losartan and Hypertrophy, Left Ventricular studies

Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
losartan : A biphenylyltetrazole where a 1,1'-biphenyl group is attached at the 5-position and has an additional trisubstituted imidazol-1-ylmethyl group at the 4'-position

Hypertrophy, Left Ventricular: Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality.

Research Excerpts

Excerpt	Relevance	Reference
"All-cause mortality was examined in relation to in-treatment digoxin use in 937 hypertensive patients with ECG left ventricular hypertrophy in atrial fibrillation at baseline (n = 134) or who developed atrial fibrillation during follow-up (n = 803), randomly assigned to losartan or atenolol-based treatment, in post-hoc analysis of a substudy of the Losartan Intervention For Endpoint Reduction in hypertension (LIFE) trial."	9.20	Digoxin use and risk of mortality in hypertensive patients with atrial fibrillation. ( Boman, K; Dahlöf, B; Devereux, RB; Hille, DA; Kjeldsen, SE; Okin, PM; Wachtell, K, 2015)
"The aim of this study was to evaluate the effects of lercanidipine or barnidipine on echocardiographic parameters, in hypertensive, type 2 diabetics with left ventricular hypertrophy."	9.20	Barnidipine or Lercanidipine on Echocardiographic Parameters in Hypertensive, Type 2 Diabetics with Left Ventricular Hypertrophy: A Randomized Clinical Trial. ( D'Angelo, A; Derosa, G; Franzetti, I; Maffioli, P; Mugellini, A; Pesce, RM; Querci, F, 2015)
"Nine hundred thirty-nine participants in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy had measurable LVM at enrolment."	9.17	Systolic left ventricular function according to left ventricular concentricity and dilatation in hypertensive patients: the Losartan Intervention For Endpoint reduction in hypertension study. ( Aurigemma, GP; Bang, CN; Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Køber, L; Roman, MJ; Wachtell, K, 2013)
"The aim of this study was to evaluate the effects of losartan on left ventricular (LV) hypertrophy and fibrosis in patients with nonobstructive hypertrophic cardiomyopathy (HCM)."	9.17	Effects of losartan on left ventricular hypertrophy and fibrosis in patients with nonobstructive hypertrophic cardiomyopathy. ( Abbara, S; Baggish, AL; Fifer, MA; Ghoshhajra, BB; Ho, CY; Januzzi, JL; Lowry, PA; O'Callaghan, C; Passeri, JJ; Rothman, RD; Seidman, CE; Shimada, YJ; Yannekis, G, 2013)
" We examined whether PP predicted new-onset AF in comparison with other blood pressure components in the Losartan Intervention For Endpoint reduction in hypertension study, a double-blind, randomized (losartan versus atenolol), parallel-group study, including 9193 patients with hypertension and electrocardiographic left ventricular hypertrophy."	9.16	Association of pulse pressure with new-onset atrial fibrillation in patients with hypertension and left ventricular hypertrophy: the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study. ( Ariansen, I; Dahlöf, B; Devereux, RB; Gjesdal, K; Ibsen, H; Kjeldsen, SE; Larstorp, AC; Okin, PM; Olsen, MH; Wachtell, K, 2012)
"This study was a prospective, randomized, open, blinded endpoint study to assess the effects of angiotensin II type 1 receptor blocker, losartan, compared with calcium channel blocker, amlodipine, on left ventricular (LV) diastolic function and atherosclerosis of the carotid artery in Japanese patients with mild-to-moderate hypertension, LV hypertrophy, diastolic dysfunction and preserved systolic function."	9.15	The effect of losartan and amlodipine on left ventricular diastolic function and atherosclerosis in Japanese patients with mild-to-moderate hypertension (J-ELAN) study. ( Akehi, N; Ebisuno, S; Fukui, S; Hori, M; Horiguchi, Y; Katsube, Y; Kobayashi, K; Kodama, M; Ohtsu, H; Ota, M; Ozaki, H; Sakai, A; Shimonagata, T; Takayasu, K; Yamamoto, K; Yamazaki, T, 2011)
"The Aliskiren in Left Ventricular Hypertrophy (ALLAY) trial randomised 465 hypertensive overweight subjects with LVH to the direct renin inhibitor aliskiren 300 mg, losartan 100 mg or the combination and followed patients for 9 months."	9.15	Suppression of aldosterone mediates regression of left ventricular hypertrophy in patients with hypertension. ( Appelbaum, E; Dahlöf, B; Desai, A; Lukashevich, V; Pouleur, AC; Prescott, MF; Smith, BA; Solomon, SD; Uno, H, 2011)
"Eight thousand one hundred ninety-four LIFE patients with hypertension and left ventricular hypertrophy with available baseline hemoglobin measurements were randomized to losartan- or atenolol-based treatment and followed for 4."	9.14	Prognostic importance of hemoglobin in hypertensive patients with electrocardiographic left ventricular hypertrophy: the Losartan Intervention For End point reduction in hypertension (LIFE) study. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Ibsen, H; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Narayan, P; Nieminen, MS; Olsen, MH; Omvik, P; Oparil, S; Wachtell, K; Wedel, H, 2009)
"We randomized 465 patients with hypertension, increased ventricular wall thickness, and body mass index >25 kg/m(2) to receive aliskiren 300 mg, losartan 100 mg, or their combination daily for 9 months."	9.14	Effect of the direct Renin inhibitor aliskiren, the Angiotensin receptor blocker losartan, or both on left ventricular mass in patients with hypertension and left ventricular hypertrophy. ( Appelbaum, E; Berglund, T; Cherif Papst, C; Dahlöf, B; Lukashevich, V; Manning, WJ; Smith, BA; Solomon, SD; Verma, A, 2009)
"ECG strain was evaluated at baseline and after 1 year of therapy in 7409 hypertensive patients in the LIFE study (Losartan Intervention For End-point reduction in hypertension) treated in a blinded manner with atenolol- or losartan-based regimens."	9.14	Prognostic value of changes in the electrocardiographic strain pattern during antihypertensive treatment: the Losartan Intervention for End-Point Reduction in Hypertension Study (LIFE). ( Dahlöf, B; Devereux, RB; Edelman, JM; Kjeldsen, SE; Nieminen, MS; Oikarinen, L; Okin, PM; Toivonen, L; Viitasalo, M, 2009)
"The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study compared effects of losartan-based versus atenolol-based therapy on cardiovascular events in 9193 patients with hypertension and LVH."	9.14	Predictors of cardiovascular events in patients with hypertension and left ventricular hypertrophy: the Losartan Intervention for Endpoint reduction in hypertension study. ( Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fyhrquist, F; Hille, DA; Ibsen, H; Julius, S; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Lyle, PA; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wedel, H, 2009)
"It is unclear whether serum uric acid (SUA) is associated with development of new-onset diabetes (NOD) in patients with hypertension and left ventricular hypertrophy (LVH)."	9.14	Serum uric acid is associated with new-onset diabetes in hypertensive patients with left ventricular hypertrophy: The LIFE Study. ( Dahlöf, B; Devereux, RB; Høieggen, A; Ibsen, H; Kjeldsen, SE; Larstorp, AC; Lindholm, L; Okin, PM; Olsen, MH; Wachtell, K; Wiik, BP, 2010)
"8 years of randomized losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint Reduction in Hypertension Echocardiography substudy."	9.13	Gender differences in left ventricular structure and function during antihypertensive treatment: the Losartan Intervention for Endpoint Reduction in Hypertension Study. ( Boman, K; Cramariuc, D; de Simone, G; Devereux, RB; Gerdts, E; Okin, PM; Wachtell, K, 2008)
" These posthoc analyses from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study evaluated losartan- versus atenolol-based therapy on the primary composite end point of cardiovascular death, stroke, and myocardial infarction and other end points in 4963 women."	9.13	Effects of losartan in women with hypertension and left ventricular hypertrophy: results from the Losartan Intervention for Endpoint Reduction in Hypertension Study. ( Dahlöf, B; Devereux, RB; Franco, V; Gerdts, E; Hille, DA; Kjeldsen, SE; Lyle, PA; Manhem, K; Okin, PM; Oparil, S; Os, I, 2008)
"Hypertensive patients with electrocardiographic-left ventricular hypertrophy were randomized to losartan-based or atenolol-based treatment and followed for 4."	9.13	Left bundle branch block and cardiovascular morbidity and mortality in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction in Hypertension study. ( Dahlöf, B; Devereux, RB; Ibsen, H; Jern, S; Kjeldsen, SE; Li, Z; Nieminen, MS; Okin, PM; Wachtell, K, 2008)
"The Losartan Intervention for Endpoint reduction in hypertension (LIFE) study demonstrated the clinical benefit of losartan-based therapy in hypertensive patients with left ventricular hypertrophy (LVH), mainly due to a highly significant 25% reduction in the relative risk of stroke compared with an atenolol-based regimen, for a similar reduction in blood pressure."	9.12	Cost-effectiveness of losartan-based therapy in patients with hypertension and left ventricular hypertrophy: a UK-based economic evaluation of the Losartan Intervention for Endpoint reduction in hypertension (LIFE) study. ( Burke, TA; Carides, G; McInnes, G, 2006)
"The Effect of Losartan and Amlodipine on Left Ventricular Diastolic Function in Patients With Mild-to-Moderate Hypertension (J-ELAN) study is a multicenter, prospective, randomized trial designed to assess the effects of losartan and amlodipine on LV diastolic function in hypertensive patients with LV diastolic dysfunction in the absence of systolic dysfunction."	9.12	Effect of losartan and amlodipine on left ventricular diastolic function in patients with mild-to-moderate hypertension (J-ELAN): rationale and design. ( , 2006)
"Our current aims were to investigate whether 1) baseline urinary albumin-to-creatinine ratio (UACR) predicted cardiovascular outcomes, 2) changes in UACR differed between treatments, 3) benefits of losartan were related to its influence on UACR, and 4) reduction in albuminuria reduced cardiovascular events."	9.12	Does albuminuria predict cardiovascular outcomes on treatment with losartan versus atenolol in patients with diabetes, hypertension, and left ventricular hypertrophy? The LIFE study. ( Borch-Johnsen, K; Dahlöf, B; Ibsen, H; Lindholm, LH; Lyle, PA; Mogensen, CE; Olsen, MH; Snapinn, SM; Wachtell, K; Wan, Y, 2006)
"In the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study, there was a 25% risk reduction for stroke with angiotensin receptor blocker-based therapy (losartan) as compared with beta-blocker-based therapy (atenolol) despite comparable blood pressure reductions."	9.12	Long-term effects of a losartan- compared with an atenolol-based treatment regimen on carotid artery plaque development in hypertensive patients with left ventricular hypertrophy: ICARUS, a LIFE substudy. ( Fossum, E; Høieggen, A; Ibsen, H; Julius, S; Kjeldsen, SE; Olsen, MH; Reims, HM; Wachtell, K; Wan, Y, 2006)
"A total of 9193 hypertensive patients (1195 with diabetes) in the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study were treated with losartan- or atenolol-based regimens and followed up with serial ECG and blood pressure determinations at baseline and 6 months and then yearly until death or study end."	9.12	Impact of diabetes mellitus on regression of electrocardiographic left ventricular hypertrophy and the prediction of outcome during antihypertensive therapy: the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study. ( Dahlöf, B; Devereux, RB; Edelman, JM; Gerdts, E; Harris, KE; Jern, S; Julius, S; Kjeldsen, SE; Lindholm, LH; Okin, PM; Snapinn, SM, 2006)
"LIFE was a randomized, double-blind trial comparing losartan-based and atenolol-based treatment regimens on the primary composite endpoint of death, myocardial infarction (MI), or stroke in 9193 patients aged 55-80 years with hypertension and left ventricular hypertrophy."	9.12	Blood pressure reduction and antihypertensive medication use in the losartan intervention for endpoint reduction in hypertension (LIFE) study in patients with hypertension and left ventricular hypertrophy. ( Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Harris, KE; Hille, DA; Ibsen, H; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Wedel, H, 2007)
"The Losartan Intervention For Endpoint reduction (LIFE) study was a randomized, doubleblind trial that compared the effects of losartan-based treatment with those of atenolol-based treatment on cardiovascular disease (CVD)-related morbidity and mortality in 9193 patients with hypertension and left-ventricular hypertrophy (LVH)."	9.12	An economic assessment of losartan-based versus atenolol-based therapy in patients with hypertension and left-ventricular hypertrophy: results from the Losartan Intervention For Endpoint reduction (LIFE) study adapted to The Netherlands. ( Atthobari, J; Boersma, C; Carides, GW; Postma, MJ; Voors, AA, 2007)
"The Losartan Intervention for Endpoint reduction in hypertension (LIFE) study was designed to compare losartan- vs atenolol-based antihypertensive treatment on cardiovascular morbidity and mortality in a population of 9193 hypertensive patients with left ventricular hypertrophy (LVH)."	9.11	Population impact of losartan use on stroke in the European Union (EU): projections from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. ( Burke, TA; Carides, GW; Dahlöf, B; Devereux, RB; Diener, HC; Edelman, JM; Krobot, K, 2004)
" We measured the QRS duration and QT intervals from the baseline 12-lead electrocardiograms in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study, which included hypertensive patients with electrocardiographic evidence of left ventricular hypertrophy randomized to either losartan-based or atenolol-based treatment to lower blood pressure."	9.11	QRS duration and QT interval predict mortality in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention for Endpoint Reduction in Hypertension Study. ( Dahlöf, B; Devereux, RB; Jern, S; Nieminen, MS; Oikarinen, L; Okin, PM; Toivonen, L; Viitasalo, M, 2004)
"To assess the influence of age on changes in left ventricular (LV) mass and geometry during antihypertensive treatment, we related age to clinical and echocardiographic findings before and after 4 years of antihypertensive treatment in a subset of 560 hypertensive patients without known concurrent disease in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which randomized patients to blinded losartan- or atenolol-based treatment."	9.11	Impact of age on left ventricular hypertrophy regression during antihypertensive treatment with losartan or atenolol (the LIFE study). ( Dahlöf, B; Devereux, RB; Gerdts, E; Nieminen, MS; Palmieri, V; Roman, MJ; Smith, G; Wachtell, K, 2004)
"To examine a possible relationship between baseline albuminuria and effect of losartan versus atenolol on cardiovascular (CV) events in hypertensive patients with left ventricular hypertrophy, the effect of losartan versus atenolol on albuminuria, and whether the benefits of losartan versus atenolol could be explained by influence of losartan on albuminuria."	9.11	Does albuminuria predict cardiovascular outcome on treatment with losartan versus atenolol in hypertension with left ventricular hypertrophy? A LIFE substudy. ( Borch-Johnsen, K; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Mogensen, CE; Nieminen, MS; Olsen, MH; Omvik, P; Oparil, S; Wachtell, K; Wan, Y, 2004)
"An echocardiographic substudy of the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial was designed to test the ability of losartan to reduce left ventricular (LV) mass more than atenolol."	9.11	Regression of hypertensive left ventricular hypertrophy by losartan compared with atenolol: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial. ( Boman, K; Dahlöf, B; Devereux, RB; Edelman, JM; Gerdts, E; Harris, KE; Nieminen, MS; Papademetriou, V; Rokkedal, J; Wachtell, K, 2004)
"The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study showed that treatment with the angiotensin II type-1 receptor antagonist losartan reduces overall stroke risk compared with conventional therapy with the beta-blocker atenolol."	9.11	Stroke reduction in hypertensive adults with cardiac hypertrophy randomized to losartan versus atenolol: the Losartan Intervention For Endpoint reduction in hypertension study. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fyhrquist, F; Harris, KE; Ibsen, H; Julius, S; Kizer, JR; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wachtell, K; Wedel, H, 2005)
"As part of the Losartan Intervention For End point reduction in hypertension (LIFE) study, 342 hypertensive patients with AF and LV hypertrophy were assigned to losartan- or atenolol-based therapy for 1,471 patient-years of follow-up."	9.11	Cardiovascular morbidity and mortality in hypertensive patients with a history of atrial fibrillation: The Losartan Intervention For End Point Reduction in Hypertension (LIFE) study. ( Aurup, P; Dahlöf, B; Devereux, RB; Gerdts, E; Hornestam, B; Ibsen, H; Julius, S; Kjeldsen, SE; Lehto, M; Lindholm, LH; Nieminen, MS; Olsen, MH; Rokkedal, J; Slotwiner, DJ; Wachtell, K, 2005)
"In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study 9,193 hypertensive patients and patients with electrocardiogram-documented left ventricular hypertrophy were randomized to once-daily losartan- or atenolol-based antihypertensive therapy."	9.11	Angiotensin II receptor blockade reduces new-onset atrial fibrillation and subsequent stroke compared to atenolol: the Losartan Intervention For End Point Reduction in Hypertension (LIFE) study. ( Dahlöf, B; Devereux, RB; Gerdts, E; Hornestam, B; Ibsen, H; Julius, S; Kjeldsen, SE; Lehto, M; Lindholm, LH; Nieminen, MS; Olsen, MH; Wachtell, K, 2005)
"We studied the impact of smoking in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which showed superiority of losartan over atenolol for reduction of composite risk of cardiovascular death, stroke and myocardial infarction in hypertensives with left ventricular hypertrophy."	9.11	Losartan benefits over atenolol in non-smoking hypertensive patients with left ventricular hypertrophy: the LIFE study. ( Beevers, G; Brady, WE; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Reims, HM; Wedel, H, 2004)
"The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study reported that a losartan-based antihypertensive regimen reduced cardiovascular morbidity and mortality (composite of cardiovascular death, stroke, and myocardial infarction) more than therapy based on atenolol in patients with left ventricular hypertrophy and isolated systolic hypertension (ISH)."	9.11	The effects of losartan compared to atenolol on stroke in patients with isolated systolic hypertension and left ventricular hypertrophy. The LIFE study. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Harris, KE; Ibsen, H; Julius, S; Kizer, JR; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Lyle, PA; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wedel, H, 2005)
"In 183 patients with hypertension and electrocardiographic left ventricular (LV) hypertrophy, enrolled in the LIFE Study, we measured BP and serum Nt-proANP and Nt-proBNP by immunoassay after 2 weeks of placebo treatment and after 1, 2, 4, 6, 12, 24, 36 and 48 months of randomized treatment with losartan- or atenolol-based antihypertensive regimens."	9.11	Opposite effects of losartan and atenolol on natriuretic peptides in patients with hypertension and left ventricular hypertrophy: a LIFE substudy. ( Bang, LE; Devereux, RB; Fossum, E; Hall, C; Hildebrandt, PR; Ibsen, H; Olsen, MH; Rokkedal, J; Tuxen, C; Wachtell, K, 2005)
" We investigated whether body build was independently associated with higher cardiovascular risk and whether treatment with losartan relative to atenolol influenced the impact of body build on the primary composite end point of cardiovascular death, stroke, and myocardial infarction and on cardiovascular death in patients with hypertension and left ventricular hypertrophy in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study."	9.11	Body build and risk of cardiovascular events in hypertension and left ventricular hypertrophy: the LIFE (Losartan Intervention For Endpoint reduction in hypertension) study. ( Beevers, G; Dahlöf, B; de Faire, U; de Simone, G; Devereux, RB; Fyhrquist, F; Hille, DA; Ibsen, H; Julius, S; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Palmieri, V; Wachtell, K, 2005)
"We explored the impact of baseline left ventricular hypertrophy (LVH) and losartan treatment on renal and cardiovascular (CV) events in 1,513 patients from the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial, which studied the effects of losartan on the progression of renal disease and/or death in patients with type 2 diabetes and nephropathy."	9.11	Adverse effects of left ventricular hypertrophy in the reduction of endpoints in NIDDM with the angiotensin II antagonist losartan (RENAAL) study. ( Boner, G; Brenner, BM; Cooper, ME; Crow, RS; de Zeeuw, D; Dickson, T; Kowey, PR; McCarroll, K; Parving, HH; Shahinfar, S, 2005)
"We conducted a subgroup analysis in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study to determine whether aspirin interacted with the properties of losartan, an angiotensin-II receptor antagonist."	9.11	The effect of losartan versus atenolol on cardiovascular morbidity and mortality in patients with hypertension taking aspirin: the Losartan Intervention for Endpoint Reduction in hypertension (LIFE) study. ( Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fossum, E; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Moan, A; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wedel, H, 2005)
"A total of 754 hypertensive patients with left ventricular hypertrophy (LVH) by Cornell voltage-duration product or Sokolow-Lyon voltage criteria on a screening electrocardiogram had their LV mass measured by echocardiogram at enrolment in the Losartan Intervention For Endpoint Reduction (LIFE) trial, and after 12 and 24 months of blinded therapy with losartan-based or atenolol-based regimens."	9.10	Progressive hypertrophy regression with sustained pressure reduction in hypertension: the Losartan Intervention For Endpoint Reduction study. ( Bella, JN; Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Liu, JE; Nieminen, MS; Palmieri, V; Papademetriou, V; Wachtell, K, 2002)
"To compare the effects of the angiotensin II antagonist, losartan, with those of atenolol on left ventricular hypertrophy (LVH), blood pressure and neurohormone concentrations in hypertensive patients with LVH."	9.10	Effects of losartan and atenolol on left ventricular mass and neurohormonal profile in patients with essential hypertension and left ventricular hypertrophy. ( Aurup, P; Barrios, V; Dahlof, B; Diez, J; Johansson, M; Nicholls, MG; Smith, RD; Yu, CM; Zanchetti, A, 2002)
"In the LIFE study, with a double-masked, randomized, parallel-group design, 9193 patients (46% men) with hypertension (mean age 67 years, average pressure 174/98 mmHg after placebo run-in) and electrocardiogram-documented left ventricular hypertrophy were randomly assigned to once-daily losartan- or atenolol-based antihypertensive treatment and followed for at least 4 years (mean 4."	9.10	Risk of new-onset diabetes in the Losartan Intervention For Endpoint reduction in hypertension study. ( Aurup, P; Beevers, G; Borch-Johnsen, K; Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Olsen, MH; Omvik, P; Oparil, S; Snapinn, S; Wachtell, K; Wedel, H, 2002)
"To test the hypothesis that losartan improves outcome better than atenolol in patients with isolated systolic hypertension and electrocardiographically documented left ventricular hypertrophy (ECG-LVH)."	9.10	Effects of losartan on cardiovascular morbidity and mortality in patients with isolated systolic hypertension and left ventricular hypertrophy: a Losartan Intervention for Endpoint Reduction (LIFE) substudy. ( Aurup, P; Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Edelman, J; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, S; Wedel, H, 2002)
" The aim of the LIFE-study was to establish whether treatment with the angiotensin-II AT 1-receptor antagonist, losartan, reduced cardiovascular events more effectively than treatment with the betablocker atenolol in patients with hypertension and left ventricular hypertrophy."	9.10	[The effect of losartan versus atenolol on cardiovascular morbidity and mortality in patients with hypertension and ECG-verified left ventricular hypertrophy in the LIFE-study]. ( Dahlöf, B; Ibsen, H; Kjeldsen, SE; Lindholm, LH; Pedersen, OL, 2003)
" Thirty chronically hemodialyzed uremic patients with hypertension were randomly assigned to receive the AT1-R antagonist losartan (n = 10), the angiotensin-converting enzyme (ACD) inhibitor enalapril (n = 10), or calcium antagonist amlodipine (n = 10)."	9.10	Angiotensin II type 1 receptor antagonist, losartan, causes regression of left ventricular hypertrophy in end-stage renal disease. ( Iwasaka, T; Masaki, H; Matsubara, H; Nishikawa, M; Nishiue, T; Shibasaki, Y, 2002)
" In an 8-week, randomized, double-blind, placebo-controlled trial in patients with mild-to-moderate hypertension, the antihypertensive effects of candesartan cilexetil 16 mg were maintained after a missed dose, whereas systolic and diastolic blood pressure increased toward baseline levels after a missed dose of losartan 100 mg."	9.09	Comparison of angiotensin II receptor blockers: impact of missed doses of candesartan cilexetil and losartan in systemic hypertension. ( Dell'Oro, R; Grassi, G; Mancia, G; Turri, C, 1999)
" After a 4-week placebo run-in period, 25 patients with mild-to-moderate essential hypertension were randomly allocated to active treatment with Losartan 50 mg titrated to Losartan 50 mg/hydrochlorothiazide (HCT) 12."	9.09	Effects of losartan titrated to Losartan/Hydrochlorothiazide and amlodipine on left ventricular mass in patients with mild-to-moderate hypertension. A double-blind randomized controlled study. ( Battegay, E; Dieterle, T; Martina, B; Weinbacher, M, 1999)
"To compare the regression of left ventricular hypertrophy in patients with moderate hypertension treated with enalapril, losartan or a combination of the two drugs at lower doses."	9.09	Reduction in left ventricular hypertrophy in hypertensive patients treated with enalapril, losartan or the combination of enalapril and losartan. ( Avanza, AC; El Aouar, LM; Mill, JG, 2000)
"The Losartan Intervention For Endpoint (LIFE) reduction in hypertension study is a double-blind, prospective, parallel-group study comparing the effects of losartan with those of atenolol on the reduction of cardiovascular complications in patients (n = 9,194) with essential hypertension and with electrocardiographically (ECG) documented left ventricular hypertrophy (LVH)."	9.09	Lowering of blood pressure and predictors of response in patients with left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint. ( Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Wedel, H, 2000)
"The Losartan Intervention For Endpoint reduction in hypertension (LIFE) trial, in which hypertensive patients with ECG LV hypertrophy (Cornell voltage-duration product, > 2440 mm x ms and/or SV1 + RV(5-6) > 38 mm) were randomized to > or = 4 years double-blinded treatment with losartan or atenolol."	9.09	Left ventricular wall stresses and wall stress-mass-heart rate products in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint reduction in hypertension. ( Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Nieminen, MS; Okin, PM; Palmieri, V; Papademetriou, V; Roman, MJ; Wachtell, K, 2000)
"Losartan reduces blood pressure in patients with essential hypertension, but the long-term central hemodynamic effects at rest and during exercise are not known."	9.09	Long-term central hemodynamic effects at rest and during exercise of losartan in essential hypertension. ( Gerdts, E; Lund-Johansen, P; Myking, OL; Omvik, P, 2000)
"The Losartan Intervention For Endpoint (LIFE) reduction in hypertension study is a double-blind, prospective, parallel group study designed to compare the effects of losartan with those of atenolol on the reduction of cardiovascular morbidity and mortality."	9.09	Baseline characteristics in relation to electrocardiographic left ventricular hypertrophy in hypertensive patients: the Losartan intervention for endpoint reduction (LIFE) in hypertension study. The Life Study Investigators. ( Dahlöf, B; Devereux, RB; Jern, S; Julius, S; Kjeldsen, SE; Okin, PM, 2000)
"The purpose of our study was to evaluate the antihypertensive efficacy, tolerability and effects on left ventricular mass of losartan over 10 months in patients with essential hypertension."	9.08	[The effectiveness and tolerability of losartan and effect on left ventricular mass in patients with essential hypertension]. ( Acitorio, M; Aquino, D; Caccavale, A; Coppolino, P; Cosimi, R; Iacono, A; Iarussi, D; Ratti, G; Rocereto, A; Tedesco, MA, 1998)
"This study evaluated the anti-hypertensive efficacy, tolerability and effects on left ventricular mass of losartan, a selective angiotensin II receptor antagonist, after 22 months in patients with essential hypertension."	9.08	Effects of losartan on hypertension and left ventricular mass: a long-term study. ( Aquino, D; di Salvo, G; Galzerano, D; Iacono, A; Iarussi, D; Limongelli, G; Mennella, S; Ratti, G; Tedesco, MA, 1998)
"-Losartan was the first available orally administered selective antagonist of the angiotensin II type 1 receptor developed for the treatment of hypertension."	9.08	Characteristics of 9194 patients with left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint Reduction in Hypertension. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Hedner, T; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Wedel, H, 1998)
" Thus, the observed outcomes benefits favoring losartan may involve other possible mechanisms, including differential effects of losartan and atenolol on LVH regression, left atrial diameter, atrial fibrillation, brain natriuretic peptide, vascular structure, thrombus formation/platelet aggregation, serum uric acid, albuminuria, new-onset diabetes, and lipid metabolism."	8.84	Potential mechanisms of stroke benefit favoring losartan in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. ( Dahlöf, B; Devereux, RB, 2007)
"Prehypertensive losartan treatment may lead to long‑term inhibition of the development of left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs)."	7.85	Hypomethylation of Agtrap is associated with long-term inhibition of left ventricular hypertrophy in prehypertensive losartan-treated spontaneously hypertensive rats. ( Lian, GL; Lin, X; Wang, HJ; Wang, TJ; Xie, LD; Xu, CS; Zhong, HB, 2017)
"This study examined the antifibrotic effect of losartan, an angiotensin II type 1 receptor antagonist, in an animal model of heart fibrosis induced by long-term intense exercise."	7.79	Losartan prevents heart fibrosis induced by long-term intensive exercise in an animal model. ( Benito, B; Brugada, J; Gay-Jordi, G; Guash, E; Mont, L; Nattel, S; Serrano-Mollar, A, 2013)
"Treatment with the selective VDR activator paricalcitol reduces myocardial fibrosis and preserves diastolic LV function due to pressure overload in a mouse model."	7.78	The vitamin D receptor activator paricalcitol prevents fibrosis and diastolic dysfunction in a murine model of pressure overload. ( Cannon, MV; de Boer, RA; Mahmud, H; Meems, LM; Ruifrok, WP; Silljé, HH; van Gilst, WH; Voors, AA, 2012)
"Treatment of hypertensive patients with a losartan-based regimen was associated with greater regression of electrocardiographic (ECG) left ventricular hypertrophy (LVH) than atenolol-based therapy in the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study, independent of blood pressure (BP) changes."	7.76	Greater regression of electrocardiographic left ventricular hypertrophy during hydrochlorothiazide therapy in hypertensive patients. ( Dahlöf, B; Devereux, RB; Edelman, JM; Hille, DA; Kjeldsen, SE; Lindholm, LH; Okin, PM, 2010)
"We examined lipid levels in the Losartan Intervention For Endpoint reduction in hypertension study and their impact on the primary composite endpoint of cardiovascular death, myocardial infarction, or stroke."	7.75	Effects of losartan compared with atenolol on lipids in patients with hypertension and left ventricular hypertrophy: the Losartan Intervention For Endpoint reduction in hypertension study. ( Beevers, G; Dahlöf, B; de Faire, U; de Simone, G; Devereux, RB; Fyhrquist, F; Ibsen, H; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Lyle, PA; Nieminen, MS; Olsen, MH; Omvik, P; Oparil, S; Wachtell, K; Wedel, H, 2009)
"To investigate the effects of losartan on left ventricular hypertrophy (LVH) and plasma transforming growth factor-beta1 (TGF-beta1) in elderly patients with essential hypertension (EH)."	7.75	[Effects of losartan on left ventricular hypertrophy and plasma transforming growth factor-beta1 in elderly patients with hypertension]. ( Bai, SC; Huang, P; Lai, WY; Li, Y; Su, L; Wu, ZL; Xu, DL, 2009)
" We prospectively compared MWS derived from linear echocardiographic dimensions with MR strain(in) in septal and posterior locations in 27 subjects with ECG LV hypertrophy in the Losartan Intervention for Endpoint Reduction in Hypertension Study."	7.74	Marked regional left ventricular heterogeneity in hypertensive left ventricular hypertrophy patients: a losartan intervention for endpoint reduction in hypertension (LIFE) cardiovascular magnetic resonance and echocardiographic substudy. ( Bella, JN; Biederman, RW; Calhoun, D; Dell'Italia, LJ; Devereux, RB; Doyle, M; Kortright, E; Oparil, S; Perry, G; Pohost, GM; Young, AA, 2008)
"Treatment of hypertensive patients with electrocardiographic left ventricular hypertrophy with losartan-based therapy is associated with lower incidence of diabetes mellitus and greater regression of hypertrophy than atenolol-based therapy."	7.74	In-treatment resolution or absence of electrocardiographic left ventricular hypertrophy is associated with decreased incidence of new-onset diabetes mellitus in hypertensive patients: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) ( Dahlöf, B; Devereux, RB; Harris, KE; Jern, S; Kjeldsen, SE; Lindholm, LH; Okin, PM, 2007)
"In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, the primary composite end point of cardiovascular death, stroke, and myocardial infarction was reduced by losartan versus atenolol in patients with hypertension and left ventricular hypertrophy."	7.73	Pulse pressure and effects of losartan or atenolol in patients with hypertension and left ventricular hypertrophy. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fyhrquist, F; Hille, DA; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Lyle, PA; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wedel, H, 2005)
"The Losartan Intervention For Endpoint reduction in hypertension study (LIFE) was a double-masked, randomized trial of losartan versus atenolol in 9193 patients with essential hypertension and left ventricular hypertrophy (LVH) ascertained by electrocardiography."	7.73	Cost effectiveness of losartan in patients with hypertension and LVH: an economic evaluation for Sweden of the LIFE trial. ( Burke, TA; Carides, GW; Dahlöf, B; Dasbach, EJ; Jönsson, B; Lindholm, LH, 2005)
" To assess the relations of LV mass and function with Hgb delivery (ie, the physiological carrier of oxygen), we calculated the product of Hgb concentration and Doppler-derived cardiac output in 864 hypertensive participants with electrocardiographic LVH (359 women) in the Losartan Intervention for End Point Reduction in Hypertension echocardiography substudy."	7.73	Association of hemoglobin delivery with left ventricular structure and function in hypertensive patients: Losartan Intervention for End Point Reduction in Hypertension Study. ( Boman, K; Dahlöf, B; de Simone, G; Devereux, RB; Fyhrquist, F; Gerdts, E; Hoieggen, A; Narayan, P; Nieminen, MS; Papademetriou, V; Wachtell, K, 2006)
"The LIFE (Losartan Intervention For Endpoint reduction in hypertension) study demonstrated a 13% relative risk reduction in the primary composite endpoint (myocardial infarction, stroke or death) for patients with hypertension and electrocardiographically diagnosed left ventricular hypertrophy (LVH) treated with losartan compared with atenolol."	7.73	A cost-utility analysis of losartan versus atenolol in the treatment of hypertension with left ventricular hypertrophy. ( Anis, AH; Brisson, M; Nosyk, B; Singh, S; Sun, H; Woolcott, J, 2006)
"Twenty four hour blood pressure (BP) monitoring was carried out and structural state of left ventricular myocardium assessed in 20 patients with mild and moderate hypertension before and after 24 weeks of therapy with Hyzaar - fixed dose combination of losartan (50 mg) and hydrochlorothiazide (12."	7.72	[Therapy of patients with arterial hypertension with fixed dose combination of losartan and hydrochlorothiazide. Effect on 24 hour blood pressure and left-ventricular hypertrophy]. ( Chazova, IE; Dmitriev, VV; Ratova, LG; Sinitsin, VE; Stukalova, OV, 2003)
"The Losartan Intervention For Endpoint Reduction (LIFE) study demonstrated a clear mortality benefit in treating hypertensive patients with electrocardiogram (ECG) evidence of left ventricular hypertrophy (LVH) with losartan rather than atenolol."	7.72	How much echo left ventricular hypertrophy would be missed in diabetics by applying the Losartan Intervention For Endpoint Reduction electrocardiogram criteria to select patients for angiotensin receptor blockade? ( Dawson, A; Donnelly, LA; Morris, AD; Pringle, SD; Rana, BS; Struthers, AD, 2004)
"To investigate the different effects of an angiotensin II type 1 (AT(1)) receptor antagonist, losartan, and an angiotensin converting enzyme (ACE) inhibitor, fosinopril, on cardiomyocyte apoptosis, myocardial fibrosis, and angiotensin II (Ang II) in the left ventricle of spontaneously hypertensive rats (SHRs)."	7.71	Apoptosis, myocardial fibrosis and angiotensin II in the left ventricle of hypertensive rats treated with fosinopril or losartan. ( Liang, X; Sun, M; Xie, X; Yang, T; Yu, G; Zhao, S, 2002)
"We studied the effects of chronic losartan (Los) treatment on contractile function of isolated right ventricular (RV) trabeculae from rat hearts 12 wk after left ventricular (LV) myocardial infarction (MI) had been induced by ligation of the left anterior descending artery at 4 wk of age."	7.71	Losartan prevents contractile dysfunction in rat myocardium after left ventricular myocardial infarction. ( Daniëls, MC; de Tombe, PP; Keller, RS, 2001)
" ECG LVH by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria was used to select patients for the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study."	7.70	Effect of obesity on electrocardiographic left ventricular hypertrophy in hypertensive patients : the losartan intervention for endpoint (LIFE) reduction in hypertension study. ( Dahlöf, B; Devereux, RB; Jern, S; Kjeldsen, SE; Okin, PM, 2000)
"Losartan, a recently developed nonpeptide angiotensin II (AII) receptor antagonist, was orally administered for 14 days to mice with viral myocarditis, beginning 7 days after encephalomyocarditis virus inoculation."	7.69	Comparative effects of losartan, captopril, and enalapril on murine acute myocarditis due to encephalomyocarditis virus. ( Araki, M; Imai, S; Kanda, T; Kobayashi, I; Murata, K; Suzuki, T, 1995)
" These results suggest that inhibition of generation of angiotensin II and AT1 receptor blockade are equally effective in preventing important features of ventricular remodeling after myocardial infarction."	7.69	Comparative effects of chronic angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade on cardiac remodeling after myocardial infarction in the rat. ( Drexler, H; Holtz, J; Meybrunn, M; Riede, UN; Schieffer, B; Seitz, S; Wirger, A, 1994)
"Psoriasis has a similar prevalence in hypertensive patients as in the general population."	6.79	Psoriasis is associated with subsequent atrial fibrillation in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint study. ( Bang, CN; Devereux, RB; Gottlieb, AB; Køber, L; Okin, PM; Wachtell, K, 2014)
"Losartan treatment was associated with preserved fibrinolytic balance compared to a more prothrombotic fibrinolytic and hemostatic state in the atenolol group."	6.75	Effects of atenolol or losartan on fibrinolysis and von Willebrand factor in hypertensive patients with left ventricular hypertrophy. ( Andersson, J; Boman, JH; Boman, K; Dahlöf, B; Olofsson, M, 2010)
"Electrocardiographic left ventricular hypertrophy (LVH) predicts cardiovascular morbidity and mortality, and regression of ECG LVH may predict improved prognosis in hypertensive patients."	6.71	Regression of electrocardiographic left ventricular hypertrophy by losartan versus atenolol: The Losartan Intervention for Endpoint reduction in Hypertension (LIFE) Study. ( Aurup, P; Dahlof, B; Devereux, RB; Edelman, JM; Harris, KE; Jern, S; Julius, S; Kjeldsen, SE; Nieminen, MS; Okin, PM; Snapinn, S, 2003)
"Hypertension is a major risk factor for morbidity and mortality."	6.71	Long-term plasma catecholamines in patients with hypertension and left ventricular hypertrophy treated with losartan or atenolol: ICARUS, a LIFE substudy. ( Fossum, E; Høieggen, A; Ibsen, H; Julius, S; Kjeldsen, SE; Olsen, MH; Reims, HM; Wachtell, K, 2004)
"In hypertensive left ventricular hypertrophy (LVH), myocardial texture is altered by a disproportionate increase in fibrosis, but there is insufficient clinical evidence whether antihypertensive therapy or individual agents can induce regression of myocardial fibrosis."	6.71	Different effects of antihypertensive therapies based on losartan or atenolol on ultrasound and biochemical markers of myocardial fibrosis: results of a randomized trial. ( Ciulla, MM; Dahlöf, B; Dìez, J; Esposito, A; Gilles, L; López, B; Magrini, F; Nicholls, MG; Paliotti, R; Smith, RD; Zanchetti, A, 2004)
"Patients with hypertension have different types of left ventricular (LV) geometry, but the impact of blood pressure (BP) reduction on LV geometry change during antihypertensive treatment remains unclear."	6.70	Change of left ventricular geometric pattern after 1 year of antihypertensive treatment: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. ( Bella, JN; Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Nieminen, MS; Papademetriou, V; Rokkedal, J; Smith, G; Wachtell, K, 2002)
"Losartan/HCTZ is an effective combination therapy, lowering blood pressure (BP) to a greater extent than losartan or HCTZ alone in patients with hypertension."	6.45	Losartan/Hydrochlorothiazide: a review of its use in the treatment of hypertension and for stroke risk reduction in patients with hypertension and left ventricular hypertrophy. ( Keating, GM, 2009)
"Losartan (Cozaar) is an angiotensin AT1 receptor antagonist."	6.43	Losartan: a review of its use in stroke risk reduction in patients with hypertension and left ventricular hypertrophy. ( Moen, MD; Wagstaff, AJ, 2005)
"Losartan 50-100 mg/day was compared with atenolol 50-100 mg/day in patients with essential hypertension and left ventricular hypertrophy (LVH) [n = 9,193] in the randomized, double-blind Losartan Intervention For Endpoint reduction in hypertension (LIFE) study."	6.42	Losartan: in the reduction of stroke risk in patients with hypertension and left ventricular hypertrophy. ( Keating, GM; Waugh, J, 2003)
"Losartan is an orally active, selective, nonpeptide, angiotensin-II Type I-receptor antagonist, and was the first drug marketed in this class."	6.42	Losartan for the treatment of hypertension and left ventricular hypertrophy: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. ( Devereux, RB; Lyle, PA, 2004)
"The renin-angiotensin system, through the effects of angiotensin II, may be involved in the pathogenesis of essential hypertension and associated left ventricular hypertrophy."	6.18	[Losartan and the LIFE-study. Antihypertensive treatment with AT1-receptor antagonist]. ( Kjeldsen, SE; Omvik, P, 1996)
"Losartan treatment decreased systolic pressure and yellow-red collagen fiber content in all areas, whereas spironolactone treatment decreased green collagen fiber content without decreasing systolic pressure."	5.29	Left ventricular fibrosis in renovascular hypertensive rats. Effect of losartan and spironolactone. ( Appay, MD; Bariety, J; Heudes, D; Hinglais, N; Michel, JB; Nicoletti, A; Philippe, M; Sassy-Prigent, C, 1995)
"9 years follow-up in 9193 patients with hypertension randomized to losartan- or atenolol-based regimens."	5.24	Combining ECG Criteria for Left Ventricular Hypertrophy Improves Risk Prediction in Patients With Hypertension. ( Devereux, RB; Hille, DA; Kjeldsen, SE; Okin, PM, 2017)
"Baseline estimated GFR (eGFR) and change in eGFR during follow-up were examined in relation to average on-treatment SBP in 8778 hypertensive patients with ECG left ventricular hypertrophy (LVH) randomly assigned to losartan- or atenolol-based treatment."	5.22	Impact of achieved systolic blood pressure on renal function in hypertensive patients. ( Devereux, RB; Kjeldsen, SE; Okin, PM, 2016)
"All-cause mortality was examined in relation to in-treatment digoxin use in 937 hypertensive patients with ECG left ventricular hypertrophy in atrial fibrillation at baseline (n = 134) or who developed atrial fibrillation during follow-up (n = 803), randomly assigned to losartan or atenolol-based treatment, in post-hoc analysis of a substudy of the Losartan Intervention For Endpoint Reduction in hypertension (LIFE) trial."	5.20	Digoxin use and risk of mortality in hypertensive patients with atrial fibrillation. ( Boman, K; Dahlöf, B; Devereux, RB; Hille, DA; Kjeldsen, SE; Okin, PM; Wachtell, K, 2015)
" The risk of new-onset AF was examined in relation to last in-treatment SBP before AF diagnosis or last in-study measurement in the absence of new AF in 8831 hypertensive patients with ECG left ventricular hypertrophy with no history of AF, in sinus rhythm on their baseline ECG, randomly assigned to losartan- or atenolol-based treatment."	5.20	Effect of lower on-treatment systolic blood pressure on the risk of atrial fibrillation in hypertensive patients. ( Dahlöf, B; Devereux, RB; Hille, DA; Kjeldsen, SE; Larstorp, AC; Okin, PM; Wachtell, K, 2015)
"The aim of this study was to evaluate the effects of lercanidipine or barnidipine on echocardiographic parameters, in hypertensive, type 2 diabetics with left ventricular hypertrophy."	5.20	Barnidipine or Lercanidipine on Echocardiographic Parameters in Hypertensive, Type 2 Diabetics with Left Ventricular Hypertrophy: A Randomized Clinical Trial. ( D'Angelo, A; Derosa, G; Franzetti, I; Maffioli, P; Mugellini, A; Pesce, RM; Querci, F, 2015)
" atenolol-based treatment in the LIFE study, we tested whether BP variability assessed as SD and range for BP6-24 months measured at 6, 12, 18 and 24 months of treatment was associated with target organ damage (TOD) defined by LVH on ECG and urine albumin/creatinine ratio at 24 months, and predicted the composite endpoint (CEP) of cardiovascular death, nonfatal myocardial infarction (MI) or stroke occurring after 24 months (CEP = 630 events)."	5.20	Blood pressure variability predicts cardiovascular events independently of traditional cardiovascular risk factors and target organ damage: a LIFE substudy. ( Dahlöf, B; Devereux, RB; Ibsen, H; Kjeldsen, SE; Lindholm, LH; Mancia, G; Okin, PM; Olsen, MH; Rothwell, PM; Vishram, JK; Wachtell, K, 2015)
"8 years' losartan- versus atenolol-based antihypertensive treatment reduced left ventricular hypertrophy and cardiovascular end points, including cardiovascular death and stroke."	5.20	Left Ventricular Wall Stress-Mass-Heart Rate Product and Cardiovascular Events in Treated Hypertensive Patients: LIFE Study. ( Bang, CN; Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Hille, DA; Nieminen, MS; Palmieri, V; Papademetriou, V; Roman, MJ; Wachtell, K, 2015)
"Incident AF was examined in 518 black and 8,313 nonblack hypertensive patients with electrocardiographic left ventricular hypertrophy (LVH) with no history of AF in sinus rhythm on their baseline electrocardiogram, who were randomly assigned to losartan- or atenolol-based treatment."	5.19	Racial differences in incident atrial fibrillation among hypertensive patients during antihypertensive therapy. ( Bang, CN; Dahlöf, B; Devereux, RB; Hille, DA; Julius, S; Kjeldsen, SE; Okin, PM; Wachtell, K, 2014)
"8 years randomized losartan- or atenolol-based antihypertensive treatment in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study and classified as having ISH (n = 128) if systolic BP ≥ 160 mmHg and diastolic BP < 90 mmHg, or non-ISH divided into two groups by systolic BP ≥ 160 mmHg (non-ISH ≥ 160 mmHg) (n = 645) and systolic BP < 160 mm Hg (n = 100) (non-ISH < 160 mmHg), respectively."	5.19	Impact of isolated systolic hypertension on normalization of left ventricular structure during antihypertensive treatment (the LIFE study). ( Abdelhai, YM; Boman, K; Dahlöf, B; De Simone, G; Devereux, RB; Gerdts, E; Lønnebakken, MT; Mancusi, C; Wachtell, K, 2014)
"The relationship of SCD to new-onset AF was evaluated in 8831 hypertensive patients with electrocardiographic left ventricular hypertrophy with no history of AF, in sinus rhythm on their baseline electrocardiogram, randomly assigned to losartan- or atenolol-based treatment."	5.17	Relationship of sudden cardiac death to new-onset atrial fibrillation in hypertensive patients with left ventricular hypertrophy. ( Bang, CN; Dahlöf, B; Devereux, RB; Hille, DA; Kjeldsen, SE; Okin, PM; Wachtell, K, 2013)
" In multivariable Cox analyses, adjusting for randomized treatment, age, sex, race, prior anti-hypertensive therapy, baseline uric acid, serum creatinine and glucose entered as standard covariates, and in-treatment non-HDL cholesterol, Cornell product left ventricular hypertrophy, diastolic and systolic pressure, BMI, hydrochlorothiazide and statin use as time-varying covariates, the lowest quartile of in-treatment HDL remained associated with a nearly 9-fold increased risk of new diabetes (hazard ratio 8."	5.17	In-treatment HDL cholesterol levels and development of new diabetes mellitus in hypertensive patients: the LIFE Study. ( Dahlöf, B; Devereux, RB; Hille, DA; Kjeldsen, SE; Lindholm, LH; Okin, PM; Wiik, BP, 2013)
"Nine hundred thirty-nine participants in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy had measurable LVM at enrolment."	5.17	Systolic left ventricular function according to left ventricular concentricity and dilatation in hypertensive patients: the Losartan Intervention For Endpoint reduction in hypertension study. ( Aurigemma, GP; Bang, CN; Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Køber, L; Roman, MJ; Wachtell, K, 2013)
"The aim of this study was to evaluate the effects of losartan on left ventricular (LV) hypertrophy and fibrosis in patients with nonobstructive hypertrophic cardiomyopathy (HCM)."	5.17	Effects of losartan on left ventricular hypertrophy and fibrosis in patients with nonobstructive hypertrophic cardiomyopathy. ( Abbara, S; Baggish, AL; Fifer, MA; Ghoshhajra, BB; Ho, CY; Januzzi, JL; Lowry, PA; O'Callaghan, C; Passeri, JJ; Rothman, RD; Seidman, CE; Shimada, YJ; Yannekis, G, 2013)
"8 years randomized treatment in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy."	5.17	Impact of overweight and obesity on cardiac benefit of antihypertensive treatment. ( Boman, K; Dahlöf, B; de Simone, G; Devereux, RB; Gerdts, E; Lund, BP; Nieminen, MS; Okin, PM; Wachtell, K, 2013)
"To compare the effects of losartan and amlodipine on myocardial structure and function in hypertensive patients with Type 2 diabetes and left ventricular hypertrophy."	5.16	Losartan and amlodipine on myocardial structure and function: a prospective, randomized, clinical trial. ( Corradi, L; Derosa, G; Destro, M; Fogari, R; Lazzari, P; Mugellini, A; Preti, P; Zoppi, A, 2012)
"In the Losartan Intervention For Endpoint reduction in Hypertension (LIFE) study, a double-blinded, randomized, parallel-group study, 9193 hypertensive patients with electrocardiogram (ECG)-documented left ventricular hypertrophy (LVH), randomized to once-daily losartan- or atenolol-based antihypertensive therapy were followed for a mean of 4."	5.16	Impact of alcohol habits and smoking on the risk of new-onset atrial fibrillation in hypertensive patients with ECG left ventricular hypertrophy: the LIFE study. ( Ariansen, I; Dahlöf, B; Devereux, RB; Gjesdal, K; Ibsen, H; Kjeldsen, SE; Okin, PM; Olsen, MH; Reims, HM; Wachtell, K, 2012)
"HYPOTHESIS/ INTRODUCTION: We investigated whether diabetes modified the effectiveness of renin-angiotensin-aldosterone system (RAAS) inhibition on left ventricular hypertrophy (LVH) regression in hypertensive patients in the Aliskiren in Left Ventricular Hypertrophy (ALLAY) trial."	5.16	Influence of diabetes on efficacy of aliskiren, losartan or both on left ventricular mass regression. ( Appelbaum, E; Dahlof, B; Pouleur, AC; Prescott, M; Smith, B; Solomon, SD; Takeuchi, M; Vardeny, O; Verma, A, 2012)
" We sought to determine, in a pre-dialysis cohort on atenolol, whether Losartan might attenuate left ventricular hypertrophy post arteriovenous fistula creation in end stage kidney disease."	5.16	Can losartan and blood pressure control peri arteriovenous fistula creation ameliorate the early associated left ventricular hypertrophic response a randomised placebo controlled trial. ( Aggarwal, A; Alexiou, A; Karapanagiotidis, S; Kinghorn, A; Lee, G; Pedagogos, E; Raspudic, M; Yapanis, A; Zentner, D, 2012)
"Data from all patients with at least two echocardiographic examinations in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) echocardiographic substudy (n = 801); high-risk patients on losartan- vs."	5.16	Contrasting hemodynamic mechanisms of losartan- vs. atenolol-based antihypertensive treatment: a LIFE study. ( Bella, JN; Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Greve, AM; Lønnebakken, MT; Nieminen, MS; Okin, PM; Olsen, MH; Omvik, P; Palmieri, V; Wachtell, K, 2012)
"A total of 9,027 patients with hypertension and ECG-LVH and without a history of HF were randomized to losartan- or atenolol-based treatment in the Losartan Intervention For Endpoint reduction in hypertension study."	5.16	Regression of ECG-LVH is associated with lower risk of new-onset heart failure and mortality in patients with isolated systolic hypertension; The LIFE study. ( Dahlöf, B; Devereux, RB; Ibsen, H; Kjeldsen, SE; Larstorp, AC; Okin, PM; Olsen, MH; Wachtell, K, 2012)
" We examined whether PP predicted new-onset AF in comparison with other blood pressure components in the Losartan Intervention For Endpoint reduction in hypertension study, a double-blind, randomized (losartan versus atenolol), parallel-group study, including 9193 patients with hypertension and electrocardiographic left ventricular hypertrophy."	5.16	Association of pulse pressure with new-onset atrial fibrillation in patients with hypertension and left ventricular hypertrophy: the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study. ( Ariansen, I; Dahlöf, B; Devereux, RB; Gjesdal, K; Ibsen, H; Kjeldsen, SE; Larstorp, AC; Okin, PM; Olsen, MH; Wachtell, K, 2012)
"This study was a prospective, randomized, open, blinded endpoint study to assess the effects of angiotensin II type 1 receptor blocker, losartan, compared with calcium channel blocker, amlodipine, on left ventricular (LV) diastolic function and atherosclerosis of the carotid artery in Japanese patients with mild-to-moderate hypertension, LV hypertrophy, diastolic dysfunction and preserved systolic function."	5.15	The effect of losartan and amlodipine on left ventricular diastolic function and atherosclerosis in Japanese patients with mild-to-moderate hypertension (J-ELAN) study. ( Akehi, N; Ebisuno, S; Fukui, S; Hori, M; Horiguchi, Y; Katsube, Y; Kobayashi, K; Kodama, M; Ohtsu, H; Ota, M; Ozaki, H; Sakai, A; Shimonagata, T; Takayasu, K; Yamamoto, K; Yamazaki, T, 2011)
"The Aliskiren in Left Ventricular Hypertrophy (ALLAY) trial randomised 465 hypertensive overweight subjects with LVH to the direct renin inhibitor aliskiren 300 mg, losartan 100 mg or the combination and followed patients for 9 months."	5.15	Suppression of aldosterone mediates regression of left ventricular hypertrophy in patients with hypertension. ( Appelbaum, E; Dahlöf, B; Desai, A; Lukashevich, V; Pouleur, AC; Prescott, MF; Smith, BA; Solomon, SD; Uno, H, 2011)
"The Telmisartan and Losartan Cardiac Evaluation Trial, a multicenter, prospective, randomized, open-labeled, blinded-endpoint trial, was designed to compare the effects of two angiotensin II receptor blockers (ARBs), telmisartan and losartan, on cardiovascular protection in Japanese patients with mild to moderate essential hypertension."	5.15	Effects of telmisartan and losartan on cardiovascular protection in Japanese hypertensive patients. ( Hasegawa, H; Kobayashi, Y; Komuro, I; Mizuguchi, T; Namiki, T; Narumi, H; Ohtsuka, M; Takano, H, 2011)
"Eight thousand one hundred ninety-four LIFE patients with hypertension and left ventricular hypertrophy with available baseline hemoglobin measurements were randomized to losartan- or atenolol-based treatment and followed for 4."	5.14	Prognostic importance of hemoglobin in hypertensive patients with electrocardiographic left ventricular hypertrophy: the Losartan Intervention For End point reduction in hypertension (LIFE) study. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Ibsen, H; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Narayan, P; Nieminen, MS; Olsen, MH; Omvik, P; Oparil, S; Wachtell, K; Wedel, H, 2009)
"We randomized 465 patients with hypertension, increased ventricular wall thickness, and body mass index >25 kg/m(2) to receive aliskiren 300 mg, losartan 100 mg, or their combination daily for 9 months."	5.14	Effect of the direct Renin inhibitor aliskiren, the Angiotensin receptor blocker losartan, or both on left ventricular mass in patients with hypertension and left ventricular hypertrophy. ( Appelbaum, E; Berglund, T; Cherif Papst, C; Dahlöf, B; Lukashevich, V; Manning, WJ; Smith, BA; Solomon, SD; Verma, A, 2009)
"ECG strain was evaluated at baseline and after 1 year of therapy in 7409 hypertensive patients in the LIFE study (Losartan Intervention For End-point reduction in hypertension) treated in a blinded manner with atenolol- or losartan-based regimens."	5.14	Prognostic value of changes in the electrocardiographic strain pattern during antihypertensive treatment: the Losartan Intervention for End-Point Reduction in Hypertension Study (LIFE). ( Dahlöf, B; Devereux, RB; Edelman, JM; Kjeldsen, SE; Nieminen, MS; Oikarinen, L; Okin, PM; Toivonen, L; Viitasalo, M, 2009)
"A total of 937 hypertensive patients with ECG LVH were studied by echocardiography in the Losartan Intervention For Endpoint reduction in hypertension study."	5.14	Exercise and cardiovascular outcomes in hypertensive patients in relation to structure and function of left ventricular hypertrophy: the LIFE study. ( Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Nieminen, MS; Olofsson, M; Papademetriou, V; Wachtell, K, 2009)
"8 years of randomized losartan- or atenolol-based treatment within the echocardiographic substudy of the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study."	5.14	Pulse pressure, left ventricular function and cardiovascular events during antihypertensive treatment (the LIFE study). ( Dahlöf, B; Devereux, RB; Franklin, S; Gerdts, E; Nieminen, M; Papademetriou, V; Rieck, A; Wachtell, K, 2009)
"The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study compared effects of losartan-based versus atenolol-based therapy on cardiovascular events in 9193 patients with hypertension and LVH."	5.14	Predictors of cardiovascular events in patients with hypertension and left ventricular hypertrophy: the Losartan Intervention for Endpoint reduction in hypertension study. ( Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fyhrquist, F; Hille, DA; Ibsen, H; Julius, S; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Lyle, PA; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wedel, H, 2009)
"This pharmacogenetics substudy from the Losartan Intervention for Endpoint reduction in Hypertension study in patients with hypertension and left ventricular hypertrophy (LVH) treated with the angiotensin receptor blocker losartan versus the beta-blocker atenolol for 4."	5.14	Effect of ACE insertion/deletion and 12 other polymorphisms on clinical outcomes and response to treatment in the LIFE study. ( Benn, M; Berg, K; Dahlöf, B; de Faire, U; Edelman, JM; Eliasson, E; Fyhrquist, F; Hille, DA; Ibsen, H; Kontula, K; Lyle, PA; Nordestgaard, BG; Os, I; Sandberg, M; Sethi, AA; Wong, PH, 2010)
"It is unclear whether serum uric acid (SUA) is associated with development of new-onset diabetes (NOD) in patients with hypertension and left ventricular hypertrophy (LVH)."	5.14	Serum uric acid is associated with new-onset diabetes in hypertensive patients with left ventricular hypertrophy: The LIFE Study. ( Dahlöf, B; Devereux, RB; Høieggen, A; Ibsen, H; Kjeldsen, SE; Larstorp, AC; Lindholm, L; Okin, PM; Olsen, MH; Wachtell, K; Wiik, BP, 2010)
"In this study, effective BP control was obtained with losartan and ramipril and LVH was found to be regressed significantly in the hypertensive patients with ADPKD."	5.14	A comparison of the effects of ramipril and losartan on blood pressure control and left ventricle hypertrophy in patients with autosomal dominant polycystic kidney disease. ( Kaynar, K; Kiriş, A; Koşucu, P; Orem, C; Ozkan, G; Ulusoy, S, 2010)
" Patients were treated with losartan- or atenolol-based regimens and followed with serial ECGs annually which were used to determine HR and ECG left ventricular hypertrophy by Cornell product and Sokolow-Lyon voltage criteria."	5.13	Incidence of atrial fibrillation in relation to changing heart rate over time in hypertensive patients: the LIFE study. ( Dahlöf, B; Devereux, RB; Edelman, JM; Hille, DA; Julius, S; Kjeldsen, SE; Lindholm, LH; Nieminen, MS; Okin, PM; Wachtell, K, 2008)
"The relation of ECG strain and albuminuria to new-onset HF was examined in 7,786 hypertensive patients with no history of HF, who were randomly assigned to treatment with losartan or atenolol."	5.13	Combination of the electrocardiographic strain pattern and albuminuria for the prediction of new-onset heart failure in hypertensive patients: the LIFE study. ( Borch-Johnsen, K; Dahlöf, B; Devereux, RB; Ibsen, H; Julius, S; Kjeldsen, SE; Lindholm, LH; Nieminen, MS; Oikarinen, L; Okin, PM; Olsen, MH; Toivonen, L; Viitasalo, M; Wachtell, K, 2008)
"8 years of randomized losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint Reduction in Hypertension Echocardiography substudy."	5.13	Gender differences in left ventricular structure and function during antihypertensive treatment: the Losartan Intervention for Endpoint Reduction in Hypertension Study. ( Boman, K; Cramariuc, D; de Simone, G; Devereux, RB; Gerdts, E; Okin, PM; Wachtell, K, 2008)
" These posthoc analyses from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study evaluated losartan- versus atenolol-based therapy on the primary composite end point of cardiovascular death, stroke, and myocardial infarction and other end points in 4963 women."	5.13	Effects of losartan in women with hypertension and left ventricular hypertrophy: results from the Losartan Intervention for Endpoint Reduction in Hypertension Study. ( Dahlöf, B; Devereux, RB; Franco, V; Gerdts, E; Hille, DA; Kjeldsen, SE; Lyle, PA; Manhem, K; Okin, PM; Oparil, S; Os, I, 2008)
" We examined whether 'in-treatment' wall motion abnormalities predicted outcome in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension echocardiographic substudy."	5.13	Clinical impact of 'in-treatment' wall motion abnormalities in hypertensive patients with left ventricular hypertrophy: the LIFE study. ( Boman, K; Cicala, S; Dahlöf, B; de Simone, G; Devereux, RB; Gerdts, E; Nieminen, MS; Wachtell, K, 2008)
"Hypertensive patients with electrocardiographic-left ventricular hypertrophy were randomized to losartan-based or atenolol-based treatment and followed for 4."	5.13	Left bundle branch block and cardiovascular morbidity and mortality in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction in Hypertension study. ( Dahlöf, B; Devereux, RB; Ibsen, H; Jern, S; Kjeldsen, SE; Li, Z; Nieminen, MS; Okin, PM; Wachtell, K, 2008)
"The Losartan Intervention for Endpoint reduction in hypertension (LIFE) study demonstrated the clinical benefit of losartan-based therapy in hypertensive patients with left ventricular hypertrophy (LVH), mainly due to a highly significant 25% reduction in the relative risk of stroke compared with an atenolol-based regimen, for a similar reduction in blood pressure."	5.12	Cost-effectiveness of losartan-based therapy in patients with hypertension and left ventricular hypertrophy: a UK-based economic evaluation of the Losartan Intervention for Endpoint reduction in hypertension (LIFE) study. ( Burke, TA; Carides, G; McInnes, G, 2006)
"The Effect of Losartan and Amlodipine on Left Ventricular Diastolic Function in Patients With Mild-to-Moderate Hypertension (J-ELAN) study is a multicenter, prospective, randomized trial designed to assess the effects of losartan and amlodipine on LV diastolic function in hypertensive patients with LV diastolic dysfunction in the absence of systolic dysfunction."	5.12	Effect of losartan and amlodipine on left ventricular diastolic function in patients with mild-to-moderate hypertension (J-ELAN): rationale and design. ( , 2006)
"Our current aims were to investigate whether 1) baseline urinary albumin-to-creatinine ratio (UACR) predicted cardiovascular outcomes, 2) changes in UACR differed between treatments, 3) benefits of losartan were related to its influence on UACR, and 4) reduction in albuminuria reduced cardiovascular events."	5.12	Does albuminuria predict cardiovascular outcomes on treatment with losartan versus atenolol in patients with diabetes, hypertension, and left ventricular hypertrophy? The LIFE study. ( Borch-Johnsen, K; Dahlöf, B; Ibsen, H; Lindholm, LH; Lyle, PA; Mogensen, CE; Olsen, MH; Snapinn, SM; Wachtell, K; Wan, Y, 2006)
"In the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study, there was a 25% risk reduction for stroke with angiotensin receptor blocker-based therapy (losartan) as compared with beta-blocker-based therapy (atenolol) despite comparable blood pressure reductions."	5.12	Long-term effects of a losartan- compared with an atenolol-based treatment regimen on carotid artery plaque development in hypertensive patients with left ventricular hypertrophy: ICARUS, a LIFE substudy. ( Fossum, E; Høieggen, A; Ibsen, H; Julius, S; Kjeldsen, SE; Olsen, MH; Reims, HM; Wachtell, K; Wan, Y, 2006)
"A total of 9193 hypertensive patients (1195 with diabetes) in the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study were treated with losartan- or atenolol-based regimens and followed up with serial ECG and blood pressure determinations at baseline and 6 months and then yearly until death or study end."	5.12	Impact of diabetes mellitus on regression of electrocardiographic left ventricular hypertrophy and the prediction of outcome during antihypertensive therapy: the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study. ( Dahlöf, B; Devereux, RB; Edelman, JM; Gerdts, E; Harris, KE; Jern, S; Julius, S; Kjeldsen, SE; Lindholm, LH; Okin, PM; Snapinn, SM, 2006)
"Double-blind, randomized, parallel-group study conducted in 1995-2001 among 8831 men and women with hypertension, aged 55-80 years (median, 67 years), with electrocardiographic LVH by Cornell voltage-duration product or Sokolow-Lyon voltage, with no history of AF, without AF on the baseline electrocardiogram, and enrolled in the Losartan Intervention for Endpoint Reduction in Hypertension Study."	5.12	Regression of electrocardiographic left ventricular hypertrophy and decreased incidence of new-onset atrial fibrillation in patients with hypertension. ( Dahlöf, B; Devereux, RB; Edelman, JM; Harris, KE; Hille, DA; Jern, S; Julius, S; Kjeldsen, SE; Lindholm, LH; Nieminen, MS; Okin, PM; Wachtell, K, 2006)
"In 204 patients with hypertension and left ventricular (LV) hypertrophy we measured serum concentration of carboxy-terminal telopeptide of type I procollagen (ICTP), carboxy-terminal propeptide of type I procollagen (PICP), amino-terminal propeptide of type III procollagen (PIIINP), amino-terminal propeptide of type I procollagen (PINP) and LV mass by echocardiography at baseline and annually during 4 years of losartan- or atenolol-based antihypertensive treatment; 185 patients completed the study."	5.12	Does long-term losartan- vs atenolol-based antihypertensive treatment influence collagen markers differently in hypertensive patients? A LIFE substudy. ( Bang, LE; Christensen, MK; Devereux, RB; Fossum, E; Hildebrandt, P; Ibsen, H; Kjeldsen, SE; Olsen, MH; Rokkedal, J; Tuxen, C; Wachtell, K; Wiinberg, N, 2006)
"LIFE was a randomized, double-blind trial comparing losartan-based and atenolol-based treatment regimens on the primary composite endpoint of death, myocardial infarction (MI), or stroke in 9193 patients aged 55-80 years with hypertension and left ventricular hypertrophy."	5.12	Blood pressure reduction and antihypertensive medication use in the losartan intervention for endpoint reduction in hypertension (LIFE) study in patients with hypertension and left ventricular hypertrophy. ( Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Harris, KE; Hille, DA; Ibsen, H; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Wedel, H, 2007)
"The Losartan Intervention for End Point Reduction in Hypertension (LIFE) study included 9193 patients 55 to 80 years of age with essential hypertension and ECG LV hypertrophy by gender-adjusted Cornell product (CP) (RaVL+SV(3) [+6 mm in women])."	5.12	Regression of electrocardiographic left ventricular hypertrophy during antihypertensive therapy and reduction in sudden cardiac death: the LIFE Study. ( Dahlöf, B; Devereux, RB; Ibsen, H; Kjeldsen, SE; Lindholm, LH; Nieminen, MS; Okin, PM; Olsen, MH; Thygesen, K; Wachtell, K, 2007)
"The Losartan Intervention For Endpoint reduction (LIFE) study was a randomized, doubleblind trial that compared the effects of losartan-based treatment with those of atenolol-based treatment on cardiovascular disease (CVD)-related morbidity and mortality in 9193 patients with hypertension and left-ventricular hypertrophy (LVH)."	5.12	An economic assessment of losartan-based versus atenolol-based therapy in patients with hypertension and left-ventricular hypertrophy: results from the Losartan Intervention For Endpoint reduction (LIFE) study adapted to The Netherlands. ( Atthobari, J; Boersma, C; Carides, GW; Postma, MJ; Voors, AA, 2007)
"8479 hypertensive patients without history of heart failure who were randomly assigned to losartan or atenolol treatment."	5.12	Regression of electrocardiographic left ventricular hypertrophy is associated with less hospitalization for heart failure in hypertensive patients. ( Dahlöf, B; Devereux, RB; Edelman, JM; Harris, KE; Jern, S; Julius, S; Kjeldsen, SE; Okin, PM, 2007)
"Losartan Intervention For Endpoint reduction in hypertension (LIFE) study."	5.12	The effect of baseline physical activity on cardiovascular outcomes and new-onset diabetes in patients treated for hypertension and left ventricular hypertrophy: the LIFE study. ( Brady, WE; Dahlöf, B; Devereux, RB; Fossum, E; Gleim, GW; Hille, DA; Julius, S; Kizer, JR; Kjeldsen, SE; Lyle, PA, 2007)
"The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study showed that losartan-based treatment reduced risk of the composite endpoint of cardiovascular death, stroke and myocardial infarction compared with atenolol-based treatment in patients with hypertension and left ventricular hypertrophy with similar office blood pressure (BP) reduction."	5.12	Losartan versus atenolol on 24-hour ambulatory blood pressure. A LIFE substudy. ( Bang, LE; Hildebrandt, PR; Ibsen, H; Larsen, J; Olsen, MH; Tuxen, C; Wachtell, K; Wiinberg, N, 2007)
"The LIFE study compared losartan-based to atenolol-based therapy in 9,193 hypertensive patients with left ventricular hypertrophy (LVH)."	5.11	Cardiovascular risk reduction in hypertensive black patients with left ventricular hypertrophy: the LIFE study. ( Alderman, MH; Beevers, G; Dahlöf, B; Devereux, RB; Douglas, JG; Edelman, JM; Harris, KE; Julius, S; Kjeldsen, SE; Nesbitt, S; Randall, OS; Wright, JT, 2004)
"The Losartan Intervention for Endpoint reduction in hypertension (LIFE) study was designed to compare losartan- vs atenolol-based antihypertensive treatment on cardiovascular morbidity and mortality in a population of 9193 hypertensive patients with left ventricular hypertrophy (LVH)."	5.11	Population impact of losartan use on stroke in the European Union (EU): projections from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. ( Burke, TA; Carides, GW; Dahlöf, B; Devereux, RB; Diener, HC; Edelman, JM; Krobot, K, 2004)
" We measured the QRS duration and QT intervals from the baseline 12-lead electrocardiograms in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study, which included hypertensive patients with electrocardiographic evidence of left ventricular hypertrophy randomized to either losartan-based or atenolol-based treatment to lower blood pressure."	5.11	QRS duration and QT interval predict mortality in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention for Endpoint Reduction in Hypertension Study. ( Dahlöf, B; Devereux, RB; Jern, S; Nieminen, MS; Oikarinen, L; Okin, PM; Toivonen, L; Viitasalo, M, 2004)
"Losartan prevented more cardiovascular complications than atenolol for the same reduction in blood pressure and have positive additional effects beyond blood pressure control in patients with hypertension and left ventricular hypertrophy."	5.11	[Treatment of hypertension in patients with left ventricular hypertrophy]. ( Bratland, B; Gerhardsen, G; Gisholt, K; Kjeldsen, SE; Omvik, P; Risanger, T; Smedsrud, T, 2004)
" We analysed paired echocardiograms in 500 men and 347 women enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study at baseline and after 12 months of antihypertensive treatment with either losartan or atenolol."	5.11	Sex-related difference in regression of left ventricular hypertrophy with antihypertensive treatment: the LIFE study. ( Bella, JN; Dahlöf, B; Devereux, RB; Gerdts, E; Koren, MJ; Liu, JE; Nieminen, MS; Palmieri, V; Wachtell, K; Wright, JT; Zabalgoitia, M, 2004)
" Baseline and year-1 ECGs and echocardiograms were assessed in 584 hypertensive patients with ECG LVH by Sokolow-Lyon or Cornell voltage-duration product criteria at entry into the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy."	5.11	Regression of electrocardiographic left ventricular hypertrophy predicts regression of echocardiographic left ventricular mass: the LIFE study. ( Dahlöf, B; Devereux, RB; Jern, S; Julius, S; Kjeldsen, SE; Liu, JE; Nieminen, MS; Oikarinen, L; Okin, PM; Wachtell, K, 2004)
"To assess the influence of age on changes in left ventricular (LV) mass and geometry during antihypertensive treatment, we related age to clinical and echocardiographic findings before and after 4 years of antihypertensive treatment in a subset of 560 hypertensive patients without known concurrent disease in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which randomized patients to blinded losartan- or atenolol-based treatment."	5.11	Impact of age on left ventricular hypertrophy regression during antihypertensive treatment with losartan or atenolol (the LIFE study). ( Dahlöf, B; Devereux, RB; Gerdts, E; Nieminen, MS; Palmieri, V; Roman, MJ; Smith, G; Wachtell, K, 2004)
"The Losartan Intervention For End point reduction in hypertension (LIFE) study showed superiority of losartan over atenolol for reduction of composite risk of cardiovascular death, stroke, and myocardial infarction in hypertensives with left ventricular hypertrophy."	5.11	Alcohol consumption and cardiovascular risk in hypertensives with left ventricular hypertrophy: the LIFE study. ( Beevers, G; Brady, WE; Dahlöf, B; De Faire, U; Devereux, RB; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Reims, HM; Wedel, H, 2004)
"To examine a possible relationship between baseline albuminuria and effect of losartan versus atenolol on cardiovascular (CV) events in hypertensive patients with left ventricular hypertrophy, the effect of losartan versus atenolol on albuminuria, and whether the benefits of losartan versus atenolol could be explained by influence of losartan on albuminuria."	5.11	Does albuminuria predict cardiovascular outcome on treatment with losartan versus atenolol in hypertension with left ventricular hypertrophy? A LIFE substudy. ( Borch-Johnsen, K; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Mogensen, CE; Nieminen, MS; Olsen, MH; Omvik, P; Oparil, S; Wachtell, K; Wan, Y, 2004)
"An echocardiographic substudy of the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial was designed to test the ability of losartan to reduce left ventricular (LV) mass more than atenolol."	5.11	Regression of hypertensive left ventricular hypertrophy by losartan compared with atenolol: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial. ( Boman, K; Dahlöf, B; Devereux, RB; Edelman, JM; Gerdts, E; Harris, KE; Nieminen, MS; Papademetriou, V; Rokkedal, J; Wachtell, K, 2004)
"Double-blind, randomized, parallel-group study conducted in 1995-2001 among 9193 men and women with hypertension aged 55 through 80 years (mean, 67 years), with electrocardiographic LVH by Cornell voltage-duration product or Sokolow-Lyon voltage criteria and enrolled in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study."	5.11	Regression of electrocardiographic left ventricular hypertrophy during antihypertensive treatment and the prediction of major cardiovascular events. ( Aurup, P; Dahlöf, B; Devereux, RB; Edelman, JM; Harris, KE; Jern, S; Julius, S; Kjeldsen, SE; Lindholm, LH; Nieminen, MS; Okin, PM; Snapinn, S; Wedel, H, 2004)
"Prospective cohort substudy of the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) randomized clinical trial, conducted from 1995 to 2001."	5.11	Prognostic significance of left ventricular mass change during treatment of hypertension. ( Aurup, P; Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Harris, K; Nieminen, MS; Papademetriou, V; Rokkedal, J; Wachtell, K, 2004)
"The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study showed that treatment with the angiotensin II type-1 receptor antagonist losartan reduces overall stroke risk compared with conventional therapy with the beta-blocker atenolol."	5.11	Stroke reduction in hypertensive adults with cardiac hypertrophy randomized to losartan versus atenolol: the Losartan Intervention For Endpoint reduction in hypertension study. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fyhrquist, F; Harris, KE; Ibsen, H; Julius, S; Kizer, JR; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wachtell, K; Wedel, H, 2005)
"As part of the Losartan Intervention For End point reduction in hypertension (LIFE) study, 342 hypertensive patients with AF and LV hypertrophy were assigned to losartan- or atenolol-based therapy for 1,471 patient-years of follow-up."	5.11	Cardiovascular morbidity and mortality in hypertensive patients with a history of atrial fibrillation: The Losartan Intervention For End Point Reduction in Hypertension (LIFE) study. ( Aurup, P; Dahlöf, B; Devereux, RB; Gerdts, E; Hornestam, B; Ibsen, H; Julius, S; Kjeldsen, SE; Lehto, M; Lindholm, LH; Nieminen, MS; Olsen, MH; Rokkedal, J; Slotwiner, DJ; Wachtell, K, 2005)
"In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study 9,193 hypertensive patients and patients with electrocardiogram-documented left ventricular hypertrophy were randomized to once-daily losartan- or atenolol-based antihypertensive therapy."	5.11	Angiotensin II receptor blockade reduces new-onset atrial fibrillation and subsequent stroke compared to atenolol: the Losartan Intervention For End Point Reduction in Hypertension (LIFE) study. ( Dahlöf, B; Devereux, RB; Gerdts, E; Hornestam, B; Ibsen, H; Julius, S; Kjeldsen, SE; Lehto, M; Lindholm, LH; Nieminen, MS; Olsen, MH; Wachtell, K, 2005)
"We studied the impact of smoking in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which showed superiority of losartan over atenolol for reduction of composite risk of cardiovascular death, stroke and myocardial infarction in hypertensives with left ventricular hypertrophy."	5.11	Losartan benefits over atenolol in non-smoking hypertensive patients with left ventricular hypertrophy: the LIFE study. ( Beevers, G; Brady, WE; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Reims, HM; Wedel, H, 2004)
"The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study reported that a losartan-based antihypertensive regimen reduced cardiovascular morbidity and mortality (composite of cardiovascular death, stroke, and myocardial infarction) more than therapy based on atenolol in patients with left ventricular hypertrophy and isolated systolic hypertension (ISH)."	5.11	The effects of losartan compared to atenolol on stroke in patients with isolated systolic hypertension and left ventricular hypertrophy. The LIFE study. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Harris, KE; Ibsen, H; Julius, S; Kizer, JR; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Lyle, PA; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wedel, H, 2005)
"In 183 patients with hypertension and electrocardiographic left ventricular (LV) hypertrophy, enrolled in the LIFE Study, we measured BP and serum Nt-proANP and Nt-proBNP by immunoassay after 2 weeks of placebo treatment and after 1, 2, 4, 6, 12, 24, 36 and 48 months of randomized treatment with losartan- or atenolol-based antihypertensive regimens."	5.11	Opposite effects of losartan and atenolol on natriuretic peptides in patients with hypertension and left ventricular hypertrophy: a LIFE substudy. ( Bang, LE; Devereux, RB; Fossum, E; Hall, C; Hildebrandt, PR; Ibsen, H; Olsen, MH; Rokkedal, J; Tuxen, C; Wachtell, K, 2005)
" We investigated whether body build was independently associated with higher cardiovascular risk and whether treatment with losartan relative to atenolol influenced the impact of body build on the primary composite end point of cardiovascular death, stroke, and myocardial infarction and on cardiovascular death in patients with hypertension and left ventricular hypertrophy in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study."	5.11	Body build and risk of cardiovascular events in hypertension and left ventricular hypertrophy: the LIFE (Losartan Intervention For Endpoint reduction in hypertension) study. ( Beevers, G; Dahlöf, B; de Faire, U; de Simone, G; Devereux, RB; Fyhrquist, F; Hille, DA; Ibsen, H; Julius, S; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Palmieri, V; Wachtell, K, 2005)
"We explored the impact of baseline left ventricular hypertrophy (LVH) and losartan treatment on renal and cardiovascular (CV) events in 1,513 patients from the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial, which studied the effects of losartan on the progression of renal disease and/or death in patients with type 2 diabetes and nephropathy."	5.11	Adverse effects of left ventricular hypertrophy in the reduction of endpoints in NIDDM with the angiotensin II antagonist losartan (RENAAL) study. ( Boner, G; Brenner, BM; Cooper, ME; Crow, RS; de Zeeuw, D; Dickson, T; Kowey, PR; McCarroll, K; Parving, HH; Shahinfar, S, 2005)
"We conducted a subgroup analysis in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study to determine whether aspirin interacted with the properties of losartan, an angiotensin-II receptor antagonist."	5.11	The effect of losartan versus atenolol on cardiovascular morbidity and mortality in patients with hypertension taking aspirin: the Losartan Intervention for Endpoint Reduction in hypertension (LIFE) study. ( Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fossum, E; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Moan, A; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wedel, H, 2005)
"A total of 754 hypertensive patients with left ventricular hypertrophy (LVH) by Cornell voltage-duration product or Sokolow-Lyon voltage criteria on a screening electrocardiogram had their LV mass measured by echocardiogram at enrolment in the Losartan Intervention For Endpoint Reduction (LIFE) trial, and after 12 and 24 months of blinded therapy with losartan-based or atenolol-based regimens."	5.10	Progressive hypertrophy regression with sustained pressure reduction in hypertension: the Losartan Intervention For Endpoint Reduction study. ( Bella, JN; Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Liu, JE; Nieminen, MS; Palmieri, V; Papademetriou, V; Wachtell, K, 2002)
"To compare the effects of the angiotensin II antagonist, losartan, with those of atenolol on left ventricular hypertrophy (LVH), blood pressure and neurohormone concentrations in hypertensive patients with LVH."	5.10	Effects of losartan and atenolol on left ventricular mass and neurohormonal profile in patients with essential hypertension and left ventricular hypertrophy. ( Aurup, P; Barrios, V; Dahlof, B; Diez, J; Johansson, M; Nicholls, MG; Smith, RD; Yu, CM; Zanchetti, A, 2002)
"In the LIFE study, with a double-masked, randomized, parallel-group design, 9193 patients (46% men) with hypertension (mean age 67 years, average pressure 174/98 mmHg after placebo run-in) and electrocardiogram-documented left ventricular hypertrophy were randomly assigned to once-daily losartan- or atenolol-based antihypertensive treatment and followed for at least 4 years (mean 4."	5.10	Risk of new-onset diabetes in the Losartan Intervention For Endpoint reduction in hypertension study. ( Aurup, P; Beevers, G; Borch-Johnsen, K; Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Olsen, MH; Omvik, P; Oparil, S; Snapinn, S; Wachtell, K; Wedel, H, 2002)
"The goal of this study was to compare myocardial perfusion reserve (MPR) before and after long-term treatment with lisinopril and losartan in patients with hypertension and left ventricular hypertrophy (LVH)."	5.10	Augmentation of myocardial blood flow in hypertensive heart disease by angiotensin antagonists: a comparison of lisinopril and losartan. ( Akinboboye, OO; Bergmann, SR; Chou, RL, 2002)
"To test the hypothesis that losartan improves outcome better than atenolol in patients with isolated systolic hypertension and electrocardiographically documented left ventricular hypertrophy (ECG-LVH)."	5.10	Effects of losartan on cardiovascular morbidity and mortality in patients with isolated systolic hypertension and left ventricular hypertrophy: a Losartan Intervention for Endpoint Reduction (LIFE) substudy. ( Aurup, P; Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Edelman, J; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, S; Wedel, H, 2002)
" The aim of the LIFE-study was to establish whether treatment with the angiotensin-II AT 1-receptor antagonist, losartan, reduced cardiovascular events more effectively than treatment with the betablocker atenolol in patients with hypertension and left ventricular hypertrophy."	5.10	[The effect of losartan versus atenolol on cardiovascular morbidity and mortality in patients with hypertension and ECG-verified left ventricular hypertrophy in the LIFE-study]. ( Dahlöf, B; Ibsen, H; Kjeldsen, SE; Lindholm, LH; Pedersen, OL, 2003)
"Cardiovascular morbidity and mortality are reduced by treatment with the angiotensin II AT(1)-receptor antagonist losartan compared with conventional treatment with the beta-blocker atenolol in patients with hypertension and electrocardiogram-defined left ventricular hypertrophy, many of whom had known vascular disease."	5.10	Effects of losartan or atenolol in hypertensive patients without clinically evident vascular disease: a substudy of the LIFE randomized trial. ( Aurup, P; Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fyhrquist, F; Helle Berg, S; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, S; Wedel, H, 2003)
" Thirty chronically hemodialyzed uremic patients with hypertension were randomly assigned to receive the AT1-R antagonist losartan (n = 10), the angiotensin-converting enzyme (ACD) inhibitor enalapril (n = 10), or calcium antagonist amlodipine (n = 10)."	5.10	Angiotensin II type 1 receptor antagonist, losartan, causes regression of left ventricular hypertrophy in end-stage renal disease. ( Iwasaka, T; Masaki, H; Matsubara, H; Nishikawa, M; Nishiue, T; Shibasaki, Y, 2002)
" In an 8-week, randomized, double-blind, placebo-controlled trial in patients with mild-to-moderate hypertension, the antihypertensive effects of candesartan cilexetil 16 mg were maintained after a missed dose, whereas systolic and diastolic blood pressure increased toward baseline levels after a missed dose of losartan 100 mg."	5.09	Comparison of angiotensin II receptor blockers: impact of missed doses of candesartan cilexetil and losartan in systemic hypertension. ( Dell'Oro, R; Grassi, G; Mancia, G; Turri, C, 1999)
" After a 4-week placebo run-in period, 25 patients with mild-to-moderate essential hypertension were randomly allocated to active treatment with Losartan 50 mg titrated to Losartan 50 mg/hydrochlorothiazide (HCT) 12."	5.09	Effects of losartan titrated to Losartan/Hydrochlorothiazide and amlodipine on left ventricular mass in patients with mild-to-moderate hypertension. A double-blind randomized controlled study. ( Battegay, E; Dieterle, T; Martina, B; Weinbacher, M, 1999)
"To compare the regression of left ventricular hypertrophy in patients with moderate hypertension treated with enalapril, losartan or a combination of the two drugs at lower doses."	5.09	Reduction in left ventricular hypertrophy in hypertensive patients treated with enalapril, losartan or the combination of enalapril and losartan. ( Avanza, AC; El Aouar, LM; Mill, JG, 2000)
"The Losartan Intervention For Endpoint (LIFE) reduction in hypertension study is a double-blind, prospective, parallel-group study comparing the effects of losartan with those of atenolol on the reduction of cardiovascular complications in patients (n = 9,194) with essential hypertension and with electrocardiographically (ECG) documented left ventricular hypertrophy (LVH)."	5.09	Lowering of blood pressure and predictors of response in patients with left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint. ( Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Wedel, H, 2000)
"The Losartan Intervention For Endpoint reduction in hypertension (LIFE) trial, in which hypertensive patients with ECG LV hypertrophy (Cornell voltage-duration product, > 2440 mm x ms and/or SV1 + RV(5-6) > 38 mm) were randomized to > or = 4 years double-blinded treatment with losartan or atenolol."	5.09	Left ventricular wall stresses and wall stress-mass-heart rate products in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint reduction in hypertension. ( Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Nieminen, MS; Okin, PM; Palmieri, V; Papademetriou, V; Roman, MJ; Wachtell, K, 2000)
"Losartan reduces blood pressure in patients with essential hypertension, but the long-term central hemodynamic effects at rest and during exercise are not known."	5.09	Long-term central hemodynamic effects at rest and during exercise of losartan in essential hypertension. ( Gerdts, E; Lund-Johansen, P; Myking, OL; Omvik, P, 2000)
"We investigated whether a relationship exists between circulating transforming growth factor beta -1 (TGF-beta(1)), collagen type I metabolism, microalbuminuria, and left ventricular hypertrophy in essential hypertension and whether the ability of the angiotensin II type 1 receptor antagonist losartan to correct microalbuminuria and regress left ventricular hypertrophy in hypertensives is related to changes in TGF-beta(1) and collagen type I metabolism."	5.09	Transforming growth factor beta in hypertensives with cardiorenal damage. ( Díez, J; Laviades, C; Varo, N, 2000)
"The Losartan Intervention For Endpoint (LIFE) reduction in hypertension study is a double-blind, prospective, parallel group study designed to compare the effects of losartan with those of atenolol on the reduction of cardiovascular morbidity and mortality."	5.09	Baseline characteristics in relation to electrocardiographic left ventricular hypertrophy in hypertensive patients: the Losartan intervention for endpoint reduction (LIFE) in hypertension study. The Life Study Investigators. ( Dahlöf, B; Devereux, RB; Jern, S; Julius, S; Kjeldsen, SE; Okin, PM, 2000)
"We studied 659 participants in the LIFE (Losartan Intervention for Endpoint Reduction in Hypertension) study with both electrocardiographic and echocardiographic LV hypertrophy (68% of the echocardiographic cohort) without previous myocardial infarction."	5.09	Left ventricular function and hemodynamic features of inappropriate left ventricular hypertrophy in patients with systemic hypertension: the LIFE study. ( Bella, JN; Dahlöf, B; de Simone, G; Devereux, RB; Gerdts, E; Nieminen, MS; Palmieri, V; Papademetriou, V; Tuxen, C; Wachtell, K, 2001)
"The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) trial used left ventricular hypertrophy (LVH) on a screening ECG to identify patients at high risk for morbid events."	5.09	Relation of echocardiographic left ventricular mass and hypertrophy to persistent electrocardiographic left ventricular hypertrophy in hypertensive patients: the LIFE Study. ( Dahlöf, B; Devereux, RB; Jern, S; Julius, S; Kjeldsen, SE; Okin, PM, 2001)
"The purpose of our study was to evaluate the antihypertensive efficacy, tolerability and effects on left ventricular mass of losartan over 10 months in patients with essential hypertension."	5.08	[The effectiveness and tolerability of losartan and effect on left ventricular mass in patients with essential hypertension]. ( Acitorio, M; Aquino, D; Caccavale, A; Coppolino, P; Cosimi, R; Iacono, A; Iarussi, D; Ratti, G; Rocereto, A; Tedesco, MA, 1998)
"This study evaluated the anti-hypertensive efficacy, tolerability and effects on left ventricular mass of losartan, a selective angiotensin II receptor antagonist, after 22 months in patients with essential hypertension."	5.08	Effects of losartan on hypertension and left ventricular mass: a long-term study. ( Aquino, D; di Salvo, G; Galzerano, D; Iacono, A; Iarussi, D; Limongelli, G; Mennella, S; Ratti, G; Tedesco, MA, 1998)
"-Losartan was the first available orally administered selective antagonist of the angiotensin II type 1 receptor developed for the treatment of hypertension."	5.08	Characteristics of 9194 patients with left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint Reduction in Hypertension. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Fyhrquist, F; Hedner, T; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Nieminen, MS; Omvik, P; Oparil, S; Wedel, H, 1998)
" Thus, the observed outcomes benefits favoring losartan may involve other possible mechanisms, including differential effects of losartan and atenolol on LVH regression, left atrial diameter, atrial fibrillation, brain natriuretic peptide, vascular structure, thrombus formation/platelet aggregation, serum uric acid, albuminuria, new-onset diabetes, and lipid metabolism."	4.84	Potential mechanisms of stroke benefit favoring losartan in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. ( Dahlöf, B; Devereux, RB, 2007)
"The recent Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study was conducted in patients with essential hypertension with electrocardiogram evidence of left ventricular hypertrophy."	4.82	Implications of the LIFE trial. ( Lim, HS; Lip, GY; Nadar, S, 2003)
" Experimentally, losartan, a novel selective angiotensin II receptor type 1 antagonist has been shown to decrease cardiac hypertrophic response in models of both hypertension and volume cardiac hypertrophy as well as reverse hypertrophy in spontaneously hypertensive rats."	4.79	Effect of angiotensin II blockade on cardiac hypertrophy and remodelling: a review. ( Dahlöf, B, 1995)
"Prehypertensive losartan treatment may lead to long‑term inhibition of the development of left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs)."	3.85	Hypomethylation of Agtrap is associated with long-term inhibition of left ventricular hypertrophy in prehypertensive losartan-treated spontaneously hypertensive rats. ( Lian, GL; Lin, X; Wang, HJ; Wang, TJ; Xie, LD; Xu, CS; Zhong, HB, 2017)
"Risk of incident stroke was examined in relation to abnormal PTFV1 on a baseline ECG in 7778 hypertensive patients with ECG left ventricular hypertrophy, no history of atrial fibrillation, in sinus rhythm on their baseline ECG with no incident atrial fibrillation during follow-up, who were randomly assigned to losartan-based or atenolol-based treatment."	3.83	Electrocardiographic left atrial abnormalities and risk of incident stroke in hypertensive patients with electrocardiographic left ventricular hypertrophy. ( Devereux, RB; Kamel, H; Kjeldsen, SE; Okin, PM, 2016)
" We investigated the expression of RAS components in the heart and kidney during the development of hypertension and its perinatal treatment with losartan in young spontaneously hypertensive rats (SHR)."	3.81	Perinatally administered losartan augments renal ACE2 expression but not cardiac or renal Mas receptor in spontaneously hypertensive rats. ( Cacanyiova, S; Klimas, J; Krenek, P; Kristek, F; Kruzliak, P; Ochodnicka-Mackovicova, K; Ochodnicky, P; Olvedy, M, 2015)
" This study assessed the potential therapeutic benefit of combining the mitochondria-specific antioxidant, MitoQ10, with the low-dose angiotensin receptor blocker (ARB), losartan, on attenuation of hypertension and left ventricular hypertrophy."	3.80	Combined therapeutic benefit of mitochondria-targeted antioxidant, MitoQ10, and angiotensin receptor blocker, losartan, on cardiovascular function. ( Beattie, E; Beattie, W; Dominiczak, AF; Graham, D; Koh-Tan, CH; McLachlan, J; Murphy, MP; Nicklin, SA; Olson, E, 2014)
"Baseline and year-3 ECG LVH and left ventricular midwall shortening (MWS) were examined in 725 hypertensive patients in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy."	3.80	Relationship of left ventricular systolic function to persistence or development of electrocardiographic left ventricular hypertrophy in hypertensive patients: implications for the development of new heart failure. ( Dahlöf, B; Devereux, RB; Gerdts, E; Okin, PM; Wachtell, K, 2014)
"This study examined the antifibrotic effect of losartan, an angiotensin II type 1 receptor antagonist, in an animal model of heart fibrosis induced by long-term intense exercise."	3.79	Losartan prevents heart fibrosis induced by long-term intensive exercise in an animal model. ( Benito, B; Brugada, J; Gay-Jordi, G; Guash, E; Mont, L; Nattel, S; Serrano-Mollar, A, 2013)
" Methods Baseline and follow-up clinical and echocardiographic parameters were assessed in 939 hypertensive patients with electrocardiogram (ECG) LVH participating in the Losartan Intervention for Endpoint reduction in hypertension (LIFE) echocardiography substudy (66±7 years; 42% women; 11% with diabetes) who did not have aortic or mitral valve stenosis or prosthesis."	3.79	Mitral annular calcification and incident ischemic stroke in treated hypertensive patients: the LIFE study. ( Boman, K; Casalnuovo, G; Dahlöf, B; De Marco, M; de Simone, G; Devereux, RB; Gerdts, E; Kizer, JR; Migliore, T; Olsen, MH; Wachtell, K, 2013)
"8 years study treatment were assessed in 922 hypertensive patients in the Losartan Intervention For Endpoint reduction in hypertension echocardiography substudy."	3.78	Association of heart failure hospitalizations with combined electrocardiography and echocardiography criteria for left ventricular hypertrophy. ( Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Nieminen, MS; Okin, PM; Wachtell, K, 2012)
"Treatment with the selective VDR activator paricalcitol reduces myocardial fibrosis and preserves diastolic LV function due to pressure overload in a mouse model."	3.78	The vitamin D receptor activator paricalcitol prevents fibrosis and diastolic dysfunction in a murine model of pressure overload. ( Cannon, MV; de Boer, RA; Mahmud, H; Meems, LM; Ruifrok, WP; Silljé, HH; van Gilst, WH; Voors, AA, 2012)
"Treatment of hypertensive patients with a losartan-based regimen was associated with greater regression of electrocardiographic (ECG) left ventricular hypertrophy (LVH) than atenolol-based therapy in the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study, independent of blood pressure (BP) changes."	3.76	Greater regression of electrocardiographic left ventricular hypertrophy during hydrochlorothiazide therapy in hypertensive patients. ( Dahlöf, B; Devereux, RB; Edelman, JM; Hille, DA; Kjeldsen, SE; Lindholm, LH; Okin, PM, 2010)
"In 9193 hypertensive patients included in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, we measured urine albumin/creatinine ratio (UACR), LV hypertrophy by electrocardiography, serum high-density lipoprotein (HDL) cholesterol, and blood pressure after 2 weeks of placebo treatment and yearly during 5 years of anti-hypertensive treatment with either an atenolol- or a losartan-based regimen."	3.76	Lack of regression of left ventricular hypertrophy is associated with higher incidence of revascularization in hypertension: The LIFE Study. ( Dahlöf, B; Devereux, RB; Kjeldsen, SE; Okin, PM; Olsen, MH; Søraas, CL; Tønnessen, T; Wachtell, K, 2010)
"Baseline and third year ECG LVH and left atrial systolic diameter were examined in 663 patients in the Losartan Intervention For Endpoint reduction in hypertension echocardiographic substudy who were in sinus rhythm at baseline and had no history of atrial fibrillation."	3.76	Relationship of left atrial enlargement to persistence or development of ECG left ventricular hypertrophy in hypertensive patients: implications for the development of new atrial fibrillation. ( Dahlöf, B; Devereux, RB; Gerdts, E; Nieminen, MS; Oikarinen, L; Okin, PM; Wachtell, K, 2010)
" Here we test the therapeutic effects of two commonly used vitamin D analogs and their combination with losartan on the development of left ventricular hypertrophy."	3.76	Therapeutic effects of vitamin D analogs on cardiac hypertrophy in spontaneously hypertensive rats. ( Bhan, I; Kim, GH; Kong, J; Li, G; Li, X; Li, YC; Liu, SQ; Sun, T; Thadhani, R; Wei, M; Zhao, Q, 2010)
"We examined lipid levels in the Losartan Intervention For Endpoint reduction in hypertension study and their impact on the primary composite endpoint of cardiovascular death, myocardial infarction, or stroke."	3.75	Effects of losartan compared with atenolol on lipids in patients with hypertension and left ventricular hypertrophy: the Losartan Intervention For Endpoint reduction in hypertension study. ( Beevers, G; Dahlöf, B; de Faire, U; de Simone, G; Devereux, RB; Fyhrquist, F; Ibsen, H; Kjeldsen, SE; Lederballe-Pedersen, O; Lindholm, LH; Lyle, PA; Nieminen, MS; Olsen, MH; Omvik, P; Oparil, S; Wachtell, K; Wedel, H, 2009)
"To investigate the effects of losartan on left ventricular hypertrophy (LVH) and plasma transforming growth factor-beta1 (TGF-beta1) in elderly patients with essential hypertension (EH)."	3.75	[Effects of losartan on left ventricular hypertrophy and plasma transforming growth factor-beta1 in elderly patients with hypertension]. ( Bai, SC; Huang, P; Lai, WY; Li, Y; Su, L; Wu, ZL; Xu, DL, 2009)
" We evaluated 770 hypertensive patients with electrocardiogram findings of left ventricular hypertrophy (age 66 +/- 7 years; 42% women) enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy."	3.75	Mitral E wave deceleration time to peak E velocity ratio and cardiovascular outcome in hypertensive patients during antihypertensive treatment (from the LIFE echo-substudy). ( Aurigemma, GP; Boman, K; Chinali, M; Dahlöf, B; de Simone, G; Devereux, RB; Gerdts, E; Mishra, RK; Wachtell, K, 2009)
" We prospectively compared MWS derived from linear echocardiographic dimensions with MR strain(in) in septal and posterior locations in 27 subjects with ECG LV hypertrophy in the Losartan Intervention for Endpoint Reduction in Hypertension Study."	3.74	Marked regional left ventricular heterogeneity in hypertensive left ventricular hypertrophy patients: a losartan intervention for endpoint reduction in hypertension (LIFE) cardiovascular magnetic resonance and echocardiographic substudy. ( Bella, JN; Biederman, RW; Calhoun, D; Dell'Italia, LJ; Devereux, RB; Doyle, M; Kortright, E; Oparil, S; Perry, G; Pohost, GM; Young, AA, 2008)
" We explored, in a post hoc analysis, whether MetS predicts cardiovascular events in hypertensive patients with electrocardiographic left ventricular hypertrophy (ECG-LVH) in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study."	3.74	Clusters of metabolic risk factors predict cardiovascular events in hypertension with target-organ damage: the LIFE study. ( Dahlöf, B; de Simone, G; Devereux, RB; Hille, DA; Ibsen, H; Kjeldsen, SE; Lyle, PA; Olsen, MH; Wachtell, K, 2007)
"Losartan reduced significantly the systolic blood pressure as well as the aorta and left ventricular hypertrophy."	3.74	Beneficial effects of the combination of nifedipine and losartan in hypertensive Dahl salt-sensitive rats. ( Tinel, H, 2007)
"Treatment of hypertensive patients with electrocardiographic left ventricular hypertrophy with losartan-based therapy is associated with lower incidence of diabetes mellitus and greater regression of hypertrophy than atenolol-based therapy."	3.74	In-treatment resolution or absence of electrocardiographic left ventricular hypertrophy is associated with decreased incidence of new-onset diabetes mellitus in hypertensive patients: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) ( Dahlöf, B; Devereux, RB; Harris, KE; Jern, S; Kjeldsen, SE; Lindholm, LH; Okin, PM, 2007)
"8 years losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint reduction in hypertension (LIFE) echocardiography substudy."	3.74	Impact of left ventricular geometry on prognosis in hypertensive patients with left ventricular hypertrophy (the LIFE study). ( Cramariuc, D; Dahlöf, B; de Simone, G; Devereux, RB; Gerdts, E; Wachtell, K, 2008)
"In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, the primary composite end point of cardiovascular death, stroke, and myocardial infarction was reduced by losartan versus atenolol in patients with hypertension and left ventricular hypertrophy."	3.73	Pulse pressure and effects of losartan or atenolol in patients with hypertension and left ventricular hypertrophy. ( Beevers, G; Dahlöf, B; de Faire, U; Devereux, RB; Edelman, JM; Fyhrquist, F; Hille, DA; Ibsen, H; Julius, S; Kjeldsen, SE; Kristianson, K; Lederballe-Pedersen, O; Lindholm, LH; Lyle, PA; Nieminen, MS; Omvik, P; Oparil, S; Snapinn, SM; Wedel, H, 2005)
"Wistar rats were divided into the following 4 groups: 1) C--control (n=13); 2) AoS--aortic stenosis (n=11); 3) LIS--AoS treated with lisinopril, 20 mg/kg/day (n=11); and 4) LOS--AoS treated with losartan, 40 mg/kg/day (n=9)."	3.73	[Blockade of renin-angiotensin system attenuates cardiac remodeling in rats undergoing aortic stenosis]. ( Aragon, FF; Cicogna, AC; Cordaro, FR; Gonçalves, G; Okoshi, K; Okoshi, MP; Padovani, CR; Ribeiro, HB; Zornoff, LA, 2005)
"The Losartan Intervention For Endpoint reduction in hypertension study (LIFE) was a double-masked, randomized trial of losartan versus atenolol in 9193 patients with essential hypertension and left ventricular hypertrophy (LVH) ascertained by electrocardiography."	3.73	Cost effectiveness of losartan in patients with hypertension and LVH: an economic evaluation for Sweden of the LIFE trial. ( Burke, TA; Carides, GW; Dahlöf, B; Dasbach, EJ; Jönsson, B; Lindholm, LH, 2005)
"In 6679 hypertensive patients included in the LIFE study, we measured UACR, left ventricular hypertrophy by electrocardiography, serum cholesterol, plasma glucose and blood pressure after 2 weeks of placebo treatment and again after 1 year of anti-hypertensive treatment with either an atenolol- or a losartan-based regimen."	3.73	Reductions in albuminuria and in electrocardiographic left ventricular hypertrophy independently improve prognosis in hypertension: the LIFE study. ( Dahlöf, B; Devereux, RB; Ibsen, H; Kjeldsen, SE; Lindholm, LH; Oikarinen, L; Okin, PM; Olsen, MH; Wachtell, K, 2006)
" To assess the relations of LV mass and function with Hgb delivery (ie, the physiological carrier of oxygen), we calculated the product of Hgb concentration and Doppler-derived cardiac output in 864 hypertensive participants with electrocardiographic LVH (359 women) in the Losartan Intervention for End Point Reduction in Hypertension echocardiography substudy."	3.73	Association of hemoglobin delivery with left ventricular structure and function in hypertensive patients: Losartan Intervention for End Point Reduction in Hypertension Study. ( Boman, K; Dahlöf, B; de Simone, G; Devereux, RB; Fyhrquist, F; Gerdts, E; Hoieggen, A; Narayan, P; Nieminen, MS; Papademetriou, V; Wachtell, K, 2006)
"The LIFE (Losartan Intervention For Endpoint reduction in hypertension) study demonstrated a 13% relative risk reduction in the primary composite endpoint (myocardial infarction, stroke or death) for patients with hypertension and electrocardiographically diagnosed left ventricular hypertrophy (LVH) treated with losartan compared with atenolol."	3.73	A cost-utility analysis of losartan versus atenolol in the treatment of hypertension with left ventricular hypertrophy. ( Anis, AH; Brisson, M; Nosyk, B; Singh, S; Sun, H; Woolcott, J, 2006)
" The Losartan Intervention For Endpoint (LIFE) reduction in hypertension study provides additional data to support the use of the ACE inhibitors to lower the risk of stroke among patients with hypertension and vascular diseases."	3.72	New strategies for prevention of ischemic stroke: the LIFE study. ( Adams, HP, 2003)
"In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, a major reduction of all-cause mortality--especially cardiovascular mortality--in patients with diabetes with left ventricular hypertrophy was reported for treatment with losartan."	3.72	Effect of losartan on sudden cardiac death in people with diabetes: data from the LIFE study. ( Borch-Johnsen, K; Dahlöf, B; Edelman, JM; Ibsen, H; Lindholm, LH; Olsen, MH; Snapinn, S; Wachtell, K, 2003)
"Twenty four hour blood pressure (BP) monitoring was carried out and structural state of left ventricular myocardium assessed in 20 patients with mild and moderate hypertension before and after 24 weeks of therapy with Hyzaar - fixed dose combination of losartan (50 mg) and hydrochlorothiazide (12."	3.72	[Therapy of patients with arterial hypertension with fixed dose combination of losartan and hydrochlorothiazide. Effect on 24 hour blood pressure and left-ventricular hypertrophy]. ( Chazova, IE; Dmitriev, VV; Ratova, LG; Sinitsin, VE; Stukalova, OV, 2003)
"The Losartan Intervention For Endpoint Reduction (LIFE) study demonstrated a clear mortality benefit in treating hypertensive patients with electrocardiogram (ECG) evidence of left ventricular hypertrophy (LVH) with losartan rather than atenolol."	3.72	How much echo left ventricular hypertrophy would be missed in diabetics by applying the Losartan Intervention For Endpoint Reduction electrocardiogram criteria to select patients for angiotensin receptor blockade? ( Dawson, A; Donnelly, LA; Morris, AD; Pringle, SD; Rana, BS; Struthers, AD, 2004)
"To investigate the different effects of an angiotensin II type 1 (AT(1)) receptor antagonist, losartan, and an angiotensin converting enzyme (ACE) inhibitor, fosinopril, on cardiomyocyte apoptosis, myocardial fibrosis, and angiotensin II (Ang II) in the left ventricle of spontaneously hypertensive rats (SHRs)."	3.71	Apoptosis, myocardial fibrosis and angiotensin II in the left ventricle of hypertensive rats treated with fosinopril or losartan. ( Liang, X; Sun, M; Xie, X; Yang, T; Yu, G; Zhao, S, 2002)
"We studied the effects of chronic losartan (Los) treatment on contractile function of isolated right ventricular (RV) trabeculae from rat hearts 12 wk after left ventricular (LV) myocardial infarction (MI) had been induced by ligation of the left anterior descending artery at 4 wk of age."	3.71	Losartan prevents contractile dysfunction in rat myocardium after left ventricular myocardial infarction. ( Daniëls, MC; de Tombe, PP; Keller, RS, 2001)
" ECG LVH by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria was used to select patients for the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study."	3.70	Effect of obesity on electrocardiographic left ventricular hypertrophy in hypertensive patients : the losartan intervention for endpoint (LIFE) reduction in hypertension study. ( Dahlöf, B; Devereux, RB; Jern, S; Kjeldsen, SE; Okin, PM, 2000)
" The effect of losartan is compared to that of captopril, given at doses leading to a similar decrease of both arterial blood pressure and left ventricular hypertrophy."	3.70	Chronic losartan treatment decreases angiotensin II-mediated facilitation of noradrenaline release in the caudal artery of spontaneously hypertensive rats. ( Bravo, R; Fernández-Alfonso, MS; González, C; Ruiz-Gayo, M; Somoza, B, 2000)
"The role of angiotensin II via the angiotensin type 1 (AT1) receptor in the development of volume overload cardiac hypertrophy was investigated in adult male Wistar rats with aortic insufficiency."	3.69	Angiotensin AT1 receptor-mediated attenuation of cardiac hypertrophy due to volume overload: involvement of endothelin. ( Ishiye, M; Nakashima, M; Uematsu, T; Umemura, K, 1995)
"Losartan, a recently developed nonpeptide angiotensin II (AII) receptor antagonist, was orally administered for 14 days to mice with viral myocarditis, beginning 7 days after encephalomyocarditis virus inoculation."	3.69	Comparative effects of losartan, captopril, and enalapril on murine acute myocarditis due to encephalomyocarditis virus. ( Araki, M; Imai, S; Kanda, T; Kobayashi, I; Murata, K; Suzuki, T, 1995)
" These results suggest that inhibition of generation of angiotensin II and AT1 receptor blockade are equally effective in preventing important features of ventricular remodeling after myocardial infarction."	3.69	Comparative effects of chronic angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade on cardiac remodeling after myocardial infarction in the rat. ( Drexler, H; Holtz, J; Meybrunn, M; Riede, UN; Schieffer, B; Seitz, S; Wirger, A, 1994)
"As interactions between the renin-angiotensin and sympathetic nervous systems have been suggested in the pathogenesis of hypertension, we wanted to investigate the effect of chronic renin-angiotensin blockade with losartan and enalaprilat on the sympathetic reactivity to hypotension and on the cardiac beta-adrenergic-coupled adenylyl cyclase pathway in 12-week-old Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR)."	3.69	Effects of renin-angiotensin blockade on sympathetic reactivity and beta-adrenergic pathway in the spontaneously hypertensive rat. ( Cardinal, R; de Champlain, J; K-Laflamme, A; Oster, L, 1997)
"Reversal of left ventricular hypertrophy (LVH) in hypertensive patients appears to be a desirable goal to the reduction cardiac risk."	2.84	Effects of losartan on left ventricular mass: a three-year follow-up in elderly hypertensives with myocardial hypertrophy despite successful conventional antihypertensive treatment. ( Affricano, C; Bossini, A; Cassone, R; Gaudio, C; Lopreiato, F; Moroni, C; Scrofani, AR; Tolone, S, 2017)
"Treatment with losartan was safe, suggesting that it can be used for other indications in patients with hypertrophic cardiomyopathy, irrespective of obstructive physiology."	2.80	Efficacy and safety of the angiotensin II receptor blocker losartan for hypertrophic cardiomyopathy: the INHERIT randomised, double-blind, placebo-controlled trial. ( Ahtarovski, K; Axelsson, A; Bundgaard, H; Corell, P; Havndrup, O; Ho, C; Iversen, K; Jensen, M; Langhoff, L; Norsk, J; Vejlstrup, N, 2015)
"Psoriasis has a similar prevalence in hypertensive patients as in the general population."	2.79	Psoriasis is associated with subsequent atrial fibrillation in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint study. ( Bang, CN; Devereux, RB; Gottlieb, AB; Køber, L; Okin, PM; Wachtell, K, 2014)
"In hypertensive patients, left ventricular hypertrophy (LVH) may persist despite satisfactory blood pressure (BP) control."	2.79	Regression of Electrocardiographic Signs of Left Ventricular Hypertrophy by Combined Treatment With Thiazide Diuretic and Angiotensin-II Receptor Blocker. ( Fujiwara, H; Furukawa, Y; Kita, Y; Matsuda, M; Miyazaki, S; Sato, Y; Sawa, T; Takatsu, Y; Tanaka, M, 2014)
"Losartan treatment was associated with preserved fibrinolytic balance compared to a more prothrombotic fibrinolytic and hemostatic state in the atenolol group."	2.75	Effects of atenolol or losartan on fibrinolysis and von Willebrand factor in hypertensive patients with left ventricular hypertrophy. ( Andersson, J; Boman, JH; Boman, K; Dahlöf, B; Olofsson, M, 2010)
"The prevalence of baseline left ventricular hypertrophy (LVH) was not significantly different among three groups."	2.73	Effect of dual blockade of renin-angiotensin system on TGFbeta1 and left ventricular structure and function in hypertensive patients. ( Argano, C; Avellone, G; Colomba, D; Corrao, S; Di Chiara, T; Donatelli, M; Licata, G; Parrinello, G; Scaglione, R, 2007)
"Electrocardiographic left ventricular hypertrophy (LVH) predicts cardiovascular morbidity and mortality, and regression of ECG LVH may predict improved prognosis in hypertensive patients."	2.71	Regression of electrocardiographic left ventricular hypertrophy by losartan versus atenolol: The Losartan Intervention for Endpoint reduction in Hypertension (LIFE) Study. ( Aurup, P; Dahlof, B; Devereux, RB; Edelman, JM; Harris, KE; Jern, S; Julius, S; Kjeldsen, SE; Nieminen, MS; Okin, PM; Snapinn, S, 2003)
"Hypertension is a major risk factor for morbidity and mortality."	2.71	Long-term plasma catecholamines in patients with hypertension and left ventricular hypertrophy treated with losartan or atenolol: ICARUS, a LIFE substudy. ( Fossum, E; Høieggen, A; Ibsen, H; Julius, S; Kjeldsen, SE; Olsen, MH; Reims, HM; Wachtell, K, 2004)
"In hypertensive left ventricular hypertrophy (LVH), myocardial texture is altered by a disproportionate increase in fibrosis, but there is insufficient clinical evidence whether antihypertensive therapy or individual agents can induce regression of myocardial fibrosis."	2.71	Different effects of antihypertensive therapies based on losartan or atenolol on ultrasound and biochemical markers of myocardial fibrosis: results of a randomized trial. ( Ciulla, MM; Dahlöf, B; Dìez, J; Esposito, A; Gilles, L; López, B; Magrini, F; Nicholls, MG; Paliotti, R; Smith, RD; Zanchetti, A, 2004)
"Obesity has been shown to be associated with increased left ventricular mass (LVM) and heart sympathetic activity even in nonhypertensive subjects."	2.71	Effect of losartan and spironolactone on left ventricular mass and heart sympathetic activity in prehypertensive obese subjects: a 16-week randomized trial. ( Amador, N; Encarnación, JJ; Guízar, JM; López, M; Rodríguez, L, 2005)
"Patients with hypertension have different types of left ventricular (LV) geometry, but the impact of blood pressure (BP) reduction on LV geometry change during antihypertensive treatment remains unclear."	2.70	Change of left ventricular geometric pattern after 1 year of antihypertensive treatment: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. ( Bella, JN; Boman, K; Dahlöf, B; Devereux, RB; Gerdts, E; Nieminen, MS; Papademetriou, V; Rokkedal, J; Smith, G; Wachtell, K, 2002)
"Losartan/HCTZ is an effective combination therapy, lowering blood pressure (BP) to a greater extent than losartan or HCTZ alone in patients with hypertension."	2.45	Losartan/Hydrochlorothiazide: a review of its use in the treatment of hypertension and for stroke risk reduction in patients with hypertension and left ventricular hypertrophy. ( Keating, GM, 2009)
"Losartan (Cozaar) is an angiotensin AT1 receptor antagonist."	2.43	Losartan: a review of its use in stroke risk reduction in patients with hypertension and left ventricular hypertrophy. ( Moen, MD; Wagstaff, AJ, 2005)
"Hypertension is a major influence on the development of LVH."	2.43	Ventricular hypertrophy and hypertension: prognostic elements and implications for management. ( Devereux, RB; Krauser, DG, 2006)
"Losartan 50-100 mg/day was compared with atenolol 50-100 mg/day in patients with essential hypertension and left ventricular hypertrophy (LVH) [n = 9,193] in the randomized, double-blind Losartan Intervention For Endpoint reduction in hypertension (LIFE) study."	2.42	Losartan: in the reduction of stroke risk in patients with hypertension and left ventricular hypertrophy. ( Keating, GM; Waugh, J, 2003)
"Losartan is an orally active, selective, nonpeptide, angiotensin-II Type I-receptor antagonist, and was the first drug marketed in this class."	2.42	Losartan for the treatment of hypertension and left ventricular hypertrophy: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. ( Devereux, RB; Lyle, PA, 2004)
"Albuminuria was defined as urine albumin/creatinine ratio ≥30 mg/g."	1.91	Joint Association of Albuminuria and Left Ventricular Hypertrophy With Incident Heart Failure in Adults at High Risk With Hypertension: A Systolic Blood Pressure Intervention Trial Substudy. ( Ahmad, MI; Chen, LY; Kazibwe, R; Singh, S; Soliman, EZ; Soliman, MZ, 2023)
"Treatment with losartan reduced left ventricular dysfunction and prevented increased extracellular volume fraction, indicating that T1 mapping is sensitive to pharmacological prevention of fibrosis."	1.40	T₁ mapping detects pharmacological retardation of diffuse cardiac fibrosis in mouse pressure-overload hypertrophy. ( Fiedler, LR; Gsell, W; Habib, J; McSweeney, SJ; Prasad, SK; Price, AN; Schneider, MD; Stuckey, DJ; Thin, MZ, 2014)
" We investigated the changes of ceramide lipid components in hypertrophied immature rabbit hearts after chronic administration of the AT1 -receptor blocker, losartan."	1.39	Modulation of C16:0-ceramide in hypertrophied immature hearts by losartan. ( Itoi, T; Oka, T; Terada, N, 2013)
"Losartan was administered to individually caged rats via the drinking water (10 mg/kg/d)."	1.38	Cardiac remodeling and function following exercise and angiotensin II receptor antagonism. ( Libonati, JR, 2012)
"Hypertension is strongly associated with increased risk of subsequent heart failure."	1.35	[Hypertension and the heart]. ( Andersen, NH; Svendsen, TL; Wachtell, K, 2009)
"Nifedipine-treated animals displayed hemodynamics, LV dilatation, hypertrophy, and loss of function similar to those of the untreated group."	1.35	Comparative study of vasodilators in an animal model of chronic volume overload caused by severe aortic regurgitation. ( Arsenault, M; Beaudoin, J; Champetier, S; Couet, J; Lachance, D; Plante, E; Roussel, E, 2009)
"Arterial hypertension is the most frequent chronic disease and it is an important cause of morbidity and mortality in the developed world."	1.34	Analysis of antihypertensive drugs in the heart of animal models: a proteomic approach. ( Egido, J; Gállego-Delgado, J; Lázaro, A; Osende, JI; Vivanco, F, 2007)
"Losartan prevented the increase of HBR in the AT group."	1.34	The role of angiotensin receptor-1 blockade on electromechanical changes induced by left ventricular hypertrophy and its regression. ( Fry, CH; Gray, RP; Sheridan, DJ; Turner, MA, 2007)
"Established left ventricular hypertrophy (LVH) showed a significant alteration in the cardiac protein profile compared with normal heart."	1.33	Comparison of the protein profile of established and regressed hypertension-induced left ventricular hypertrophy. ( Barderas, MG; Duran, MC; Egido, J; Gallego-Delgado, J; Lazaro, A; Osende, JI; Vivanco, F, 2006)
" In dose-finding experiments in non-hypertrophied isolated perfused hearts, we performed dose-response curves of losartan and enalaprilat studying monophasic action potential duration at 90% repolarisation (MAPD(90%)) and ventricular fibrillation (VF) threshold."	1.32	Losartan but not enalaprilat acutely reduces reperfusion ventricular tachyarrhythmias in hypertrophied rat hearts after low-flow ischaemia. ( Beier, K; Bellahcene, M; Buser, PT; Butz, S; Driamov, S; Remondino, A; Zaugg, CE; Ziegler, A, 2004)
"Compared with WKY, SHR exhibited left ventricular hypertrophy, increased (P<0."	1.31	Chronic AT(1) blockade stimulates extracellular collagen type I degradation and reverses myocardial fibrosis in spontaneously hypertensive rats. ( Díez, J; Etayo, JC; Iraburu, MJ; López, B; Varela, M; Varo, N, 2000)
"Thirty-two patients with untreated hypertension (BP 168/96) had significantly lower levels of both MMP-9 and TIMP-1 when compared to 24 matched normotensive controls (BP 123/80) (P<0."	1.31	Matrix metalloproteinase-9 and tissue inhibitor metalloproteinase-1 levels in essential hypertension. Relationship to left ventricular mass and anti-hypertensive therapy. ( Beevers, DG; Blann, AD; Edmunds, E; Li-Saw-Hee, FL; Lip, GY, 2000)
"Because left ventricular hypertrophy is very common in renal transplant recipients, we examined the cardiovascular effects and the safety profile of the AT1 receptor antagonist losartan in hypertensive renal transplant recipients."	1.31	Regression of left ventricular hypertrophy by AT1 receptor blockade in renal transplant recipients. ( Delles, C; Fleischmann, E; Klingbeil, AU; Müller, HJ; Schmieder, RE, 2000)
"The development of hypertension and left ventricular hypertrophy was prevented by high- but not low-dose ramipril and was not affected by chronic bradykinin B2-receptor blockade."	1.30	Blockade of bradykinin B2 receptors prevents the increase in capillary density induced by chronic angiotensin-converting enzyme inhibitor treatment in stroke-prone spontaneously hypertensive rats. ( Amann, K; Gohlke, P; Kuwer, I; Mall, G; Schnell, A; Unger, T, 1997)
"By contrast, neither the concentric left ventricular hypertrophy or depressed myocardial function nor the increased beta-MHC expression were significantly altered."	1.30	Development of pressure overload induced cardiac hypertrophy is unaffected by long-term treatment with losartan. ( Rupp, H; Turcani, M, 1998)
" This dose of losartan shifted the in vivo dose-response curve of the angiotensin II-induced elevation of left ventricular systolic pressure (LVSP) to the right."	1.30	Differential effects of angiotensin II receptor blockade on pressure-induced left ventricular hypertrophy and fibrosis in rats. ( Baba, HA; Bauer, M; Irlbeck, M; Iwai, T; Schmid, KW; Zimmer, HG, 1999)
"Arterial hypertension is a cardinal precursor of congestive heart failure, and diastolic dysfunction is the most frequent mechanism for it."	1.30	[Arterial hypertension and systolic left ventricular dysfunction: therapeutic approach]. ( Anguita Sánchez, M, 1999)
"Losartan treatment decreased systolic pressure and yellow-red collagen fiber content in all areas, whereas spironolactone treatment decreased green collagen fiber content without decreasing systolic pressure."	1.29	Left ventricular fibrosis in renovascular hypertensive rats. Effect of losartan and spironolactone. ( Appay, MD; Bariety, J; Heudes, D; Hinglais, N; Michel, JB; Nicoletti, A; Philippe, M; Sassy-Prigent, C, 1995)
"Losartan and enalapril treatments decreased blood pressure and induced complete regression of LVH in this model of renovascular hypertension."	1.29	Regression of left ventricular hypertrophy in experimental renovascular hypertension: diastolic dysfunction depends more on myocardial collagen than it does on myocardial mass. ( Cespedes, C; Dussaillant, GR; Gonzalez, H; Jalil, JE, 1996)

Research

Studies (302)

Authors

Clinical Trials (19)

Trial Overview

Trial Outcomes

Percentage Change From Baseline in Extent of Left Ventricular Fibrosis at 1 Year as Assessed by Magnetic Resonance Imaging.

Percentage Change From Baseline in Left Ventricular Mass at 1 Year as Assessed by Magnetic Resonance Imaging.

Change in Left Ventricular Mass Index (LVMI) From Baseline to End of Study (Week 36)

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	39 (12.91)	18.2507
2000's	191 (63.25)	29.6817
2010's	70 (23.18)	24.3611
2020's	2 (0.66)	2.80

Authors	Studies
Kovács, MG	1
Kovács, ZZA	1
Varga, Z	1
Szűcs, G	1
Freiwan, M	1
Farkas, K	1
Kővári, B	1
Cserni, G	1
Kriston, A	1
Kovács, F	1
Horváth, P	1
Földesi, I	1
Csont, T	1
Kahán, Z	1
Sárközy, M	1
Ahmad, MI	1
Kazibwe, R	1
Soliman, MZ	1
Singh, S	2
Chen, LY	1
Soliman, EZ	1
Moroni, C	1
Tolone, S	1
Lopreiato, F	1
Scrofani, AR	1
Bossini, A	1
Affricano, C	1
Cassone, R	1
Gaudio, C	1
Okin, PM	52
Hille, DA	20
Kjeldsen, SE	73
Devereux, RB	115
Okura, T	1
Miyoshi, K	1
Irita, J	1
Enomoto, D	1
Jotoku, M	1
Nagao, T	1
Watanabe, K	1
Matsuoka, H	1
Ashihara, T	1
Higaki, J	1
Bang, CN	6
Wachtell, K	76
Dahlöf, B	114
Wiik, BP	2
Lindholm, LH	37
Kusunoki, H	1
Taniyama, Y	1
Rakugi, H	1
Morishita, R	1
Gerdts, E	41
Aurigemma, GP	7
Boman, K	26
Roman, MJ	4
Køber, L	3
McLachlan, J	1
Beattie, E	1
Murphy, MP	1
Koh-Tan, CH	1
Olson, E	1
Beattie, W	1
Dominiczak, AF	1
Nicklin, SA	1
Graham, D	1
Gottlieb, AB	1
Stuckey, DJ	1
McSweeney, SJ	1
Thin, MZ	1
Habib, J	1
Price, AN	1
Fiedler, LR	1
Gsell, W	1
Prasad, SK	1
Schneider, MD	1
Angeli, F	2
Reboldi, G	2
Verdecchia, P	2
Julius, S	34
Mancusi, C	2
De Simone, G	15
Abdelhai, YM	1
Lønnebakken, MT	3
Shimada, YJ	1
Passeri, JJ	1
Baggish, AL	1
O'Callaghan, C	1
Lowry, PA	1
Yannekis, G	1
Abbara, S	1
Ghoshhajra, BB	1
Rothman, RD	1
Ho, CY	1
Januzzi, JL	1
Seidman, CE	1
Fifer, MA	1
Freitas, F	1
Estato, V	1
Lessa, MA	1
Tibiriçá, E	1
Sawa, T	1
Sato, Y	1
Matsuda, M	1
Tanaka, M	1
Miyazaki, S	1
Furukawa, Y	1
Kita, Y	1
Takatsu, Y	1
Fujiwara, H	1
Goda, A	2
Masuyama, T	2
Cooper, RM	1
Stables, RH	1
Axelsson, A	1
Iversen, K	1
Vejlstrup, N	1
Ho, C	1
Norsk, J	1
Langhoff, L	1
Ahtarovski, K	1
Corell, P	1
Havndrup, O	1
Jensen, M	1
Bundgaard, H	1
Klimas, J	1
Olvedy, M	1
Ochodnicka-Mackovicova, K	1
Kruzliak, P	1
Cacanyiova, S	1
Kristek, F	1
Krenek, P	1
Ochodnicky, P	1
Larstorp, AC	5
Derosa, G	2
Mugellini, A	2
Querci, F	1
Franzetti, I	1
Pesce, RM	1
D'Angelo, A	1
Maffioli, P	1
Vishram, JK	1
Ibsen, H	45
Mancia, G	2
Rothwell, PM	1
Olsen, MH	35
Palmieri, V	15
Nieminen, MS	56
Papademetriou, V	17
Tanoue, MT	1
Kamel, H	1
Midtbø, H	1
Wang, TJ	1
Lian, GL	1
Lin, X	1
Zhong, HB	1
Xu, CS	1
Wang, HJ	1
Xie, LD	1
Zhao, LL	1
Chen, HJ	1
Chen, JZ	1
Yu, M	1
Ni, YL	1
Zhang, WF	1
Biederman, RW	1
Doyle, M	1
Young, AA	1
Kortright, E	1
Perry, G	1
Bella, JN	9
Oparil, S	21
Calhoun, D	1
Pohost, GM	1
Dell'Italia, LJ	1
Avanza, AC	2
Mansur, AP	1
Ramires, JA	1
Beevers, G	13
de Faire, U	20
Fyhrquist, F	21
Lederballe-Pedersen, O	18
Narayan, P	3
Omvik, P	24
Wedel, H	17
Anguita, M	1
Toledano, F	1
León, C	1
Castillo, JC	1
Solomon, SD	3
Appelbaum, E	3
Manning, WJ	1
Verma, A	2
Berglund, T	1
Lukashevich, V	2
Cherif Papst, C	1
Smith, BA	2
Lyle, PA	12
Wu, ZL	1
Xu, DL	1
Li, Y	1
Lai, WY	1
Huang, P	1
Bai, SC	1
Su, L	1
Gallego-Delgado, J	3
Connolly, SB	1
Lázaro, A	3
Sadlier, D	1
Kieran, NE	1
Sugrue, DD	1
Doran, P	1
Brady, HR	1
Osende, J	1
Egido, J	3
Oikarinen, L	11
Viitasalo, M	7
Toivonen, L	7
Edelman, JM	21
Olofsson, M	2
Mitsuhashi, H	1
Tamura, K	1
Yamauchi, J	1
Ozawa, M	1
Yanagi, M	1
Dejima, T	1
Wakui, H	1
Masuda, S	1
Azuma, K	1
Kanaoka, T	1
Ohsawa, M	1
Maeda, A	1
Tsurumi-Ikeya, Y	1
Okano, Y	1
Ishigami, T	1
Toya, Y	1
Tokita, Y	1
Ohnishi, T	1
Umemura, S	1
Jessup, JA	1
Westwood, BM	1
Chappell, MC	1
Groban, L	1
Keating, GM	2
Franklin, S	1
Rieck, A	1
Nieminen, M	1
Andersen, NH	1
Svendsen, TL	1
Morin, DP	1
John, M	1
Chinali, M	1
Mishra, RK	1
Plante, E	1
Lachance, D	1
Beaudoin, J	1
Champetier, S	1
Roussel, E	1
Arsenault, M	1
Couet, J	1
Gopinathannair, R	1
Sullivan, RM	1
Olshansky, B	1
Boman, JH	1
Andersson, J	1
Snapinn, SM	7
Nordestgaard, BG	1
Kontula, K	2
Benn, M	1
Eliasson, E	1
Berg, K	1
Sandberg, M	1
Sethi, AA	1
Wong, PH	1
Os, I	4
Bozbaş, SS	1
Bozbaş, H	1
Atar, A	1
Ulubay, G	1
Oner Eyüboğlu, F	1
Rokkedal, JE	2
Søraas, CL	1
Tønnessen, T	1
Høieggen, A	4
Lindholm, L	1
Mazzotta, G	1
Kong, J	1
Kim, GH	1
Wei, M	1
Sun, T	1
Li, G	1
Liu, SQ	1
Li, X	1
Bhan, I	1
Zhao, Q	1
Thadhani, R	1
Li, YC	1
Ulusoy, S	1
Ozkan, G	1
Orem, C	1
Kaynar, K	1
Koşucu, P	1
Kiriş, A	1
Yoshida, C	1
Naito, Y	1
Nakaboh, A	1
Matsumoto, M	1
Otsuka, M	1
Ohyanagi, M	1
Hirotani, S	1
Lee-Kawabata, M	1
Tsujino, T	1
Yamamoto, K	2
Ozaki, H	1
Takayasu, K	1
Akehi, N	1
Fukui, S	1
Sakai, A	1
Kodama, M	1
Shimonagata, T	1
Kobayashi, K	1
Ota, M	1
Horiguchi, Y	1
Ebisuno, S	1
Katsube, Y	1
Yamazaki, T	1
Ohtsu, H	1
Hori, M	2
Yamada, Y	1
Tsuboi, K	1
Hattori, T	1
Murase, T	1
Ohtake, M	1
Furukawa, M	1
Ueyama, J	1
Nishiyama, A	1
Murohara, T	1
Nagata, K	1
Silventoinen, K	1
Saijonmaa, O	1
Pouleur, AC	2
Uno, H	1
Prescott, MF	1
Desai, A	1
Lund, BP	1
Fogari, R	1
Destro, M	1
Corradi, L	1
Lazzari, P	1
Zoppi, A	1
Preti, P	1
Hasegawa, H	1
Takano, H	1
Narumi, H	1
Ohtsuka, M	1
Mizuguchi, T	1
Namiki, T	1
Kobayashi, Y	1
Komuro, I	1
Ariansen, I	2
Reims, HM	5
Gjesdal, K	2
Libonati, JR	1
Vardeny, O	1
Takeuchi, M	1
Prescott, M	1
Smith, B	1
Zentner, D	1
Pedagogos, E	1
Yapanis, A	1
Karapanagiotidis, S	1
Kinghorn, A	1
Alexiou, A	1
Lee, G	1
Raspudic, M	1
Aggarwal, A	1
Greve, AM	1
Meems, LM	1
Cannon, MV	1
Mahmud, H	1
Voors, AA	2
van Gilst, WH	1
Silljé, HH	1
Ruifrok, WP	1
de Boer, RA	1
Peng, F	1
Lin, J	1
Lin, L	1
Tang, H	1
Itoi, T	1
Oka, T	1
Terada, N	1
Gay-Jordi, G	1
Guash, E	1
Benito, B	1
Brugada, J	1
Nattel, S	1
Mont, L	1
Serrano-Mollar, A	1
De Marco, M	1
Casalnuovo, G	1
Migliore, T	1
Kizer, JR	4
Liu, JE	3
Borch-Johnsen, K	6
Zanchetti, A	3
Diez, J	6
Nicholls, MG	2
Yu, CM	1
Barrios, V	1
Aurup, P	8
Smith, RD	2
Johansson, M	1
Kristianson, K	12
Snapinn, S	7
Akinboboye, OO	1
Chou, RL	1
Bergmann, SR	1
Malik, RA	1
Edelman, J	1
Dominiak, P	1
Zidek, W	2
Massie, BM	1
Shibasaki, Y	2
Nishiue, T	2
Masaki, H	2
Matsubara, H	3
Iwasaka, T	2
Holtwick, R	1
Baba, HA	2
Ehler, E	1
Risse, D	1
Vobeta, M	1
Gehrmann, J	1
Pierkes, M	1
Kuhn, M	1
Yu, G	2
Liang, X	2
Xie, X	2
Yang, T	1
Sun, M	1
Zhao, S	2
Messerli, FH	2
Mehra, MR	1
Rokkedal, J	8
Smith, G	4
Karpov, IuA	1
Adams, HP	1
Schmieder, RE	2
Schneider, MP	1
Trenkwalder, P	1
Pedersen, OL	1
Nadar, S	1
Lim, HS	1
Lip, GY	3
Liebson, PR	1
Jern, S	14
Harris, KE	11
Xu, R	1
Zhang, Y	2
Zhang, M	1
Ge, ZM	1
Li, XC	1
Zhang, W	1
Helle Berg, S	1
Lapointe, N	2
Pourdjabbar, A	2
Rouleau, JL	2
Baumgart, P	2
Sidorenko, BA	1
Ugriumova, MO	1
Ong, HT	1
Chazova, IE	1
Ratova, LG	1
Dmitriev, VV	1
Sinitsin, VE	1
Stukalova, OV	1
Li, J	1
Li, P	1
Feng, X	1
Li, Z	2
Hou, R	1
Han, C	1
Waugh, J	1
Witham, MD	1
Davies, JI	1
Dawson, A	2
Davey, PG	1
Struthers, AD	2
Alderman, MH	1
Douglas, JG	1
Nesbitt, S	1
Randall, OS	1
Wright, JT	2
Burke, TA	3
Krobot, K	1
Carides, GW	3
Diener, HC	1
Liakishev, AA	1
Bratland, B	1

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients[NCT05637216]	Phase 2	40 participants (Anticipated)	Interventional	2023-08-17	Recruiting
A Triple-Blind, Parallel Study to Investigate the Effect of Losartan Versus Atenolol on the Reduction of Morbidity and Mortality in Hypertensive Patients With Left Ventricular Hypertrophy[NCT00338260]	Phase 3	496 participants (Actual)	Interventional	1995-06-30	Completed
Effect of Losartan in Patients With Nonobstructive Hypertrophic Cardiomyopathy[NCT01150461]	Phase 2	20 participants (Actual)	Interventional	2007-02-28	Completed
Clinical and Genetic Determinants of Disease Progression and Response to Lifestyle and Pharmacological Interventions in Patients With Hypertrophic Cardiomyopathy[NCT05366101]	Phase 2/Phase 3	168 participants (Actual)	Interventional	2019-04-01	Completed
Clinical and Genetic Determinants of Disease Progression and Response to Sacubitril/Valsartan vs Lifestyle (Physical Activity and Dietary Nitrate) in Patients With Hypertrophic Cardiomyopathy[NCT03832660]	Phase 2	168 participants (Actual)	Interventional	2019-05-03	Completed
INHibition of the Renin Angiotensin System in Hypertrophic Cardiomyopathy and the Effect on Ventricular Hypertrophy - a Randomized Intervention Trial With Losartan.[NCT01447654]	Phase 2	130 participants (Actual)	Interventional	2011-11-30	Completed
Evaluation of Some Emerging Biomarkers of Cardiovascular Risk Stratification in Hypertensive Patients: a 5-years Follow-up[NCT02064218]		0 participants	Observational	2007-11-30	Recruiting
Pilot Study of Cardiac Magnetic Resonance in Patients With Muscular Dystrophy[NCT02921321]		100 participants (Anticipated)	Observational	2014-01-31	Active, not recruiting
Assessment of Prolonged Paced QRS Duration as a Marker of Sudden Cardiac Death in Subjects With Implantable Cardioverter-defibrillators[NCT01948206]		100 participants (Actual)	Observational	2013-10-31	Terminated (stopped due to Ran out of funds)
A 36-week, Randomized, Double-blind, Multi-center, Parallel Group Study Comparing the Efficacy and Safety of Aliskiren in Combination With Losartan Compared to Losartan on the Regression of Left Ventricular Hypertrophy in Overweight Patients With Essentia[NCT00219141]	Phase 3	460 participants (Actual)	Interventional	2005-10-31	Completed
Early and Late Cardiac Effects of Arteriovenous Fistula Creation for Haemodialysis in End-stage Renal Failure and Their Possible Attenuation[NCT00602004]		52 participants (Anticipated)	Interventional	2006-10-31	Completed
Prevention of Hypertension Incidence and Diabetes Italian Assessment Study. Therapeutic Strategies of Prevention of Diabetes and Hypertension in Subjects With Metabolic Syndrome and High-Normal Blood Pressure.[NCT00456963]	Phase 4	3,000 participants (Anticipated)	Interventional	2007-09-30	Terminated (stopped due to Because of delay in approval of the protocol by a number of Ethics Commitees the trial was terminated on March 4, 2010. No patient had received any study drug.)
Angiotensin Blocking Effect of Fimasartan on Hypertensive Cardiac Disease With Left Ventricular Hypertrophy Estimated by ECG: a Prospective, Multicenter, Observational Registry[NCT03219632]		72 participants (Actual)	Observational [Patient Registry]	2012-06-05	Completed
Characterization of Myocardial Interstitial Fibrosis and Cardiomyocyte Hypertrophy by Cardiac MRI In Heart Failure: Implication on Early Remodeling and on the Transition to Heart Failure[NCT03084679]		90 participants (Anticipated)	Interventional	2017-11-01	Recruiting
Improving Outcomes in Atrial Fibrillation Patients Aided by Implantable Cardiac Monitor: Evaluation of Chronic Beta-blocker Use Versus As-needed Pharmacological Rate Control[NCT05745337]	Phase 1	20 participants (Anticipated)	Interventional	2023-02-06	Recruiting
A Pilot Study Of ALT-711 In Elderly Patients With Isolated Diastolic Heart Failure: The DIAMOND Study[NCT00043836]	Phase 2	20 participants	Interventional	2002-07-31	Completed
Psychosocial Factors and Cardiovascular Disease[NCT00005315]		0 participants	Observational	1993-09-30	Completed
Molecular Mechanisms of Volume Overload-Aim 1(SCCOR in Cardiac Dysfunction and Disease)[NCT01052428]	Phase 2/Phase 3	38 participants (Actual)	Interventional	2004-08-31	Completed
Phase 2/3 Study of Effect of AT1RB Versus ACE Inhibitor in Addition to XO Inhibitor on Progression of LV Remodeling and Dysfunction in Diabetic Patients With Acute MI.[NCT01052272]	Phase 2/Phase 3	72 participants (Actual)	Interventional	2005-07-31	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Intervention	Percentage change in fibrotic myocardium (Mean)
Losartan 50 mg PO BID	-23
Placebo	31

Intervention	Percentage change in LV mass (Mean)
Losartan 50 mg PO BID	-5
Placebo	5

Left ventricular mass index (LVMI) was measured by magnetic resonance imaging (MRI). An increase in LVMI indicates hypertrophy of the left ventricle. This could be a normal reversible response to cardiovascular conditioning (athletic heart) or an abnormal irreversible response to chronically increased volume load (preload) or increased pressure load (afterload). Thickening of the ventricular muscle results in increased left ventricular pressure, increased end-systolic volume, and decreased end-diastolic volume, causing an overall reduction in cardiac output. (NCT00219141)
Timeframe: Baseline to end of study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Cornell Voltage Duration Product as Measured by Electrocardiogram From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Diameter of Ascending Aorta as Measured by MRI From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Left Ventricular Anteroseptal Wall Thickness as Measured by MRI From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Left Ventricular Ejection Fraction as Measured by MRI From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Left Ventricular End Diastolic Mass as Measured by MRI From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Left Ventricular End Diastolic Volume as Measured by MRI From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Left Ventricular End Systolic Volume as Measured by MRI From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Left Ventricular Inferolateral Wall Thickness as Measured by MRI From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Left Ventricular Mass Index as Measured by MRI From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Left Ventricular Stroke Volume as Measured by MRI From Baseline to End of Study (Week 36)

Change in the Left Ventricular Hypertrophy (LVH) Parameter Sokolow-Lyon Voltage as Measured by Electrocardiogram From Baseline to End of Study (Week 36)

Change From Baseline in Mean 24-hour Ambulatory Diastolic and Systolic Blood Pressure From Baseline to the End of the Study (Week 36)

Intervention	g/m^2 (Least Squares Mean)
Aliskiren 300 mg	-5.51
Losartan 100 mg	-4.81
Aliskiren/Losartan 300/100 mg	-5.61

Intervention	mm * ms (Mean)
Aliskiren 300 mg	-104.97
Losartan 100 mg	-150.31
Aliskiren/Losartan 300/100 mg	-130.65

Intervention	mm (Mean)
Aliskiren 300 mg	-0.71
Losartan 100 mg	-0.64
Aliskiren/Losartan 300/100 mg	-0.86

Intervention	mm (Mean)
Aliskiren 300 mg	-0.95
Losartan 100 mg	-1.20
Aliskiren/Losartan 300/100 mg	-1.17

Intervention	percent (Mean)
Aliskiren 300 mg	0.62
Losartan 100 mg	2.02
Aliskiren/Losartan 300/100 mg	1.92

Intervention	g (Mean)
Aliskiren 300 mg	-9.81
Losartan 100 mg	-9.92
Aliskiren/Losartan 300/100 mg	-12.29

Intervention	mL (Mean)
Aliskiren 300 mg	-7.05
Losartan 100 mg	-4.52
Aliskiren/Losartan 300/100 mg	-7.03

Intervention	mL (Mean)
Aliskiren 300 mg	-3.20
Losartan 100 mg	-4.73
Aliskiren/Losartan 300/100 mg	-5.14

Intervention	mm (Mean)
Aliskiren 300 mg	-0.88
Losartan 100 mg	-0.89
Aliskiren/Losartan 300/100 mg	-0.90

Intervention	g/m^2 (Mean)
Aliskiren 300 mg	-4.87
Losartan 100 mg	-4.79
Aliskiren/Losartan 300/100 mg	-5.81

Intervention	mL (Mean)
Aliskiren 300 mg	-3.89
Losartan 100 mg	0.24
Aliskiren/Losartan 300/100 mg	-2.24

Intervention	mm (Mean)
Aliskiren 300 mg	-1.07
Losartan 100 mg	-0.97
Aliskiren/Losartan 300/100 mg	-1.43

Two 24-hour ambulatory blood pressure monitoring (ABPM) evaluations were performed, one at baseline and one at the end of the study. For each evaluation, the ABPM device was attached to the non-dominant arm of the patient. A correlation was made between the ABPM device readings and measurements taken with a mercury sphygmomanometer and stethoscope. Following the correlation procedure, blood pressure was measured at study specified intervals. (NCT00219141)
Timeframe: Baseline the end of study (Week 36)

Left Ventricular Ejection Fraction

Intervention	mm Hg (Least Squares Mean)
	Systolic	Diastolic
Aliskiren 300 mg	-2.67	-1.31
Aliskiren/Losartan 300/100 mg	-6.97	-4.11
Losartan 100 mg	-3.81	-1.92

Left Ventricular Ejection Fraction Is a calculation of heart pump function determined from the volume after complete filling minus the volume after complete contraction divided by the volume after complete filling. A value of 55% or greater is normal. (NCT01052428)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Left Ventricular End Diastolic Volume Indexed to Body Surface Area

Intervention	percent (Mean)
	Month 0 (n=19,19)	Month 3 (n=1,0)	Month 6 (n=17,19)	Month 9 (n=1,1)	Month 12 (n=14,15)	Month 15 (n=3,2)	Month 18 (n=14,18)	Month 21 (n=5,0)	Month 24 (n=16,18)
Placebo	62.62	63.90	63.80	41.90	61.70	44.70	60.95	53.79	59.95
Toprol XL	62.09	NA	61.29	54.81	62.77	68.47	62.05	NA	63.02

Left Ventricular End Diastolic Volume Indexed to Body Surface Area: As an indicator of heart size, the blood volume of the heart is related to the body size. The end diastolic volume is the blood volume of the heart at the end of filling, just before contraction. The relation of heart blood volume to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. (NCT01052428)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Left Ventricular End Systolic Volume Indexed to Body Surface Area

Intervention	ml/m^2 (Mean)
	Month 0 (n=19,19)	Month 3 (n=1,0)	Month 6 (n=17,19)	Month 9 (n=1,0)	Month 12 (n=14,15)	Month 15 (n=3,2)	Month 18 (n=14,18)	Month 21 (n=5,0)	Month 24 (n=16,18)
Placebo	91.66	90.93	90.84	70.56	88.99	82.73	90.16	85.75	87.31
Toprol XL	95.74	NA	95.24	NA	95.71	98.16	97.6	NA	95.16

Left Ventricular End Systolic Volume Indexed to Body Surface Area As an indicator of heart size, the blood volume of the heart is related to the body size. The end systolic volume is the blood volume of the heart at the end of contraction and is an index of the pump function of the heart. This relation to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. (NCT01052428)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Left Ventricular End-diastolic Mass Indexed to Left Ventricular End-diastolic Volume

Intervention	ml/m^2 (Mean)
	Month 0 (n=19,19)	Month 3 (n=1,0)	Month 6 (n=17,19)	Month 9 (n=1,0)	Month 12 (n=14,15)	Month 15 (n=3,2)	Month 18 (n=14,18)	Month 21 (n=5,0)	Month 24 (n=16,18)
Placebo	34.01	32.83	32.53	40.99	33.70	47.25	34.99	39.97	34.47
Toprol XL	35.98	NA	36.53	NA	35.89	30.97	36.72	NA	35.13

Left Ventricular End-diastolic Mass Indexed to Left Ventricular End-diastolic Volume As an indicator of heart muscle mass and heart blood volume, the mass indexed to end diastolic volume determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a three-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. (NCT01052428)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Left Ventricular End-Diastolic Radius to Wall Thickness

Intervention	g/ml (Mean)
	Month 0 (n=19,19)	Month 3 (n=1,0)	Month 6 (n=17,19)	Month 9 (n=1,1)	Month 12 (n=14,15)	Month 15 (n=3,2)	Month 18 (n=14,18)	Month 21 (n=5,0)	Month 24 (n=16,18)
Placebo	0.61	0.53	0.62	0.67	0.65	0.65	0.65	0.61	0.64
Toprol XL	0.61	NA	0.6	0.53	0.60	0.55	0.59	NA	0.62

Left Ventricular End-Diastolic Radius to Wall Thickness As an indicator of heart muscle mass and heart volume chamber diameter, the end-diastolic radius indexed to end diastolic wall thickness determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a two-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. (NCT01052428)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Peak Early Filling Rate: Rate of Change Over Time

Intervention	unitless (Mean)
	Month 0 (n=19,19)	Month 3 (n=1,0)	Month 6 (n=17,19)	Month 9 (n=1,1)	Month 12 (n=14,15)	Month 15 (n=3,2)	Month 18 (n=14,18)	Month 21 (n=5,0)	Month 24 (n=16,18)
Placebo	4.76	5.02	4.51	4.15	4.46	4.61	4.43	4.72	4.52
Toprol XL	4.69	NA	4.85	5.74	4.79	5.02	4.77	NA	4.59

Peak Early Filling Rate The peak early filling rate of change is calculated from the slope of the volume during the early filling of the heart with respect to time. The higher values indicate a very healthy heart muscle and lower values are indicative of a very stiff muscle. (NCT01052428)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Systolic Longitudinal Strain

Intervention	EDV/sec (Mean)
	Month 0 (n=19,19)	Month 3 (n=1,0)	Month 6 (n=17,19)	Month 9 (n=1,0)	Month 12 (n=14,15)	Month 15 (n=3,2)	Month 18 (n=14,18)	Month 21 (n=5,0)	Month 24 (n=16,18)
Placebo	2.27	2.58	2.38	1.56	2.26	1.83	1.95	1.73	2.17
Toprol XL	2.12	NA	2.08	NA	2.24	2.28	2.26	NA	2.25

Systolic Longitudinal Strain. By identifying two points on the heart, the strain is the difference between the distance between these two points at the end of filling of the heart and the end of contraction divided by the length at the end of filling. Thus, the measure is like the ejection fraction, however the strain is more localized to a specified segment in the heart muscle. The higher values indicate a healthy heart. (NCT01052428)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Left Ventricular Ejection Fraction (LVEF)

Intervention	percent/%Systolic interval (Mean)
	Month 0 (n=19,19)	Month 3 (n=1,0)	Month 6 (n=17,19)	Month 9 (n=1,0)	Month 12 (n=14,15)	Month 15 (n=3,2)	Month 18 (n=14,18)	Month 21 (n=5,0)	Month 24 (n=16,18)
Placebo	87.94	115.07	45.90	37.2	87.85	52.95	88.11	67.53	79.94
Toprol XL	82.55	NA	78.68	NA	80.04	88.34	79.29	NA	85.18

LVEF is a calculation of heart pump function determined from the volume after complete filling minus the volume after complete contraction divided by the volume after complete filling. A value of 55% or greater is normal. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Left Ventricular End Diastolic Volume Indexed to Body Surface Area (LVEDV/BSA)

Intervention	percent (Mean)
	Month 0 (n=17,17,18,18)	Month 6(n=14,11,11,12)	Month 9(n=1,2,0,0)	Month 12(n=12,11,11,11)	Month 15(n=3,2,1,1)	Month 18(n=10,12,8,8)	Month 21(n=3,0,0,1)	Month 24 (n=11,9,8,10)	Month 27 (n=1,1,0,1)
Candesartan Cilexetil	56.36	56.82	42.62	52.37	39.88	56.33	NA	51.70	54.17
Candesartan Cilexetil and Allopurinol	52.68	57.28	NA	56.11	54.46	57.82	56.17	55.79	54.40
Ramipril	52.19	54.20	64.98	52.76	52.13	55.02	51.27	57.18	50.73
Ramipril and Allopurinol	53.37	52.80	NA	51.74	34.89	54.05	NA	55.59	NA

LVEDV/BSA: As an indicator of heart size, the blood volume of the heart is related to the body size. The relation of heart blood volume to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Diastolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Left Ventricular End Systolic Volume Indexed to Body Surface Area (LVESV/BSA)

Intervention	ml/m^2 (Mean)
	Month 0 (n=17,17,18,18)	Month 6(n=14,11,11,12)	Month 9(n=1,2,0,0)	Month12(n=12,11,11,11)	Month 15(n=3,2,1,1)	Month 18(n=10,12,8,8)	Month 21(n=3,0,0,1)	Month 24 (n=11,9,8,10)	Month 27 (n=1,1,0,1)
Candesartan Cilexetil	78.06	78.60	93.57	85.44	90.20	82.74	NA	84.28	76.65
Candesartan Cilexetil and Allopurinol	79.03	78.01	NA	79.75	63.1	84.95	75.27	79.72	75.05
Ramipril	73.03	74.10	73.23	75.34	81.19	75.28	71.99	70.46	48.68
Ramipril and Allopurinol	78.52	86.13	NA	83.95	108.25	67.96	NA	71.63	NA

LVESV/BSA: The end systolic volume is the blood volume of the heart at the end of contraction and is an index of the pump function of the heart. This relation to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Left Ventricular End-diastolic Mass Indexed to Left Ventricular End-diastolic Volume (LVED Mass/LVEDV)

Intervention	ml/m^2 (Mean)
	Month 0 (n=17,17,18,18)	Month 6(n=14,11,11,12)	Month 9(n=1,2,0,0)	Month 12(n=12,11,11,11)	Month 15(n=3,2,1,1)	Month 18(n=10,12,8,8)	Month 21(n=3,0,0,1)	Month 24 (n=11,9,8,10)	Month 27 (n=1,1,0,1)
Candesartan Cilexetil	35.26	35.26	53.87	42.27	54.04	37.76	NA	41.72	35.13
Candesartan Cilexetil and Allopurinol	39.49	34.15	NA	36.07	28.74	37.18	32.99	35.99	34.22
Ramipril	36.20	34.77	25.64	36.82	39.42	35.30	35.23	31.17	23.98
Ramipril and Allopurinol	37.91	42.88	NA	42.34	70.48	30.39	NA	31.56	NA

LVED Mass/LVEDV: As an indicator of heart muscle mass and heart blood volume, the mass indexed to end diastolic volume determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a three-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Geometry. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Left Ventricular End-Diastolic Radius to Wall Thickness (LVED Radius/Wall Thickness)

Intervention	g/ml (Mean)
	Month 0 (n=17,17,18,18)	Month 6(n=14,11,11,12)	Month 9(n=1,2,0,0)	Month 12(n=12,11,11,11)	Month 15(n=3,2,1,1)	Month 18(n=10,12,8,8)	Month 21(n=3,0,0,1)	Month 24 (n=11,9,8,10)	Month 27 (n=1,1,0,1)
Candesartan Cilexetil	0.95	0.83	0.67	0.78	0.70	0.79	NA	0.80	0.64
Candesartan Cilexetil and Allopurinol	0.87	0.82	NA	0.86	0.68	0.80	0.69	0.82	0.69
Ramipril	0.92	0.87	0.75	0.84	0.81	0.79	0.95	0.84	0.93
Ramipril and Allopurinol	0.86	0.71	NA	0.72	0.57	0.83	NA	0.80	NA

LVED Radius/Wall thickness As an indicator of heart muscle mass and heart volume chamber diameter, the end-diastolic radius indexed to end diastolic wall thickness determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a two-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Geometry. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

LV End Systolic Maximum Shortening (LVES Max Shortening)

Intervention	unitless (Mean)
	Month 0 (n=17,17,18,18)	Month 6(n=14,11,11,12)	Month 9(n=1,2,0,0)	Month 12(n=12,11,11,11)	Month 15(n=3,2,1,1)	Month 18(n=10,12,8,8)	Month 21(n=3,0,0,1)	Month 24 (n=11,9,8,10)	Month 27 (n=1,1,0,1)
Candesartan Cilexetil	3.14	3.39	4.14	3.68	4.10	3.71	NA	3.58	4.04
Candesartan Cilexetil and Allopurinol	3.45	3.63	NA	3.42	3.90	3.56	4.24	3.56	4.29
Ramipril	3.23	3.32	3.42	3.43	3.44	3.60	2.92	3.46	3.12
Ramipril and Allopurinol	3.57	4.04	NA	4.01	4.57	3.60	NA	3.61	NA

By identifying three points in three different planes in the heart muscle, the maximum shortening is the average of the difference between the distance between these three points at the end of filling of the heart and the end of contraction divided by the length at the end of filling times 100. The maximum shortening is a three dimensional analysis. The higher values indicate a healthy heart. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Peak Early Filling Rate Normalized to EDV

Intervention	percent of length at end of filling (Mean)
	Month 0 (n=17,17,17,18)	Month 6(n=14,11,10,12)	Month 9(n=1,2,0,0)	Month 12(n=11,11,10,10)	Month 15(n=3,2,1,1)	Month 18(n=10,12,7,8)	Month 21(n=3,0,0,1)	Month 24 (n=11,9,8,10)	Month 27 (n=1,1,0,1)
Candesartan Cilexetil	16.68	17.50	19.08	17.13	16.28	17.55	NA	16.62	20.38
Candesartan Cilexetil and Allopurinol	16.00	18.50	NA	18.51	16.36	17.52	17.89	17.85	16.59
Ramipril	15.81	16.88	18.43	14.57	17.06	17.26	16.68	15.67	13.70
Ramipril and Allopurinol	15.84	18.72	NA	17.96	14.22	17.46	NA	17.52	NA

The Peak Early Filling Rate Normalized to EDV is calculated from the slope of the volume during the early filling of the heart with respect to time. The higher values indicate a very healthy heart muscle and lower values are indicative of a very stiff muscle. This is a measure of LV Diastolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

Article	Year
Investigation of the Antihypertrophic and Antifibrotic Effects of Losartan in a Rat Model of Radiation-Induced Heart Disease. International journal of molecular sciences, 2021, Nov-30, Volume: 22, Issue:23 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Chymases; Disease Models, Animal; Heart Failure; H	2021
Joint Association of Albuminuria and Left Ventricular Hypertrophy With Incident Heart Failure in Adults at High Risk With Hypertension: A Systolic Blood Pressure Intervention Trial Substudy. The American journal of cardiology, 2023, 12-01, Volume: 208 Topics: Adult; Albuminuria; Antihypertensive Agents; Blood Pressure; Electrocardiography; Heart Failure; Hum	2023
Cardiac and renal protective effects of irbesartan via peroxisome proliferator-activated receptorγ-hepatocyte growth factor pathway independent of angiotensin II Type 1a receptor blockade in mouse model of salt-sensitive hypertension. Journal of the American Heart Association, 2013, Apr-22, Volume: 2, Issue:2 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Biphenyl Compounds; Disease Models, Animal; Epithe	2013
Combined therapeutic benefit of mitochondria-targeted antioxidant, MitoQ10, and angiotensin receptor blocker, losartan, on cardiovascular function. Journal of hypertension, 2014, Volume: 32, Issue:3 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Antihypertensive Agents; Antioxidants; Cell Enlarg	2014
T₁ mapping detects pharmacological retardation of diffuse cardiac fibrosis in mouse pressure-overload hypertrophy. Circulation. Cardiovascular imaging, 2014, Volume: 7, Issue:2 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Contrast Media; Disease Models, Animal; Dose-Respo	2014
Hypertension, inflammation and atrial fibrillation. Journal of hypertension, 2014, Volume: 32, Issue:3 Topics: Antihypertensive Agents; Atrial Fibrillation; Female; Humans; Hypertension; Hypertrophy, Left Ventri	2014
Cardiac microvascular rarefaction in hyperthyroid rats is reversed by losartan, diltiazem, and propranolol. Fundamental & clinical pharmacology, 2015, Volume: 29, Issue:1 Topics: Adrenergic beta-Antagonists; Animals; Diltiazem; Hyperthyroidism; Hypertrophy, Left Ventricular; Los	2015
Left ventricular hypertrophy as a target of treatment in patients with hypertension. Circulation journal : official journal of the Japanese Circulation Society, 2014, Volume: 78, Issue:11 Topics: Angiotensin Receptor Antagonists; Electrocardiography; Humans; Hydrochlorothiazide; Hypertrophy, Lef	2014
Relationship of left ventricular systolic function to persistence or development of electrocardiographic left ventricular hypertrophy in hypertensive patients: implications for the development of new heart failure. Journal of hypertension, 2014, Volume: 32, Issue:12 Topics: Aged; Antihypertensive Agents; Electrocardiography; Female; Heart Failure; Humans; Hypertension; Hyp	2014
Can RAS inhibitors affect the course of hypertrophic cardiomyopathy? The lancet. Diabetes & endocrinology, 2015, Volume: 3, Issue:2 Topics: Angiotensin II Type 1 Receptor Blockers; Cardiomyopathy, Hypertrophic; Female; Humans; Hypertrophy,	2015
Perinatally administered losartan augments renal ACE2 expression but not cardiac or renal Mas receptor in spontaneously hypertensive rats. Journal of cellular and molecular medicine, 2015, Volume: 19, Issue:8 Topics: Angiotensin-Converting Enzyme 2; Animals; Animals, Newborn; Female; Gene Expression Regulation; Hear	2015
Relationship of diastolic function to new or persistent electrocardiographic left ventricular hypertrophy. Blood pressure, 2016, Volume: 25, Issue:6 Topics: Antihypertensive Agents; Electrocardiography; Humans; Hypertension; Hypertrophy, Left Ventricular; L	2016
Electrocardiographic left atrial abnormalities and risk of incident stroke in hypertensive patients with electrocardiographic left ventricular hypertrophy. Journal of hypertension, 2016, Volume: 34, Issue:9 Topics: Age Factors; Aged; Antihypertensive Agents; Atenolol; Atrial Function, Left; Electrocardiography; Fe	2016
Hypomethylation of Agtrap is associated with long-term inhibition of left ventricular hypertrophy in prehypertensive losartan-treated spontaneously hypertensive rats. Molecular medicine reports, 2017, Volume: 15, Issue:2 Topics: Animals; Antihypertensive Agents; Blood Pressure; DNA Methylation; Fibrosis; Hypertension; Hypertrop	2017
Losartan reduced connexin43 expression in left ventricular myocardium of spontaneously hypertensive rats. Journal of Zhejiang University. Science. B, 2008, Volume: 9, Issue:6 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Blood Pressure; Blotting, Western; Connexin 43; Hy	2008
Marked regional left ventricular heterogeneity in hypertensive left ventricular hypertrophy patients: a losartan intervention for endpoint reduction in hypertension (LIFE) cardiovascular magnetic resonance and echocardiographic substudy. Hypertension (Dallas, Tex. : 1979), 2008, Volume: 52, Issue:2 Topics: Aged; Aged, 80 and over; Antihypertensive Agents; Blood Pressure Determination; Dose-Response Relati	2008
Effects of losartan compared with atenolol on lipids in patients with hypertension and left ventricular hypertrophy: the Losartan Intervention For Endpoint reduction in hypertension study. Journal of hypertension, 2009, Volume: 27, Issue:3 Topics: Aged; Antihypertensive Agents; Blood Pressure; Cardiovascular Diseases; Cholesterol; Cholesterol, HD	2009
[Effects of losartan on left ventricular hypertrophy and plasma transforming growth factor-beta1 in elderly patients with hypertension]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2009, Volume: 29, Issue:3 Topics: Aged; Antihypertensive Agents; Female; Humans; Hypertension; Hypertrophy, Left Ventricular; Losartan	2009
Transcriptome of hypertension-induced left ventricular hypertrophy and its regression by antihypertensive therapies. Hypertension research : official journal of the Japanese Society of Hypertension, 2009, Volume: 32, Issue:5 Topics: Animals; Antihypertensive Agents; Doxazosin; Drug Therapy, Combination; Gene Expression; Gene Expres	2009
Dual ACE-inhibition and AT1 receptor antagonism improves ventricular lusitropy without affecting cardiac fibrosis in the congenic mRen2.Lewis rat. Therapeutic advances in cardiovascular disease, 2009, Volume: 3, Issue:4 Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Animals; Animals,	2009
[Hypertension and the heart]. Ugeskrift for laeger, 2009, Jun-15, Volume: 171, Issue:25 Topics: Angiotensin II Type 1 Receptor Blockers; Antihypertensive Agents; Atrial Fibrillation; Cardiovascula	2009
Mitral E wave deceleration time to peak E velocity ratio and cardiovascular outcome in hypertensive patients during antihypertensive treatment (from the LIFE echo-substudy). The American journal of cardiology, 2009, Oct-15, Volume: 104, Issue:8 Topics: Aged; Antihypertensive Agents; Blood Flow Velocity; Echocardiography, Doppler; Female; Follow-Up Stu	2009
Comparative study of vasodilators in an animal model of chronic volume overload caused by severe aortic regurgitation. Circulation. Heart failure, 2009, Volume: 2, Issue:1 Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Animals; Aortic V	2009
Slower heart rates for healthy hearts: time to redefine tachycardia? Circulation. Arrhythmia and electrophysiology, 2008, Volume: 1, Issue:5 Topics: Adrenergic beta-Antagonists; Angiotensin II Type 1 Receptor Blockers; Antihypertensive Agents; Ateno	2008
Greater regression of electrocardiographic left ventricular hypertrophy during hydrochlorothiazide therapy in hypertensive patients. American journal of hypertension, 2010, Volume: 23, Issue:7 Topics: Aged; Aged, 80 and over; Antihypertensive Agents; Atenolol; Drug Therapy, Combination; Electrocardio	2010
Lack of regression of left ventricular hypertrophy is associated with higher incidence of revascularization in hypertension: The LIFE Study. Blood pressure, 2010, Volume: 19, Issue:3 Topics: Aged; Albuminuria; Angina Pectoris; Antihypertensive Agents; Atenolol; Blood Pressure; Cholesterol,	2010
In-treatment reduced left atrial diameter during antihypertensive treatment is associated with reduced new-onset atrial fibrillation in hypertensive patients with left ventricular hypertrophy: The LIFE Study. Blood pressure, 2010, Volume: 19, Issue:3 Topics: Aged; Antihypertensive Agents; Arrhythmias, Cardiac; Atenolol; Atrial Fibrillation; Blood Pressure;	2010
Changes in electrocardiographic left ventricular hypertrophy and risk of major cardiovascular events in isolated systolic hypertension: the LIFE study. Journal of human hypertension, 2011, Volume: 25, Issue:3 Topics: Aged; Aged, 80 and over; Antihypertensive Agents; Atenolol; Electrocardiography; Female; Follow-Up S	2011
Is hydrochlorothiazide more effective on LVH in nonresponders to losartan than in those to atenolol? American journal of hypertension, 2010, Volume: 23, Issue:7 Topics: Antihypertensive Agents; Atenolol; Electrocardiography; Humans; Hydrochlorothiazide; Hypertrophy, Le	2010
Relationship of left atrial enlargement to persistence or development of ECG left ventricular hypertrophy in hypertensive patients: implications for the development of new atrial fibrillation. Journal of hypertension, 2010, Volume: 28, Issue:7 Topics: Aged; Atrial Fibrillation; Blood Pressure; Cardiomegaly; Echocardiography; Electrocardiography; Fema	2010
Therapeutic effects of vitamin D analogs on cardiac hypertrophy in spontaneously hypertensive rats. The American journal of pathology, 2010, Volume: 177, Issue:2 Topics: Aged; Animals; Antihypertensive Agents; Ergocalciferols; Humans; Hypertrophy, Left Ventricular; Losa	2010
Mechanism underlying the efficacy of combination therapy with losartan and hydrochlorothiazide in rats with salt-sensitive hypertension. Hypertension research : official journal of the Japanese Society of Hypertension, 2011, Volume: 34, Issue:7 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Antihypertensive Agents; Aorta; Blood Pressure; Dr	2011
Cardiac remodeling and function following exercise and angiotensin II receptor antagonism. European journal of applied physiology, 2012, Volume: 112, Issue:8 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Blood Pressure; Hypertrophy, Left Ventricular; Los	2012
Association of heart failure hospitalizations with combined electrocardiography and echocardiography criteria for left ventricular hypertrophy. American journal of hypertension, 2012, Volume: 25, Issue:6 Topics: Aged; Aged, 80 and over; Antihypertensive Agents; Blood Pressure; Echocardiography; Electrocardiogra	2012
The vitamin D receptor activator paricalcitol prevents fibrosis and diastolic dysfunction in a murine model of pressure overload. The Journal of steroid biochemistry and molecular biology, 2012, Volume: 132, Issue:3-5 Topics: Animals; Aorta; Atrial Natriuretic Factor; Blood Pressure; Collagen Type III; Disease Models, Animal	2012
Transient prehypertensive treatment in spontaneously hypertensive rats: a comparison of losartan and amlodipine regarding long-term blood pressure, cardiac and renal protection. International journal of molecular medicine, 2012, Volume: 30, Issue:6 Topics: Aldosterone; Amlodipine; Angiotensin II; Animals; Antihypertensive Agents; Blood Pressure; Cardioton	2012
Modulation of C16:0-ceramide in hypertrophied immature hearts by losartan. Pediatrics international : official journal of the Japan Pediatric Society, 2013, Volume: 55, Issue:3 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Animals, Newborn; Aortic Valve Stenosis; Cardiomeg	2013
Losartan prevents heart fibrosis induced by long-term intensive exercise in an animal model. PloS one, 2013, Volume: 8, Issue:2 Topics: Analysis of Variance; Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Blotting, We	2013
Mitral annular calcification and incident ischemic stroke in treated hypertensive patients: the LIFE study. American journal of hypertension, 2013, Volume: 26, Issue:4 Topics: Aged; Aged, 80 and over; Calcinosis; Cardiomyopathies; Echocardiography; Female; Humans; Hypertensio	2013
[Better prognosis in hypertension and left ventricular hypertrophy. LIFE Study sets new standard]. MMW Fortschritte der Medizin, 2002, May-16, Volume: 144, Issue:20 Topics: Aged; Aged, 80 and over; Angiotensin Receptor Antagonists; Antihypertensive Agents; Atenolol; Dose-R	2002
A blood pressure independent association between glomerular albumin leakage and electrocardiographic left ventricular hypertrophy. The LIFE Study. Losartan Intervention For Endpoint reduction. Journal of human hypertension, 2002, Volume: 16, Issue:8 Topics: Aged; Albuminuria; Antihypertensive Agents; Blood Pressure; Creatinine; Female; Follow-Up Studies; H	2002
No morbidity-mortality. Commentary. Diabetic medicine : a journal of the British Diabetic Association, 2002, Volume: 19 Suppl 5 Topics: Adrenergic beta-Antagonists; Aged; Angiotensin II; Angiotensin Receptor Antagonists; Atenolol; Diabe	2002
[Isolated systolic hypertension. "AT1 blocker preferred over beta-blocker"]. MMW Fortschritte der Medizin, 2002, Sep-19, Volume: 144, Issue:38 Topics: Adrenergic beta-Antagonists; Angiotensin Receptor Antagonists; Antihypertensive Agents; Atenolol; Cl	2002
[German Hypertension League on the LIFE Study. New evaluation of AT1 receptor antagonists]. MMW Fortschritte der Medizin, 2002, Sep-19, Volume: 144, Issue:38 Topics: Adrenergic beta-Antagonists; Aged; Angiotensin Receptor Antagonists; Antihypertensive Agents; Atenol	2002
[What are the consequences of the LIFE Study for general practice]. MMW Fortschritte der Medizin, 2002, Sep-19, Volume: 144, Issue:38 Topics: Adrenergic beta-Antagonists; Aged; Angiotensin Receptor Antagonists; Antihypertensive Agents; Atenol	2002
Left but not right cardiac hypertrophy in atrial natriuretic peptide receptor-deficient mice is prevented by angiotensin type 1 receptor antagonist losartan. Journal of cardiovascular pharmacology, 2002, Volume: 40, Issue:5 Topics: Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Guanylate Cyclase; Hemodynamics;	2002
Apoptosis, myocardial fibrosis and angiotensin II in the left ventricle of hypertensive rats treated with fosinopril or losartan. Chinese medical journal, 2002, Volume: 115, Issue:9 Topics: Angiotensin II; Animals; Antihypertensive Agents; Apoptosis; Blood Pressure; Fibrosis; Fosinopril; H	2002
Crumbling of left ventricular hypertrophy as a surrogate end point (the Losartan for Intervention for Endpoint Reduction in Hypertension [LIFE] Study). The American journal of cardiology, 2002, Nov-15, Volume: 90, Issue:10 Topics: Antihypertensive Agents; Humans; Hypertension; Hypertrophy, Left Ventricular; Losartan; Randomized C	2002
New strategies for prevention of ischemic stroke: the LIFE study. Current neurology and neuroscience reports, 2003, Volume: 3, Issue:1 Topics: Aged; Aged, 80 and over; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Atenolol	2003
[Left ventricular hypertrophy. Recent aspects of diagnosis and therapy]. MMW Fortschritte der Medizin, 2002, Oct-17, Volume: 144, Issue:42 Topics: Adrenergic beta-Antagonists; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Aten	2002
[Is one antihypertensive agent as good as another?]. MMW Fortschritte der Medizin, 2002, Nov-07, Volume: 144, Issue:45 Topics: Aged; Antihypertensive Agents; Arteriosclerosis; Drug Therapy, Combination; Humans; Hypertension; Hy	2002
[Losartan in isolated systolic hypertension--convincing results of a LIFE sub-group study]. MMW Fortschritte der Medizin, 2003, Jan-16, Volume: 145, Issue:1-2 Topics: Aged; Antihypertensive Agents; Atenolol; Cause of Death; Double-Blind Method; Humans; Hypertension;	2003
The LIFE study: the straw that should break the camel's back. European heart journal, 2003, Volume: 24, Issue:6 Topics: Antihypertensive Agents; Atenolol; Humans; Hypertension; Hypertrophy, Left Ventricular; Losartan; My	2003
Summaries for patients. Benefits of losartan in patients with hypertension and left ventricular hypertrophy but no vascular disease. Annals of internal medicine, 2003, Aug-05, Volume: 139, Issue:3 Topics: Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Angiotensin Receptor Antagonists; Antihyperten	2003
The OPTIMAAL study, not so optimal: the lessons of LIFE, RENAAL and IDNT. The Canadian journal of cardiology, 2003, Volume: 19, Issue:9 Topics: Adult; Aged; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Captopril;	2003
Effect of losartan on sudden cardiac death in people with diabetes: data from the LIFE study. Lancet (London, England), 2003, Aug-23, Volume: 362, Issue:9384 Topics: Aged; Antihypertensive Agents; Arrhythmias, Cardiac; Atenolol; Atrial Fibrillation; Comorbidity; Dea	2003
[LIFE study proves preventive action. With losartan to do even more against stroke]. MMW Fortschritte der Medizin, 2003, Volume: 145 Suppl 1 Topics: Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Antihypertensive Agents; Atenolol; Diabetes Co	2003
LIFE: losartan versus atenolol. Lancet (London, England), 2003, Oct-25, Volume: 362, Issue:9393 Topics: Antihypertensive Agents; Atenolol; Comorbidity; Death, Sudden, Cardiac; Diabetes Mellitus; Drug Ther	2003
[Therapy of patients with arterial hypertension with fixed dose combination of losartan and hydrochlorothiazide. Effect on 24 hour blood pressure and left-ventricular hypertrophy]. Kardiologiia, 2003, Volume: 43, Issue:10 Topics: Adult; Aged; Antihypertensive Agents; Diuretics; Drug Therapy, Combination; Female; Humans; Hydrochl	2003
Effects of losartan on pressure overload-induced cardiac gene expression profiling in rats. Clinical and experimental pharmacology & physiology, 2003, Volume: 30, Issue:11 Topics: Animals; Gene Expression Profiling; Hypertrophy, Left Ventricular; Losartan; Male; Myocardium; Oligo	2003
Hypothetical economic analysis of screening for left ventricular hypertrophy in high-risk normotensive populations. QJM : monthly journal of the Association of Physicians, 2004, Volume: 97, Issue:2 Topics: Antihypertensive Agents; Cardiovascular Diseases; Chlorthalidone; Cost-Benefit Analysis; Echocardiog	2004
Losartan but not enalaprilat acutely reduces reperfusion ventricular tachyarrhythmias in hypertrophied rat hearts after low-flow ischaemia. The Journal of pharmacy and pharmacology, 2004, Volume: 56, Issue:4 Topics: Action Potentials; Animals; Anti-Arrhythmia Agents; Dose-Response Relationship, Drug; Enalaprilat; H	2004
Prevention of angiotensin II-induced hypertension, cardiovascular hypertrophy and oxidative stress by acetylsalicylic acid in rats. Journal of hypertension, 2004, Volume: 22, Issue:4 Topics: Angiotensin II; Animals; Antihypertensive Agents; Antioxidants; Aorta; Aspirin; Body Weight; Cells,	2004
Electrocardiographic strain pattern and prediction of cardiovascular morbidity and mortality in hypertensive patients. Hypertension (Dallas, Tex. : 1979), 2004, Volume: 44, Issue:1 Topics: Aged; Antihypertensive Agents; Atenolol; Cardiovascular Diseases; Electrocardiography; Female; Human	2004
How much echo left ventricular hypertrophy would be missed in diabetics by applying the Losartan Intervention For Endpoint Reduction electrocardiogram criteria to select patients for angiotensin receptor blockade? Journal of hypertension, 2004, Volume: 22, Issue:7 Topics: Aged; Angiotensin II Type 1 Receptor Blockers; Diabetes Mellitus, Type 2; Echocardiography; Electroc	2004
[Optimizing antihypertensive therapy. In 5 years 35,000 strokes are preventable]. MMW Fortschritte der Medizin, 2004, Jul-08, Volume: 146, Issue:27-28 Topics: Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Angiotensin II Type 1 Receptor Blockers; Antih	2004
Pulse pressure and effects of losartan or atenolol in patients with hypertension and left ventricular hypertrophy. Hypertension (Dallas, Tex. : 1979), 2005, Volume: 45, Issue:4 Topics: Aged; Aged, 80 and over; Antihypertensive Agents; Atenolol; Blood Pressure; Cardiovascular Diseases;	2005
Keeping tabs on your heart while treating BP. The Johns Hopkins medical letter health after 50, 2005, Volume: 17, Issue:3 Topics: Antihypertensive Agents; Atenolol; Humans; Hypertension; Hypertrophy, Left Ventricular; Losartan	2005
[Myocardial remodeling after experimental acute myocardial infarction in rats. Effect of renin-angiotensin-aldosterone blockade]. Arquivos brasileiros de cardiologia, 2005, Volume: 84, Issue:1 Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Animals; Disease	2005
[Blockade of renin-angiotensin system attenuates cardiac remodeling in rats undergoing aortic stenosis]. Arquivos brasileiros de cardiologia, 2005, Volume: 84, Issue:4 Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Animals; Aortic V	2005
Letter regarding article by Devereux et al, "regression of hypertensive left ventricular hypertrophy by losartan compared with atenolol: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial". Circulation, 2005, Jun-07, Volume: 111, Issue:22 Topics: Antihypertensive Agents; Atenolol; Clinical Trials as Topic; Humans; Hypertension; Hypertrophy, Left	2005
Cost effectiveness of losartan in patients with hypertension and LVH: an economic evaluation for Sweden of the LIFE trial. Journal of hypertension, 2005, Volume: 23, Issue:7 Topics: Aged; Antihypertensive Agents; Atenolol; Clinical Trials as Topic; Cost-Benefit Analysis; Double-Bli	2005
Enlarged hearts, larger threats. But reducing heart-muscle mass can blunt cardiac dangers. Heart advisor, 2005, Volume: 8, Issue:4 Topics: Antihypertensive Agents; Atenolol; Humans; Hypertrophy, Left Ventricular; Losartan	2005
The effect of angiotensin receptor blockade ARB on the regression of left ventricular hypertrophy in hemodialysis patients: comparison between patients with D allele and non-D allele ACE gene polymorphism. Clinical nephrology, 2005, Volume: 64, Issue:5 Topics: Alleles; Angiotensin II Type 1 Receptor Blockers; Female; Humans; Hypertrophy, Left Ventricular; Los	2005
Losartan and acute myocardial infarction in insulin-resistant Zucker fatty rats: reduced ventricular arrhythmias and improved survival. Canadian journal of physiology and pharmacology, 2005, Volume: 83, Issue:11 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Arrhythmias, Cardiac; Blood Pressure; Gene Express	2005
Comparison of the protein profile of established and regressed hypertension-induced left ventricular hypertrophy. Journal of proteome research, 2006, Volume: 5, Issue:2 Topics: Amino Acid Sequence; Animals; Antihypertensive Agents; Blood Pressure; Doxazosin; Electrophoresis, G	2006
Reductions in albuminuria and in electrocardiographic left ventricular hypertrophy independently improve prognosis in hypertension: the LIFE study. Journal of hypertension, 2006, Volume: 24, Issue:4 Topics: Aged; Albuminuria; Antihypertensive Agents; Atenolol; Blood Glucose; Blood Pressure; Cholesterol; Cr	2006
Association of hemoglobin delivery with left ventricular structure and function in hypertensive patients: Losartan Intervention for End Point Reduction in Hypertension Study. Hypertension (Dallas, Tex. : 1979), 2006, Volume: 47, Issue:5 Topics: Aged; Aged, 80 and over; Antihypertensive Agents; Blood Flow Velocity; Cardiac Output; Echocardiogra	2006
A cost-utility analysis of losartan versus atenolol in the treatment of hypertension with left ventricular hypertrophy. PharmacoEconomics, 2006, Volume: 24, Issue:4 Topics: Adrenergic beta-Antagonists; Aged; Angiotensin II Type 1 Receptor Blockers; Atenolol; Cohort Studies	2006
[Antihypertensive therapy: risk stratification in diabetes and cardiac diseases]. MMW Fortschritte der Medizin, 2006, Mar-16, Volume: 148, Issue:11 Topics: Adrenergic beta-Antagonists; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme	2006
[AT1 receptor antagonist lorsartan and organ protection. Managing hypertension a different way]. MMW Fortschritte der Medizin, 2006, Mar-30, Volume: 148, Issue:13 Topics: Angiotensin II Type 1 Receptor Blockers; Antihypertensive Agents; Diabetic Nephropathies; Humans; Hy	2006
[Hypertensive patient with enlarged heart. Caution, risk of atrial fibrillation!]. MMW Fortschritte der Medizin, 2006, May-25, Volume: 148, Issue:21 Topics: Antihypertensive Agents; Atrial Fibrillation; Clinical Trials as Topic; Drug Therapy, Combination; E	2006
Analysis of antihypertensive drugs in the heart of animal models: a proteomic approach. Methods in molecular biology (Clifton, N.J.), 2007, Volume: 357 Topics: Animals; Antihypertensive Agents; Disease Models, Animal; Electrophoresis, Gel, Two-Dimensional; Hea	2007
The role of angiotensin receptor-1 blockade on electromechanical changes induced by left ventricular hypertrophy and its regression. Cardiovascular research, 2007, Feb-01, Volume: 73, Issue:3 Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Aorta, Thoracic; Constriction; Ele	2007
Enhanced activity of ventricular Na+-HCO3- cotransport in pressure overload hypertrophy. American journal of physiology. Heart and circulatory physiology, 2007, Volume: 293, Issue:2 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Aorta, Abdominal; Disease Models, Animal; Heart Ve	2007
Clusters of metabolic risk factors predict cardiovascular events in hypertension with target-organ damage: the LIFE study. Journal of human hypertension, 2007, Volume: 21, Issue:8 Topics: Aged; Cardiovascular Diseases; Electrocardiography; Female; Humans; Hypertension; Hypertrophy, Left	2007
Beneficial effects of the combination of nifedipine and losartan in hypertensive Dahl salt-sensitive rats. Journal of cardiovascular pharmacology, 2007, Volume: 50, Issue:1 Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Aorta; Blood Pressure; Calcium Channel Blockers; D	2007
Left ventricular hypertrophy reversal and prevention of diabetes: two birds with one stone? Hypertension (Dallas, Tex. : 1979), 2007, Volume: 50, Issue:5 Topics: Antihypertensive Agents; Clinical Trials as Topic; Comorbidity; Diabetes Mellitus; Electrocardiograp	2007
In-treatment resolution or absence of electrocardiographic left ventricular hypertrophy is associated with decreased incidence of new-onset diabetes mellitus in hypertensive patients: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Hypertension (Dallas, Tex. : 1979), 2007, Volume: 50, Issue:5 Topics: Aged; Aged, 80 and over; Antihypertensive Agents; Atenolol; Blood Pressure; Comorbidity; Diabetes Me	2007
Ambulatory blood pressure adds to explaining benefits of AT-1 receptor blockade in the treatment of left ventricular hypertrophy. Blood pressure, 2007, Volume: 16, Issue:6 Topics: Aged; Aged, 80 and over; Angiotensin II Type 1 Receptor Blockers; Atenolol; Blood Pressure; Blood Pr	2007
Impact of left ventricular geometry on prognosis in hypertensive patients with left ventricular hypertrophy (the LIFE study). European journal of echocardiography : the journal of the Working Group on Echocardiography of the European Society of Cardiology, 2008, Volume: 9, Issue:6 Topics: Aged; Aged, 80 and over; Antihypertensive Agents; Atenolol; Female; Heart Ventricles; Humans; Hypert	2008
AT1 receptor participates in the cardiac hypertrophy induced by resistance training in rats. American journal of physiology. Regulatory, integrative and comparative physiology, 2008, Volume: 295, Issue:2 Topics: Adaptation, Physiological; Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Blottin	2008
Angiotensin AT1 receptor-mediated attenuation of cardiac hypertrophy due to volume overload: involvement of endothelin. European journal of pharmacology, 1995, Jun-23, Volume: 280, Issue:1 Topics: Amino Acid Sequence; Angiotensin II; Angiotensin Receptor Antagonists; Animals; Antihypertensive Age	1995
Comparative effects of losartan, captopril, and enalapril on murine acute myocarditis due to encephalomyocarditis virus. Journal of cardiovascular pharmacology, 1995, Volume: 26, Issue:1 Topics: Acute Disease; Administration, Oral; Angiotensin-Converting Enzyme Inhibitors; Animals; Antihyperten	1995
Left ventricular fibrosis in renovascular hypertensive rats. Effect of losartan and spironolactone. Hypertension (Dallas, Tex. : 1979), 1995, Volume: 26, Issue:1 Topics: Angiotensin II; Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Biochemical Phen	1995
Regression of cardiac hypertrophy and myosin isoenzyme patterns by losartan and captopril in renovascular hypertensive rats. Zhongguo yao li xue bao = Acta pharmacologica Sinica, 1994, Volume: 15, Issue:3 Topics: Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Biphenyl Compounds; Captopril; H	1994
Comparative effects of chronic angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade on cardiac remodeling after myocardial infarction in the rat. Circulation, 1994, Volume: 89, Issue:5 Topics: Angiotensin II; Angiotensin Receptor Antagonists; Animals; Biphenyl Compounds; Coronary Circulation;	1994
Reduction of development of left ventricular hypertrophy in salt-loaded Dahl salt-sensitive rats by angiotensin II receptor inhibition. American journal of hypertension, 1996, Volume: 9, Issue:3 Topics: Analysis of Variance; Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Biphenyl C	1996
Angiotensin II increases left ventricular mass without affecting myosin isoform mRNAs. Hypertension (Dallas, Tex. : 1979), 1996, Volume: 28, Issue:2 Topics: Angiotensin II; Animals; Antihypertensive Agents; Biphenyl Compounds; Heart Ventricles; Hemodynamics	1996
Losartan reduces cardiac mass and improves coronary flow reserve in the spontaneously hypertensive rat. Journal of hypertension, 1996, Volume: 14, Issue:5 Topics: Angiotensin II; Angiotensin Receptor Antagonists; Animals; Biphenyl Compounds; Coronary Circulation;	1996
Osteopontin is produced by rat cardiac fibroblasts and mediates A(II)-induced DNA synthesis and collagen gel contraction. The Journal of clinical investigation, 1996, Nov-15, Volume: 98, Issue:10 Topics: Angiotensin II; Animals; Antibodies, Blocking; Antibodies, Monoclonal; Biphenyl Compounds; Blotting,	1996
Regression of left ventricular hypertrophy in experimental renovascular hypertension: diastolic dysfunction depends more on myocardial collagen than it does on myocardial mass. Journal of hypertension, 1996, Volume: 14, Issue:9 Topics: Animals; Biphenyl Compounds; Blood Pressure; Collagen; Diastole; Enalapril; Hypertension, Renovascul	1996
Blockade of bradykinin B2 receptors prevents the increase in capillary density induced by chronic angiotensin-converting enzyme inhibitor treatment in stroke-prone spontaneously hypertensive rats. Hypertension (Dallas, Tex. : 1979), 1997, Volume: 29, Issue:1 Pt 2 Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Biphenyl Compounds; Bradykinin; Bradykinin Recept	1997
Enalapril and losartan reduced cardiac mass and improved coronary hemodynamics in SHR. Hypertension (Dallas, Tex. : 1979), 1997, Volume: 29, Issue:1 Pt 2 Topics: Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Biphenyl Compounds; Blood Pressu	1997
The effect of Losartan, an angiotensin II antagonist, on cardiac function, mass and morphology in rats after repeated hyperbaric exposures. Scandinavian journal of clinical and laboratory investigation, 1997, Volume: 57, Issue:3 Topics: Adaptation, Physiological; Angiotensin II; Animals; Atmospheric Pressure; Biphenyl Compounds; Body W	1997
Effects of renin-angiotensin blockade on sympathetic reactivity and beta-adrenergic pathway in the spontaneously hypertensive rat. Hypertension (Dallas, Tex. : 1979), 1997, Volume: 30, Issue:2 Pt 1 Topics: Adenylyl Cyclases; Angiotensin-Converting Enzyme Inhibitors; Angiotensins; Animals; Antihypertensive	1997
Effects of angiotensin II receptor blockade on hypoxia-induced right ventricular hypertrophy in rats. Journal of molecular and cellular cardiology, 1997, Volume: 29, Issue:11 Topics: Angiotensin Receptor Antagonists; Animals; Cell Hypoxia; Cell Size; Female; Glucosephosphate Dehydro	1997
Angiotensin II blockade followed by growth hormone as adjunctive therapy after experimental myocardial infarction. Journal of cardiac failure, 1998, Volume: 4, Issue:3 Topics: Angiotensin II; Angiotensin Receptor Antagonists; Animals; Anti-Arrhythmia Agents; Blood Flow Veloci	1998
Angiotensin receptor antagonism with losartan and the regression of left ventricular hypertrophy. Journal of human hypertension, 1998, Volume: 12, Issue:8 Topics: Angiotensin Receptor Antagonists; Antihypertensive Agents; Humans; Hypertrophy, Left Ventricular; Lo	1998
Chronic effects of early started angiotensin converting enzyme inhibition and angiotensin AT1-receptor subtype blockade in rats with myocardial infarction: role of bradykinin. Cardiovascular research, 1998, Volume: 39, Issue:2 Topics: Adrenergic beta-Antagonists; Analysis of Variance; Angiotensin I; Angiotensin Receptor Antagonists;	1998
Development of pressure overload induced cardiac hypertrophy is unaffected by long-term treatment with losartan. Molecular and cellular biochemistry, 1998, Volume: 188, Issue:1-2 Topics: Administration, Oral; Animals; Hypertension; Hypertrophy, Left Ventricular; Losartan; Male; Myocardi	1998
Inhibition of beta-myosin heavy chain gene expression in pressure overload rat heart by losartan and captopril. Zhongguo yao li xue bao = Acta pharmacologica Sinica, 1997, Volume: 18, Issue:1 Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Aortic Coarctat	1997
Differential effects of angiotensin II receptor blockade on pressure-induced left ventricular hypertrophy and fibrosis in rats. Journal of molecular and cellular cardiology, 1999, Volume: 31, Issue:2 Topics: Angiotensin Receptor Antagonists; Animals; Cell Size; Female; Fibrosis; Heart Ventricles; Hypertroph	1999
Losartan inhibits the post-transcriptional synthesis of collagen type I and reverses left ventricular fibrosis in spontaneously hypertensive rats. Journal of hypertension, 1999, Volume: 17, Issue:1 Topics: Animals; Antihypertensive Agents; Biomarkers; Blood Pressure; Blotting, Northern; Cardiomyopathies;	1999
Central vasopressin is modulated by chronic blockade of the renin-angiotensin system in experimental left ventricular hypertrophy. American journal of hypertension, 1999, Volume: 12, Issue:3 Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Blood Pressure; Brain Chemistry; Hypertrophy, Lef	1999
Effects of antihypertensive treatment on cardiac IGF-1 during prevention of ventricular hypertrophy in the rat. Life sciences, 1999, Volume: 64, Issue:18 Topics: Animals; Antihypertensive Agents; Blood Pressure; Enalapril; Heart; Hypertrophy, Left Ventricular; I	1999
Angiotensin-converting enzyme inhibition and AT1 receptor blockade modify the pressure-natriuresis relationship by additive mechanisms in rats with human renin and angiotensinogen genes. Journal of the American Society of Nephrology : JASN, 1999, Volume: 10, Issue:8 Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Angiotensinogen; Animals	1999
[Arterial hypertension and systolic left ventricular dysfunction: therapeutic approach]. Revista espanola de cardiologia, 1999, Volume: 52 Suppl 3 Topics: Amlodipine; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Calcium Channel Block	1999
Effect of obesity on electrocardiographic left ventricular hypertrophy in hypertensive patients : the losartan intervention for endpoint (LIFE) reduction in hypertension study. Hypertension (Dallas, Tex. : 1979), 2000, Volume: 35, Issue:1 Pt 1 Topics: Aged; Antihypertensive Agents; Body Mass Index; Electrocardiography; Female; Humans; Hypertension; H	2000
Myocardial renin is neither necessary nor sufficient to initiate or maintain ventricular hypertrophy. American journal of physiology. Regulatory, integrative and comparative physiology, 2000, Volume: 278, Issue:3 Topics: Angiotensins; Animals; Antihypertensive Agents; Desoxycorticosterone; Hypertrophy, Left Ventricular;	2000
Chronic AT(1) blockade stimulates extracellular collagen type I degradation and reverses myocardial fibrosis in spontaneously hypertensive rats. Hypertension (Dallas, Tex. : 1979), 2000, Volume: 35, Issue:6 Topics: Angiotensin Receptor Antagonists; Animals; Blood Pressure; Collagen; Collagenases; Extracellular Mat	2000
Matrix metalloproteinase-9 and tissue inhibitor metalloproteinase-1 levels in essential hypertension. Relationship to left ventricular mass and anti-hypertensive therapy. International journal of cardiology, 2000, Volume: 75, Issue:1 Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Blood Pressure; Collagen; E	2000
Regression of left ventricular hypertrophy by AT1 receptor blockade in renal transplant recipients. American journal of hypertension, 2000, Volume: 13, Issue:12 Topics: Adult; Angiotensin Receptor Antagonists; Antihypertensive Agents; Echocardiography; Erythropoiesis;	2000
Gap junction remodeling in hypertrophied left ventricles of aortic-banded rats: prevention by angiotensin II type 1 receptor blockade. Journal of molecular and cellular cardiology, 2001, Volume: 33, Issue:2 Topics: Angiotensin Receptor Antagonists; Animals; Anti-Arrhythmia Agents; Aorta; Blotting, Western; Connexi	2001
Chronic losartan treatment decreases angiotensin II-mediated facilitation of noradrenaline release in the caudal artery of spontaneously hypertensive rats. Life sciences, 2000, Nov-17, Volume: 67, Issue:26 Topics: Angiotensin II; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals;	2000
Restoration of normal ventricular electrophysiology in renovascular hypertensive rabbits after treatment with losartan. Journal of cardiovascular pharmacology, 2001, Volume: 37, Issue:3 Topics: Action Potentials; Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Hyper	2001
Differential effect of chronic antihypertensive treatment on vascular smooth muscle cell phenotype in spontaneously hypertensive rats. Hypertension (Dallas, Tex. : 1979), 2001, Volume: 37, Issue:5 Topics: Animals; Antihypertensive Agents; Blood Pressure; Captopril; Cell Cycle; Cell Division; Cells, Cultu	2001
Losartan prevents contractile dysfunction in rat myocardium after left ventricular myocardial infarction. American journal of physiology. Heart and circulatory physiology, 2001, Volume: 281, Issue:5 Topics: Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Calcium; Female; Heart Failure;	2001
Diverse effects of chronic treatment with losartan, fosinopril, and amlodipine on apoptosis, angiotensin II in the left ventricle of hypertensive rats. International journal of cardiology, 2001, Volume: 81, Issue:2-3 Topics: Amlodipine; Angiotensin II; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibito	2001
Effect of angiotensin type I-receptor blockade on left ventricular remodeling in pressure overload hypertrophy. Journal of cardiac failure, 2001, Volume: 7, Issue:4 Topics: Angiotensin Receptor Antagonists; Animals; Blood Pressure; Disease Models, Animal; Echocardiography;	2001
Correlates of pulse pressure reduction during antihypertensive treatment (losartan or atenolol) in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study). The American journal of cardiology, 2002, Feb-15, Volume: 89, Issue:4 Topics: Aged; Aged, 80 and over; Albumins; Antihypertensive Agents; Atenolol; Blood Pressure; Creatinine; El	2002
[Stress intolerance in diastolic dysfunction. A case for AT1 blocker?]. MMW Fortschritte der Medizin, 2002, Jan-17, Volume: 144, Issue:1-2 Topics: Antihypertensive Agents; Diastole; Exercise Test; Heart Failure; Humans; Hypertension; Hypertrophy,	2002
[Hypertension plus left ventricular hypertrophy. Prognosis can now be significantly improved]. MMW Fortschritte der Medizin, 2002, Apr-04, Volume: 144, Issue:14 Topics: Antihypertensive Agents; Atenolol; Humans; Hypertension; Hypertrophy, Left Ventricular; Losartan; Pr	2002
ARB superior to beta blocker in preventing adverse outcomes in older, high-risk hypertensive patients. Geriatrics, 2002, Volume: 57, Issue:5 Topics: Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Antihypertensive Agents; Atenolol; Humans; Hyp	2002

losartan and Hypertrophy, Left Ventricular