avapro has been researched along with Left Ventricular Hypertrophy in 46 studies
Irbesartan: A spiro compound, biphenyl and tetrazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION, and in the treatment of kidney disease.
irbesartan : A biphenylyltetrazole that is an angiotensin II receptor antagonist used mainly for the treatment of hypertension.
| Excerpt | Relevance | Reference |
|---|---|---|
| "5 mg hydrochorothiazide + 5 mg amlodipine, 86 patients with resistant hypertension were randomized to the add-on 25 mg spironolactone (MRB group, n = 46) or 5 mg ramipril (RASB group, n = 40) groups for 12 weeks." | 9.19 | Greater efficacy of aldosterone blockade and diuretic reinforcement vs. dual renin-angiotensin blockade for left ventricular mass regression in patients with resistant hypertension. ( Azizi, M; Bobrie, G; Chatellier, G; Frank, M; Ménard, J; Perdrix, L; Plouin, PF, 2014) |
| "In a multi-center, single-arm, prospective study, we investigated the efficacy and safety of the fixed irbesartan/hydrochlorothiazide combination in Chinese patients with moderate to severe hypertension." | 9.17 | Efficacy and safety of a fixed combination of irbesartan/hydrochlorothiazide in Chinese patients with moderate to severe hypertension. ( Dai, QY; Huang, QF; Li, Y; Ma, GS; Sheng, CS; Wang, JG, 2013) |
| "The MPI was measured at baseline and after 48 weeks of antihypertensive treatment in 93 participants of the SILVHIA trial, where individuals with primary hypertension and left ventricular hypertrophy were randomized to double blind treatment with either irbesartan or atenolol." | 9.14 | The effects of antihypertensive treatment on the doppler-derived myocardial performance index in patients with hypertensive left ventricular hypertrophy: results from the Swedish irbesartan in left ventricular hypertrophy investigation versus atenolol (SI ( Arnlöv, J; Kahan, T; Liljedahl, S; Lind, L, 2009) |
| "We determined the association between the TGF-beta1 genotype and regression of LV mass in 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, randomized in a double-blind study to receive treatment for 48 weeks with either the AT1-receptor antagonist irbesartan or the beta1-adrenoceptor blocker atenolol." | 9.11 | Transforming growth factor beta1 genotype and change in left ventricular mass during antihypertensive treatment--results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA). ( Billberger, K; Hallberg, P; Kahan, T; Karlsson, J; Kurland, L; Liljedahl, U; Lind, L; Malmqvist, K; Melhus, H; Michaelsson, K; Nyström, F; Ohman, KP; Syvänen, AC, 2004) |
| "Patients with mild to moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind fashion to treatment with either the angiotensin II type 1 receptor antagonist irbesartan (n = 48) or the beta(1)-adrenergic receptor blocker atenolol (n = 49) as monotherapy." | 9.11 | Angiotensinogen gene polymorphisms: relationship to blood pressure response to antihypertensive treatment. Results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial. ( Kahan, T; Karlsson, J; Kurland, L; Liljedahl, U; Lind, L; Malmqvist, K; Melhus, H; Syvänen, AC, 2004) |
| "Studies suggest that endothelin-1 contributes to the pathogenesis of hypertension." | 9.11 | Gender-specific association between preproendothelin-1 genotype and reduction of systolic blood pressure during antihypertensive treatment--results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA). ( Hallberg, P; Kahan, T; Karlsson, J; Kurland, L; Liljedahl, U; Lind, L; Malmqvist, K; Melhus, H; Michaëlsson, K; Nyström, F; Ohman, KP; Syvänen, AC, 2004) |
| "The aim of this study was to comparatively assess the effects of irbesartan and amlodipine monotherapies on left ventricular mass index (LVMI) in patients with mild to moderate untreated hypertension and echocardiographically determined left ventricular hypertrophy (LVH)." | 9.10 | Comparative effects of irbesartan versus amlodipine on left ventricular mass index in hypertensive patients with left ventricular hypertrophy. ( Fedele, F; Fera, MS; Ferri, FM; Gaudio, C; Giovannini, M; Pannarale, G; Puddu, PE; Vittore, A; Vizza, CD, 2003) |
| "Patients with mild-to-moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind study to receive treatment with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan (n = 43), or the beta1-adrenergic receptor blocker atenolol (n = 43)." | 9.10 | Aldosterone synthase (CYP11B2) -344 C/T polymorphism is related to antihypertensive response: result from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial. ( Hägg, A; Kahan, T; Karlsson, J; Kurland, L; Lind, L; Malmqvist, K; Melhus, H; Nyström, F; Ohman, P, 2002) |
| "The CYP2C9 genotype seems to predict the DBP response to irbesartan, but not to atenolol, in patients with essential hypertension." | 9.10 | The CYP2C9 genotype predicts the blood pressure response to irbesartan: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial. ( Hallberg, P; Kahan, T; Karlsson, J; Kurland, L; Lind, L; Malmqvist, K; Melhus, H; Nyström, F; Ohman, KP, 2002) |
| "Patients with essential hypertension and echocardiographically diagnosed LVH were included in a double-blind study to receive treatment with either the angiotensin II type 1 receptor (AT1-receptor) antagonist irbesartan (n = 41), or the beta-1 adrenergic receptor blocker atenolol (n = 43) as monotherapy for 3 months." | 9.10 | Polymorphisms in the angiotensinogen and angiotensin II type 1 receptor gene are related to change in left ventricular mass during antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol ( ( Hägg, A; Kahan, T; Karlsson, J; Kurland, L; Lind, L; Malmqvist, K; Melhus, H; Nyström, F; Ohman, P, 2002) |
| "We determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol." | 9.10 | B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial. ( Hallberg, P; Kahan, T; Karlsson, J; Kurland, L; Lind, L; Malmqvist, K; Melhus, H; Michaëlsson, K; Nyström, F; Ohman, KP, 2003) |
| "The SILVER (Study of Irbesartan in Left VEntricular hypertrophy Regression) trial is designed to test the hypothesis that the newly developed angiontensin-II receptor antagonist, irbesartan, will produce a greater reduction in left ventricular (LV) mass than felodipine ER, in a population of hypertensive patients defined by seated diastolic blood pressure (SeDBP) in the range 95-115 mmHg or seated systolic blood pressure (SeSBP) in the range 160-200 mm Hg." | 9.08 | Comparison of irbesartan vs felodipine in the regression after 1 year of left ventricular hypertrophy in hypertensive patients (the SILVER trial). Study of Irbesartan in Left VEntricular hypertrophy Regression. ( Agabiti Rosei, E; Bregman, B; Brudi, P; Clairefond, P; Cohen, A; Dubourg, O; Gosse, P; Guéret, P; Williams, B, 1998) |
| "Thus, 115 hypertensive patients with left ventricular hypertrophy were randomized to receive double-blind irbesartan or atenolol, with additional therapy if needed." | 6.71 | Long-term effects of irbesartan and atenolol on the renin-angiotensin-aldosterone system in human primary hypertension: the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA). ( Kahan, T; Lind, L; Malmqvist, K; Nyström, F; Ohman, KP, 2003) |
| "Patients with hypertension and left ventricular hypertrophy (n = 66) with a seated diastolic BP 90-115 mmHg (average of three measurements one minute apart by nurses)." | 6.70 | Nurse-recorded and ambulatory blood pressure predicts treatment-induced reduction of left ventricular hypertrophy equally well in hypertension: results from the Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA) study. ( Kahan, T; Malmqvist, K; Nyström, F; Ohman, KP, 2002) |
| "5 mg hydrochorothiazide + 5 mg amlodipine, 86 patients with resistant hypertension were randomized to the add-on 25 mg spironolactone (MRB group, n = 46) or 5 mg ramipril (RASB group, n = 40) groups for 12 weeks." | 5.19 | Greater efficacy of aldosterone blockade and diuretic reinforcement vs. dual renin-angiotensin blockade for left ventricular mass regression in patients with resistant hypertension. ( Azizi, M; Bobrie, G; Chatellier, G; Frank, M; Ménard, J; Perdrix, L; Plouin, PF, 2014) |
| "In a multi-center, single-arm, prospective study, we investigated the efficacy and safety of the fixed irbesartan/hydrochlorothiazide combination in Chinese patients with moderate to severe hypertension." | 5.17 | Efficacy and safety of a fixed combination of irbesartan/hydrochlorothiazide in Chinese patients with moderate to severe hypertension. ( Dai, QY; Huang, QF; Li, Y; Ma, GS; Sheng, CS; Wang, JG, 2013) |
| "The MPI was measured at baseline and after 48 weeks of antihypertensive treatment in 93 participants of the SILVHIA trial, where individuals with primary hypertension and left ventricular hypertrophy were randomized to double blind treatment with either irbesartan or atenolol." | 5.14 | The effects of antihypertensive treatment on the doppler-derived myocardial performance index in patients with hypertensive left ventricular hypertrophy: results from the Swedish irbesartan in left ventricular hypertrophy investigation versus atenolol (SI ( Arnlöv, J; Kahan, T; Liljedahl, S; Lind, L, 2009) |
| "Patients with mild to moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind fashion to treatment with either the angiotensin II type 1 receptor antagonist irbesartan (n = 48) or the beta(1)-adrenergic receptor blocker atenolol (n = 49) as monotherapy." | 5.11 | Angiotensinogen gene polymorphisms: relationship to blood pressure response to antihypertensive treatment. Results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial. ( Kahan, T; Karlsson, J; Kurland, L; Liljedahl, U; Lind, L; Malmqvist, K; Melhus, H; Syvänen, AC, 2004) |
| "We determined the association between the TGF-beta1 genotype and regression of LV mass in 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, randomized in a double-blind study to receive treatment for 48 weeks with either the AT1-receptor antagonist irbesartan or the beta1-adrenoceptor blocker atenolol." | 5.11 | Transforming growth factor beta1 genotype and change in left ventricular mass during antihypertensive treatment--results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA). ( Billberger, K; Hallberg, P; Kahan, T; Karlsson, J; Kurland, L; Liljedahl, U; Lind, L; Malmqvist, K; Melhus, H; Michaelsson, K; Nyström, F; Ohman, KP; Syvänen, AC, 2004) |
| " The aim of this trial was to compare the effects of irbesartan versus atenolol on LVH in subjects with essential hypertension." | 5.11 | Effect of irbesartan versus atenolol on left ventricular mass and voltage: results of the CardioVascular Irbesartan Project. ( Delles, C; Klingbeil, AU; Kolloch, RE; Krekler, M; Ludwig, M; Schmieder, RE; Schneider, MP; Stumpe, KO, 2004) |
| "Studies suggest that endothelin-1 contributes to the pathogenesis of hypertension." | 5.11 | Gender-specific association between preproendothelin-1 genotype and reduction of systolic blood pressure during antihypertensive treatment--results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA). ( Hallberg, P; Kahan, T; Karlsson, J; Kurland, L; Liljedahl, U; Lind, L; Malmqvist, K; Melhus, H; Michaëlsson, K; Nyström, F; Ohman, KP; Syvänen, AC, 2004) |
| "Patients with mild to moderate primary hypertension and LV hypertrophy were randomized in a double-blind fashion to treatment with either the angiotensin II type 1 receptor antagonist irbesartan (n = 48) or the beta1 adrenoreceptor blocker atenolol (n = 49)." | 5.11 | Single nucleotide polymorphisms predict the change in left ventricular mass in response to antihypertensive treatment. ( Kahan, T; Kurland, L; Liljedahl, U; Lind, L; Malmqvist, K; Melhus, H; Syvänen, AC, 2004) |
| "The aim of this study was to comparatively assess the effects of irbesartan and amlodipine monotherapies on left ventricular mass index (LVMI) in patients with mild to moderate untreated hypertension and echocardiographically determined left ventricular hypertrophy (LVH)." | 5.10 | Comparative effects of irbesartan versus amlodipine on left ventricular mass index in hypertensive patients with left ventricular hypertrophy. ( Fedele, F; Fera, MS; Ferri, FM; Gaudio, C; Giovannini, M; Pannarale, G; Puddu, PE; Vittore, A; Vizza, CD, 2003) |
| "We evaluated the influence of this polymorphism on the change in left ventricular mass index in 90 patients with essential hypertension and echocardiographically diagnosed left ventricular hypertrophy, randomised in a double-blind study to receive treatment with either the angiotensin II type I receptor antagonist irbesartan or the beta1-adrenoceptor blocker atenolol for 48 weeks." | 5.10 | Adipocyte-derived leucine aminopeptidase genotype and response to antihypertensive therapy. ( Hallberg, P; Kahan, T; Kurland, L; Liljedahl, U; Lind, L; Malmqvist, K; Melhus, H; Michaëlsson, K; Nyström, F; Ohman, KP; Syvänen, AC, 2003) |
| "We determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol." | 5.10 | B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial. ( Hallberg, P; Kahan, T; Karlsson, J; Kurland, L; Lind, L; Malmqvist, K; Melhus, H; Michaëlsson, K; Nyström, F; Ohman, KP, 2003) |
| "The CYP2C9 genotype seems to predict the DBP response to irbesartan, but not to atenolol, in patients with essential hypertension." | 5.10 | The CYP2C9 genotype predicts the blood pressure response to irbesartan: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial. ( Hallberg, P; Kahan, T; Karlsson, J; Kurland, L; Lind, L; Malmqvist, K; Melhus, H; Nyström, F; Ohman, KP, 2002) |
| "Patients with essential hypertension and echocardiographically diagnosed LVH were included in a double-blind study to receive treatment with either the angiotensin II type 1 receptor (AT1-receptor) antagonist irbesartan (n = 41), or the beta-1 adrenergic receptor blocker atenolol (n = 43) as monotherapy for 3 months." | 5.10 | Polymorphisms in the angiotensinogen and angiotensin II type 1 receptor gene are related to change in left ventricular mass during antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol ( ( Hägg, A; Kahan, T; Karlsson, J; Kurland, L; Lind, L; Malmqvist, K; Melhus, H; Nyström, F; Ohman, P, 2002) |
| "Patients with mild-to-moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind study to receive treatment with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan (n = 43), or the beta1-adrenergic receptor blocker atenolol (n = 43)." | 5.10 | Aldosterone synthase (CYP11B2) -344 C/T polymorphism is related to antihypertensive response: result from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial. ( Hägg, A; Kahan, T; Karlsson, J; Kurland, L; Lind, L; Malmqvist, K; Melhus, H; Nyström, F; Ohman, P, 2002) |
| "The Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA)." | 5.09 | Regression of left ventricular hypertrophy in human hypertension with irbesartan. ( Edner, M; Hägg, A; Held, C; Kahan, T; Lind, L; Malmqvist, K; Müller-Brunotte, R; Nyström, F; Ohman, KP; Osbakken, MD; Ostergern, J, 2001) |
| "The SILVER (Study of Irbesartan in Left VEntricular hypertrophy Regression) trial is designed to test the hypothesis that the newly developed angiontensin-II receptor antagonist, irbesartan, will produce a greater reduction in left ventricular (LV) mass than felodipine ER, in a population of hypertensive patients defined by seated diastolic blood pressure (SeDBP) in the range 95-115 mmHg or seated systolic blood pressure (SeSBP) in the range 160-200 mm Hg." | 5.08 | Comparison of irbesartan vs felodipine in the regression after 1 year of left ventricular hypertrophy in hypertensive patients (the SILVER trial). Study of Irbesartan in Left VEntricular hypertrophy Regression. ( Agabiti Rosei, E; Bregman, B; Brudi, P; Clairefond, P; Cohen, A; Dubourg, O; Gosse, P; Guéret, P; Williams, B, 1998) |
| "In normal mice, HS diet induces septum-predominant LVH and fibrosis through activation of the cardiac RAS-ERK pathway, which can be blocked by irbesartan or ramipril, indicating a key role of the cardiac RAS in HS diet-induced LVH." | 3.76 | The cardiac renin-angiotensin system is responsible for high-salt diet-induced left ventricular hypertrophy in mice. ( Adamy, C; Berdeaux, A; Crozatier, B; Hittinger, L; Le Corvoisier, P; Michel, JB; Sambin, L; Su, J, 2010) |
| "Thus, 115 hypertensive patients with left ventricular hypertrophy were randomized to receive double-blind irbesartan or atenolol, with additional therapy if needed." | 2.71 | Long-term effects of irbesartan and atenolol on the renin-angiotensin-aldosterone system in human primary hypertension: the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA). ( Kahan, T; Lind, L; Malmqvist, K; Nyström, F; Ohman, KP, 2003) |
| "Patients with hypertension and left ventricular hypertrophy (n = 66) with a seated diastolic BP 90-115 mmHg (average of three measurements one minute apart by nurses)." | 2.70 | Nurse-recorded and ambulatory blood pressure predicts treatment-induced reduction of left ventricular hypertrophy equally well in hypertension: results from the Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA) study. ( Kahan, T; Malmqvist, K; Nyström, F; Ohman, KP, 2002) |
| "Irbesartan reduces left ventricular hypertrophy and increases probability of maintenance of sinus rhythm after cardioversion of atrial fibrillation." | 2.48 | [Irbesartan in clinical practice]. ( Malishevskiĭ, MV, 2012) |
| "Left ventricular hypertrophy has been associated with the prolongation of QT-time, and an increased risk of ventricular arrhythmias." | 1.32 | Asynchronous development of electrical remodeling and cardiac hypertrophy in the complete AV block dog. ( Leunissen, JD; Londoño, C; Ramakers, C; Schoenmakers, M; van Opstal, JM; Vos, MA, 2003) |
| "We tested the hypothesis that long-term administration of the specific angiotensin II subtype 1 (AT1)-receptor blocker BMS-186295 will regress hypertrophy and modify left ventricular angiotensin converting enzyme (ACE) expression in rats with ascending aortic stenosis." | 1.30 | Angiotensin AT1 receptor inhibition. Effects on hypertrophic remodeling and ACE expression in rats with pressure-overload hypertrophy due to ascending aortic stenosis. ( Benedict, CR; Bishop, SP; Chafizadeh, E; Douglas, PS; Ho, KK; Lee, MA; Lindpaintner, K; Lorell, BH; Weigner, M; Weinberg, EO, 1997) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 3 (6.52) | 18.2507 |
| 2000's | 27 (58.70) | 29.6817 |
| 2010's | 14 (30.43) | 24.3611 |
| 2020's | 2 (4.35) | 2.80 |
| Authors | Studies |
|---|---|
| Huang, C | 1 |
| Huang, Y | 1 |
| Zhong, Q | 1 |
| Cai, A | 1 |
| Feng, YQ | 1 |
| Zhang, J | 1 |
| Yang, L | 1 |
| Ding, Y | 1 |
| Vignier, N | 1 |
| Le Corvoisier, P | 2 |
| Blard, C | 1 |
| Sambin, L | 2 |
| Azibani, F | 1 |
| Schlossarek, S | 1 |
| Delcayre, C | 1 |
| Carrier, L | 1 |
| Hittinger, L | 2 |
| Su, JB | 1 |
| Huang, QF | 1 |
| Sheng, CS | 1 |
| Li, Y | 1 |
| Ma, GS | 1 |
| Dai, QY | 1 |
| Wang, JG | 1 |
| Kusunoki, H | 1 |
| Taniyama, Y | 1 |
| Rakugi, H | 1 |
| Morishita, R | 1 |
| Peters, CD | 1 |
| Kjærgaard, KD | 1 |
| Jespersen, B | 1 |
| Christensen, KL | 1 |
| Jensen, JD | 1 |
| Jekell, A | 1 |
| Malmqvist, K | 17 |
| Wallén, NH | 1 |
| Mörtsell, D | 2 |
| Kahan, T | 19 |
| Degirmenci, H | 1 |
| Açikel, M | 1 |
| Bakirci, EM | 1 |
| Duman, H | 1 |
| Demirelli, S | 1 |
| Tas, H | 1 |
| Simsek, Z | 1 |
| Karakelleoglu, S | 1 |
| Aksakal, E | 1 |
| Erol, MK | 1 |
| Chen, Q | 1 |
| Pang, L | 1 |
| Huang, S | 1 |
| Lei, W | 1 |
| Huang, D | 1 |
| Azizi, M | 1 |
| Perdrix, L | 1 |
| Bobrie, G | 1 |
| Frank, M | 1 |
| Chatellier, G | 1 |
| Ménard, J | 1 |
| Plouin, PF | 1 |
| Liljedahl, S | 1 |
| Lind, L | 13 |
| Arnlöv, J | 1 |
| Adamy, C | 1 |
| Crozatier, B | 1 |
| Berdeaux, A | 1 |
| Michel, JB | 1 |
| Su, J | 1 |
| Oghlakian, GO | 1 |
| Sipahi, I | 1 |
| Fang, JC | 1 |
| Burger, D | 1 |
| Montezano, AC | 1 |
| Nishigaki, N | 1 |
| He, Y | 1 |
| Carter, A | 1 |
| Touyz, RM | 1 |
| Shang, W | 1 |
| Han, P | 1 |
| Yang, CB | 1 |
| Gu, XW | 1 |
| Zhang, W | 1 |
| Xu, LP | 1 |
| Fu, ST | 1 |
| Su, DF | 2 |
| Xie, HH | 2 |
| Nako, H | 1 |
| Kataoka, K | 1 |
| Koibuchi, N | 1 |
| Dong, YF | 1 |
| Toyama, K | 1 |
| Yamamoto, E | 1 |
| Yasuda, O | 1 |
| Ichijo, H | 1 |
| Ogawa, H | 1 |
| Kim-Mitsuyama, S | 1 |
| Malishevskiĭ, MV | 1 |
| Nyström, F | 10 |
| Ohman, KP | 8 |
| Zukowska-Szczechowska, E | 1 |
| Gosek, K | 1 |
| Grzeszczak, W | 1 |
| Hallberg, P | 6 |
| Karlsson, J | 7 |
| Kurland, L | 10 |
| Melhus, H | 10 |
| Edner, M | 4 |
| Bergfeldt, L | 1 |
| Karpov, IuA | 1 |
| Michaëlsson, K | 4 |
| Schoenmakers, M | 1 |
| Ramakers, C | 1 |
| van Opstal, JM | 1 |
| Leunissen, JD | 1 |
| Londoño, C | 1 |
| Vos, MA | 1 |
| Liljedahl, U | 6 |
| Syvänen, AC | 6 |
| Gaudio, C | 1 |
| Ferri, FM | 1 |
| Giovannini, M | 1 |
| Pannarale, G | 1 |
| Puddu, PE | 1 |
| Vittore, A | 1 |
| Fera, MS | 1 |
| Vizza, CD | 1 |
| Fedele, F | 1 |
| Billberger, K | 1 |
| Schneider, MP | 1 |
| Klingbeil, AU | 1 |
| Delles, C | 1 |
| Ludwig, M | 1 |
| Kolloch, RE | 1 |
| Krekler, M | 1 |
| Stumpe, KO | 1 |
| Schmieder, RE | 1 |
| Müller-Brunotte, R | 3 |
| Shen, FM | 1 |
| Zhang, XF | 1 |
| Jiang, YY | 1 |
| Park, CG | 1 |
| Ahn, JC | 1 |
| Hong, SJ | 1 |
| Kim, EJ | 1 |
| Lee, SJ | 1 |
| Park, SM | 2 |
| Seo, HS | 1 |
| Oh, DJ | 1 |
| Ring, M | 1 |
| Bella, JN | 1 |
| Held, C | 2 |
| Hashemi, N | 1 |
| Weinberg, EO | 1 |
| Lee, MA | 1 |
| Weigner, M | 1 |
| Lindpaintner, K | 1 |
| Bishop, SP | 1 |
| Benedict, CR | 1 |
| Ho, KK | 1 |
| Douglas, PS | 1 |
| Chafizadeh, E | 1 |
| Lorell, BH | 1 |
| Spinale, FG | 1 |
| Holzgrefe, HH | 1 |
| Walker, JD | 1 |
| Mukherjee, R | 1 |
| Kribbs, SB | 1 |
| Powell, JR | 1 |
| Antonaccio, M | 1 |
| Cohen, A | 1 |
| Bregman, B | 1 |
| Agabiti Rosei, E | 1 |
| Williams, B | 1 |
| Dubourg, O | 1 |
| Clairefond, P | 1 |
| Brudi, P | 1 |
| Gosse, P | 1 |
| Guéret, P | 1 |
| Hägg, A | 3 |
| Osbakken, MD | 1 |
| Ostergern, J | 1 |
| Schiffrin, EL | 1 |
| Park, JB | 1 |
| Pu, Q | 1 |
| Ohman, P | 2 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Saving Residual Renal Function Among Haemodialysis Patients Receiving Irbesartan - a Double Blind Randomised Study[NCT00791830] | Phase 3 | 82 participants (Actual) | Interventional | 2009-04-30 | Completed | ||
| Randomized, Double-blind Evaluation of the Effects of Irbesartan and Atenolol on Cardiovascular Structure and Function in Subjects With Hypertension and Left Ventricular Hypertrophy[NCT00389168] | Phase 2/Phase 3 | 115 participants (Actual) | Interventional | 1995-04-30 | Completed | ||
| Evaluation of Renal Sodium Excretion After Salt Loading in Heart Failure With Preserved Ejection Fraction[NCT03837470] | Early Phase 1 | 14 participants (Actual) | Interventional | 2019-05-06 | Completed | ||
| Double-blind, Randomized, Parallel Design Study Comparing Effectiveness of Losartan vs. Hydrochlorothiazide in Reversing or Preventing the Progression of the Remodeling of Resistance Arteries in Pre-hypertensive Pre-diabetic Subjects[NCT00388388] | Phase 2 | 1 participants (Actual) | Interventional | 2007-03-31 | Terminated (stopped due to Few subjects recruited, sponsor withdrew support.) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Difference in Diastolic Blood Pressure. Repeated measures multivariable analysis of variance (MANOVA) at time points 0, 12, 24, and 48 weeks (NCT00389168)
Timeframe: Baseline to 48 weeks
| Intervention | mm Hg (Mean) |
|---|---|
| Atenolol | -16.3 |
| Irbesartan | -18.8 |
Changes in common carotid artery intima-media thickness, assessed by ultrasonography. (NCT00389168)
Timeframe: Baseline to 48 weeks
| Intervention | mm (Mean) |
|---|---|
| Atenolol | 0.03 |
| Irbesartan | -0.01 |
Safety was assessed by non-directed questions, and all observed and volunteered adverse events were recorded at each study visit. Serious adverse events were defined by, and reported according to the regulations of good clinical practice (GCP). none were considered related to the study medication. (NCT00389168)
Timeframe: Treatment period was baseline to 48 weeks
| Intervention | Participants (Number) |
|---|---|
| Atenolol | 5 |
| Irbesartan | 5 |
Repeated measures multivariate analysis of variance (MANOVA) at time points 0, 12, 24, and 48 weeks. Data are presented as left ventricular mass in gram (g) indexed for body mass index (in m^2). (NCT00389168)
Timeframe: Baseline and 48 weeks
| Intervention | g/m^2 (Mean) | ||
|---|---|---|---|
| 12 weeks | 24 weeks | 48 weeks | |
| Atenolol | -1 | -6 | -14 |
| Irbesartan | -9 | -14 | -26 |
Venous plasma concentrations of angiotensin II were measured in order to study the possible associations between the activity of the renin-angiotensin-aldosteone system and changes in left ventricular mass. Further analyses of other components of the renin-angiotensin-aldosterone system and of other hormonal system (e.g. the sympathetic nervous system) have also been performed and published. Repeated measures MANOVA at time points 0, 12, 24, and 48 weeks. Data were log-transformed to avoid skewness before statistical evaluation. However, tabular data are given as mean values with 95% confidence to improve readability. (NCT00389168)
Timeframe: Baseline to 48 weeks
| Intervention | pmol/L (Mean) | ||
|---|---|---|---|
| Weel 12 | Week 24 | Week 48 | |
| Atenolol | -1.0 | -0.8 | -0.2 |
| Irbesartan | 3.0 | 3.3 | 10.0 |
Changes in left ventricular diastolic function from baseline to week 48 will be evaluated as the difference in E/A ratio. Conventional pulsed wave Doppler echocardiography was used for recordings of mitral inflow in. The peak of early (E) and late (A) mitral flow velocities were measured, and the E/A-ratio was calculated. Repeated measures MANOVA at time points 0, 12, 24, and 48 weeks. Some echocardiographic recordings at some time point may be of insufficient quality or missing, and the number of observations may not always correspond to the total number of participants at all time points. (NCT00389168)
Timeframe: Baseline to 48 weeks
| Intervention | ratio (Mean) | ||
|---|---|---|---|
| Week 12 | Week 24 | Week 48 | |
| Atenolol | 0.18 | 0.16 | 0.13 |
| Irbesartan | 0.10 | 0.04 | 0.10 |
4 reviews available for avapro and Left Ventricular Hypertrophy
| Article | Year |
|---|---|
Treatment of heart failure with preserved ejection fraction: have we been pursuing the wrong paradigm?
Topics: Adrenergic beta-Antagonists; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme | 2011 |
[Irbesartan in clinical practice].
Topics: Angiotensin II Type 1 Receptor Blockers; Antihypertensive Agents; Biphenyl Compounds; Blood Pressure | 2012 |
[Irbesartan--antihypertensive treatment in patients with heart failure and diabetes mellitus].
Topics: Antihypertensive Agents; Biphenyl Compounds; Diabetes Complications; Heart Failure; Humans; Hyperten | 2002 |
[Clinical hypertensiology: analysis of trials completed in 2001-2002].
Topics: Adrenergic beta-Antagonists; Adult; Aged; Aged, 80 and over; Angiotensin-Converting Enzyme Inhibitor | 2002 |
26 trials available for avapro and Left Ventricular Hypertrophy
16 other studies available for avapro and Left Ventricular Hypertrophy
| Article | Year |
|---|---|
Prevalence of and risk factors for abnormal left ventricular geometrical patterns in hypertensive subjects administered irbesartan.
Topics: Aged; Antihypertensive Agents; Cross-Sectional Studies; Electrocardiography; Female; Heart Ventricle | 2021 |
Effects of irbesartan on phenotypic alterations in monocytes and the inflammatory status of hypertensive patients with left ventricular hypertrophy.
Topics: Aged; Anti-Inflammatory Agents; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Antihyperte | 2021 |
AT1 blockade abolishes left ventricular hypertrophy in heterozygous cMyBP-C null mice: role of FHL1.
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Biphenyl Compounds; Blood Pressure; Carrier Protei | 2014 |
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.
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Biphenyl Compounds; Disease Models, Animal; Epithe | 2013 |
Comparison of effects of nebivolol, carvedilol and irbesartan on left ventricular hypertrophy associated with hypertension.
Topics: Adrenergic beta-Antagonists; Adult; Aged; Antihypertensive Agents; Biphenyl Compounds; Carbazoles; C | 2014 |
Effects of emodin and irbesartan on ventricular fibrosis in Goldblatt hypertensive rats.
Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Biphenyl Compounds; Blotting, West | 2014 |
The cardiac renin-angiotensin system is responsible for high-salt diet-induced left ventricular hypertrophy in mice.
Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Animals; Autoradi | 2010 |
Endothelial microparticle formation by angiotensin II is mediated via Ang II receptor type I/NADPH oxidase/ Rho kinase pathways targeted to lipid rafts.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Acetophenones; Adaptor Proteins, Signal Transducing; | 2011 |
Synergism of irbesartan and amlodipine on hemodynamic amelioration and organ protection in spontaneously hypertensive rats.
Topics: Amlodipine; Animals; Antihypertensive Agents; Baroreflex; Biphenyl Compounds; Blood Pressure; Drug S | 2011 |
Novel mechanism of angiotensin II-induced cardiac injury in hypertensive rats: the critical role of ASK1 and VEGF.
Topics: Angiotensin II; Animals; Antihypertensive Agents; Apoptosis; Biphenyl Compounds; Blood Pressure; Blo | 2012 |
Asynchronous development of electrical remodeling and cardiac hypertrophy in the complete AV block dog.
Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Biphenyl Compounds; Bradycardia; Chymases; | 2003 |
Blood pressure variability, baroreflex sensitivity and organ damage in spontaneously hypertensive rats treated with various antihypertensive drugs.
Topics: Animals; Antihypertensive Agents; Aorta; Atenolol; Baroreflex; Biphenyl Compounds; Blood Pressure; C | 2006 |
Efficacy of irbesartan on left ventricular mass and arterial stiffness in hypertensive patients.
Topics: Adult; Aged; Angiotensin II Type 1 Receptor Blockers; Aorta; Biphenyl Compounds; Female; Humans; Hyp | 2006 |
Treatment of diastolic dysfunction in hypertensive left ventricular hypertrophy.
Topics: Adrenergic beta-Antagonists; Angiotensin II Type 1 Receptor Blockers; Antihypertensive Agents; Ateno | 2006 |
Angiotensin AT1 receptor inhibition. Effects on hypertrophic remodeling and ACE expression in rats with pressure-overload hypertrophy due to ascending aortic stenosis.
Topics: Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Aorta; Aortic Valve Stenosis; Bi | 1997 |
Angiotensin II subtype-1 receptor blockade during the development of left ventricular hypertrophy in dogs: effects on ventricular and myocyte function.
Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensiv | 1997 |