avapro has been researched along with Cardiomyopathies in 6 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.
Cardiomyopathies: A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
| Excerpt | Relevance | Reference |
|---|---|---|
| "Angiotensin II (Ang II) can induce cardiac fibrosis, but the underlying mechanisms are incompletely understood." | 7.72 | Cardiac fibrosis occurs early and involves endothelin and AT-1 receptors in hypertension due to endogenous angiotensin II. ( Belloni, AS; Kreutz, R; Nussdorfer, GG; Paul, M; Pessina, AC; Rossi, GP; Seccia, TM, 2003) |
| " A rat model of thyrotoxicosis was established by daily intraperitoneal injections of L-thyroxine (T(4), 100 μg/kg) for 4 weeks." | 3.78 | Irbesartan prevents myocardial remodeling in experimental thyrotoxic cardiomyopathy. ( Cho, KI; Choi, BG; Jeon, YK; Kang, JH; Kim, BH; Kim, IJ; Kim, JY; Kim, SJ; Kim, SM; Kim, SS; Kim, YK, 2012) |
| "Angiotensin II (Ang II) can induce cardiac fibrosis, but the underlying mechanisms are incompletely understood." | 3.72 | Cardiac fibrosis occurs early and involves endothelin and AT-1 receptors in hypertension due to endogenous angiotensin II. ( Belloni, AS; Kreutz, R; Nussdorfer, GG; Paul, M; Pessina, AC; Rossi, GP; Seccia, TM, 2003) |
| "CT-1 was assumed to take part in the ventricular remodeling." | 1.34 | [Expression of cardiotrophin-1 and effects of irbesartan in adriamycin induced cardiomyopathy in rats]. ( Chen, Y; Li, CC; Yao, JM; Zhuang, HP, 2007) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 4 (66.67) | 29.6817 |
| 2010's | 2 (33.33) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Chen, Q | 1 |
| Pang, L | 1 |
| Huang, S | 1 |
| Lei, W | 1 |
| Huang, D | 1 |
| Kim, BH | 1 |
| Cho, KI | 1 |
| Kim, SM | 1 |
| Kim, JY | 1 |
| Choi, BG | 1 |
| Kang, JH | 1 |
| Jeon, YK | 1 |
| Kim, SS | 1 |
| Kim, SJ | 1 |
| Kim, YK | 1 |
| Kim, IJ | 1 |
| Seccia, TM | 1 |
| Belloni, AS | 1 |
| Kreutz, R | 1 |
| Paul, M | 1 |
| Nussdorfer, GG | 1 |
| Pessina, AC | 1 |
| Rossi, GP | 1 |
| Westermann, D | 1 |
| Rutschow, S | 1 |
| Jäger, S | 1 |
| Linderer, A | 1 |
| Anker, S | 1 |
| Riad, A | 1 |
| Unger, T | 1 |
| Schultheiss, HP | 1 |
| Pauschinger, M | 1 |
| Tschöpe, C | 1 |
| Müller-Brunotte, R | 1 |
| Kahan, T | 1 |
| López, B | 1 |
| Edner, M | 1 |
| González, A | 1 |
| Díez, J | 1 |
| Malmqvist, K | 1 |
| Zhuang, HP | 1 |
| Yao, JM | 1 |
| Chen, Y | 1 |
| Li, CC | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| 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 | ||
| [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 |
1 trial available for avapro and Cardiomyopathies
| Article | Year |
|---|---|
Myocardial fibrosis and diastolic dysfunction in patients with hypertension: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA).
Topics: Adrenergic beta-Antagonists; Adult; Aged; Angiotensin II Type 1 Receptor Blockers; Antihypertensive | 2007 |
5 other studies available for avapro and Cardiomyopathies
| Article | Year |
|---|---|
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 |
Irbesartan prevents myocardial remodeling in experimental thyrotoxic cardiomyopathy.
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Biphenyl Compounds; Cardiomyopathies; Echocardiogr | 2012 |
Cardiac fibrosis occurs early and involves endothelin and AT-1 receptors in hypertension due to endogenous angiotensin II.
Topics: Angiotensin II; Animals; Animals, Genetically Modified; Antihypertensive Agents; Biphenyl Compounds; | 2003 |
Contributions of inflammation and cardiac matrix metalloproteinase activity to cardiac failure in diabetic cardiomyopathy: the role of angiotensin type 1 receptor antagonism.
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Biphenyl Compounds; Cardiomyopathies; Collagen Typ | 2007 |
[Expression of cardiotrophin-1 and effects of irbesartan in adriamycin induced cardiomyopathy in rats].
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Biphenyl Compounds; Cardiomyopathies; Cytokines; D | 2007 |