Angiotensin II receptor blockade does not improve left ventricular function and remodeling in subacute mitral regurgitation in the dog
| Autor: | Chih-Chang Wei, Gilbert J. Perry, Patricia Rynders, Francis G. Spinale, S.Ray Dillon, Rupak Mukherjee, Louis J. Dell’Italia, Gerald H. Hankes |
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| Rok vydání: | 2002 |
| Předmět: |
Male
medicine.medical_specialty Angiotensin receptor Heart Ventricles Angiotensin-Converting Enzyme Inhibitors Receptor Angiotensin Type 1 Ventricular Function Left Angiotensin Receptor Antagonists Irbesartan Chymases Dogs Mitral valve Internal medicine Renin Medicine Animals Mitral regurgitation Angiotensin II receptor type 1 Ventricular Remodeling business.industry Angiotensin II Body Weight Serine Endopeptidases Hemodynamics Mitral Valve Insufficiency Blockade Disease Models Animal medicine.anatomical_structure Treatment Outcome cardiovascular system Cardiology Alabama Female Angiotensin I business Cardiology and Cardiovascular Medicine medicine.drug |
| Zdroj: | Journal of the American College of Cardiology. 39(8) |
| ISSN: | 0735-1097 |
| Popis: | ObjectivesWe hypothesized that angiotensin II type-1 (AT1) receptor blocker (AT1RB) would prevent adverse left ventricular (LV) remodeling and LV dysfunction when started at the outset of mitral regurgitation (MR).BackgroundLittle is known regarding the efficacy of AT1RB treatment of MR.MethodsMitral regurgitation was induced by chordal disruption in adult mongrel dogs. Six normal dogs (NLs) were compared to six untreated MR dogs (MR) and seven dogs treated with the receptor blocker irbesartan (MR+AT1RB) started 24 h after induction of MR (60 mg/kg p.o. b.i.d.) and continued for three months.ResultsTreatment with AT1RB decreased systemic vascular resistance but did not significantly improve cardiac output, LV end-diastolic dimension (LVEDD) or LVEDD/wall thickness compared to untreated MR dogs. Resting isolated cardiomyocyte length increased in MR versus NLs and was further increased in AT1RB dogs. Left ventricular end-systolic dimension increased to a greater extent from baseline in AT1RB dogs versus untreated MR dogs (29 ± 9% vs. 12 ± 6%, p < 0.05), despite a significantly lower LV peak systolic pressure in AT1RB dogs. Plasma-angiotensin (ANG) II was elevated greater than threefold in both MR and MR+AT1RB versus NLs. In contrast, intracardiac ANG II was increased greater than twofold in MR dogs versus NLs, but was normalized by AT1RB.ConclusionsThe use of AT1RB decreased systemic vascular resistance and attenuated local expression of the renin-angiotensin system but did not prevent adverse LV chamber and cardiomyocyte remodeling. These results suggest that blockade of the AT1receptor does not improve LV remodeling and function in the early myocardial adaptive phase of MR. |
| Databáze: | OpenAIRE |
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