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Titolo:
Effects of combination of angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist on inflammatory cellular infiltration and myocardial interstitial fibrosis after acute myocardial infarction
Autore:
Yu, CM; Tipoe, GL; Lai, KWH; Lau, CP;
Indirizzi:
Univ Hong Kong, Queen Mary Hosp, Dept Med, Div Cardiol, Hong Kong, Hong Kong, Peoples R China Univ Hong Kong Hong Kong Hong Kong Peoples R China Kong, Peoples R China Univ Hong Kong, Dept Anat, Hong Kong, Hong Kong, Peoples R China Univ HongKong Hong Kong Hong Kong Peoples R China Kong, Peoples R China
Titolo Testata:
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
fascicolo: 4, volume: 38, anno: 2001,
pagine: 1207 - 1215
SICI:
0735-1097(200110)38:4<1207:EOCOAE>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARDIAC FIBROBLASTS; RAT; COLLAGEN; HYPERTROPHY; EXPRESSION; CAPTOPRIL; LIGATION; SURVIVAL; MYOCYTES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Yu, CM Univ Hong Kong, Queen Mary Hosp, Dept Med, Div Cardiol, Pokfulam Rd, Hong Kong, Hong Kong, Peoples R China Univ Hong Kong Pokfulam Rd Hong Kong Hong Kong Peoples R China ina
Citazione:
C.M. Yu et al., "Effects of combination of angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist on inflammatory cellular infiltration and myocardial interstitial fibrosis after acute myocardial infarction", J AM COL C, 38(4), 2001, pp. 1207-1215

Abstract

OBJECTIVES The goal of this study was to compare the relative efficacy of an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin receptor blocker (ARB) in suppressing the histopathologic changes that lead to ventricular remodeling after an acute myocardial infarction (AMI). BACKGROUND Myocardial interstitial fibrosis in the noninfarcted region is a major histologic landmark resulting in cardiac dysfunction after AMI. However, the relative potency of an ACE inhibitor and ARB on suppressing the histopathologic changes was unclear. METHODS Rats with AMI were randomized to fosinopril, valsartan or a combination of the two drugs for two or four weeks. The total, type I and type III collagen and activated fibroblasts and macrophages were quantified by histomorphometry. The expression of transforming growth factor-beta 1 (TGF-beta 1) messenger ribonucleic acid (mRNA) was determined by reverse transcription polymerase chain reaction. RESULTS Acute myocardial infarction resulted in significant elevation of total (p < 0.001) and type I (p < 0.001) collagen and a twofold increase in TGF-beta 1 mPTNA expression (p < 0.001) in the septum at two and four weeks. Macrophages and activated myofibroblasts infiltrated extensively in the infarct zone. Treatment with valsartan or combination therapy normalized thetotal and type I collagen (p < 0.001) as well as TGF-beta 1 mRNA level (p < 0.01) in the septum and was associated with the suppression of macrophages and myofibroblasts in the infarct zone (p < 0.01). Fosinopril was less effective than valsartan or combination therapy. CONCLUSIONS The use of valsartan, especially combined with fosinopril, wasmore effective than fosinopril in the suppression of histopathologic changes resulting in cardiac remodeling after AMI. This study has important therapeutic implications in pharmacotherapy of clinical practice. (C) 2001 by the American College of Cardiology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 01:21:02