Literature DB >> 2142081

Preventive treatment of asymptomatic left ventricular dysfunction following myocardial infarction.

N Sharpe1, J Murphy, H Smith, S Hannan.   

Abstract

Progressive asymptomatic ventricular dilatation can occur following myocardial infarction and severe ventricular dysfunction is often present by the time clinical congestive heart failure occurs. In a randomized, double-blind trial, the effects of captopril 25 mg tid, frusemide 40 mg daily and placebo were studied in 90 patients with asymptomatic left ventricular dysfunction (ejection fraction less than 45%) 1 week following Q wave myocardial infarction. Left ventricular volumes and function were assessed at intervals during the subsequent year using two-dimensional echocardiography. The frusemide and placebo groups showed significant increases in ventricular volumes with stroke volume index unchanged and ejection fraction slightly reduced, whereas the captopril group showed a significant reduction in left ventricular end-systolic volume index with stroke volume index and ejection fraction increased. At 12 months the difference in the change in ejection fraction from baseline between the captopril and frusemide groups was 10.5% and captopril and placebo groups 9.6% (both P less than 0.0001). There was a significant difference in occurrence of clinical heart failure in the placebo group compared with the other groups (P less than 0.05). Blood pressure increased significantly within the normal range in the placebo and frusemide groups whereas there was essentially no change from baseline in the captopril group. There was no significant correlation between baseline left ventricular volumes and function and subsequent change, and anterior and inferior infarct subgroups showed similar responses within the treatment groups. In conclusion, captopril improves asymptomatic ventricular dysfunction and prevents clinical heart failure during the year following myocardial infarction. Frusemide may also prevent clinical heart failure but not progressive ventricular dilatation.

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Year:  1990        PMID: 2142081     DOI: 10.1093/eurheartj/11.suppl_b.147

Source DB:  PubMed          Journal:  Eur Heart J        ISSN: 0195-668X            Impact factor:   29.983


  6 in total

1.  Influence of tissue affinity of angiotensin-converting enzyme inhibitors on left ventricular remodeling after myocardial infarction.

Authors:  M Konermann; C Altmann; F Laschewski; W Josephs; H J Odenthal; E Horstmann; B Sanner
Journal:  Clin Cardiol       Date:  1998-04       Impact factor: 2.882

2.  Effects of angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor antagonists in rats with heart failure. Role of kinins and angiotensin II type 2 receptors.

Authors:  Y H Liu; X P Yang; V G Sharov; O Nass; H N Sabbah; E Peterson; O A Carretero
Journal:  J Clin Invest       Date:  1997-04-15       Impact factor: 14.808

Review 3.  Central hemodynamic effects of diuretic therapy in chronic heart failure.

Authors:  B Silke
Journal:  Cardiovasc Drugs Ther       Date:  1993-01       Impact factor: 3.727

4.  General practitioners and the treatment of myocardial infarction: the place of thrombolytic treatment.

Authors:  M C Colquhoun
Journal:  Br Heart J       Date:  1993-09

Review 5.  Captopril. A review of its pharmacology and therapeutic efficacy after myocardial infarction and in ischaemic heart disease.

Authors:  G L Plosker; D McTavish
Journal:  Drugs Aging       Date:  1995-09       Impact factor: 3.923

6.  Blood signature of pre-heart failure: a microarrays study.

Authors:  Fatima Smih; Franck Desmoulin; Matthieu Berry; Annie Turkieh; Romain Harmancey; Jason Iacovoni; Charlotte Trouillet; Clement Delmas; Atul Pathak; Olivier Lairez; François Koukoui; Pierre Massabuau; Jean Ferrieres; Michel Galinier; Philippe Rouet
Journal:  PLoS One       Date:  2011-06-24       Impact factor: 3.240

  6 in total

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