Review: The revised role of ACE-inhibition after myocardial infarction in the thrombolytic/primary PCI era

Abstract

Many studies have investigated the process of left ventricular (LV) dilatation and the effects of angiotensin-converting enzyme (ACE) inhibitors after myocardial infarction (MI). It has been generally accepted that progression of LV dilatation is a major predictor of heart failure and death after MI. Also, attenuation of LV dilatation is thought to be one of the main mechanisms by which ACE inhibitors (ACE-Is) produce their beneficial effects. However, evidence for this hypothesis came from studies that were performed before thrombolytic therapy and primary percutaneous coronary intervention (PCI) were routinely used after acute MI. Nowadays, reperfusion is obtained much more frequently and LV dilatation after MI has become less prevalent. Nevertheless, ACE-Is proved effective in reducing cardiac morbidity and mortality. Therefore, mechanisms other than attenuation of LV dilatation, such as anti-atherosclerotic effects or plaque stabilisation, may explain the long-term beneficial effects of ACE-Is after MI.In the present overview, we evaluate the role of LV dilatation and the effects of ACE-Is after MI in the thrombolytic/primary PCI era and provide recommendations on ACE-I use in clinical practice. IntroductionAcute myocardial infarction (MI) is followed by complex alterations in left ventricular (LV) architecture, referred to as LV remodelling. After large anterior infarctions, LV remodelling may become a generalised progressive process, continuing over months to years and eventually leading to heart failure and death.1,2 An integral part of LV remodelling is LV dilatation. During the last decades, many randomised controlled trials have been conducted to investigate the effect of various interventions on the progression of LV dilatation, cardiac morbidity and mortality. These trials have resulted in two major advances in the treatment of MI. First, early reperfusion of the infarct-related artery (e.g. by administration of thrombolytic therapy or direct percutaneous coronary intervention [PCI]) proved effective in preventing or minimising LV dilatation and reducing cardiac morbidity and mortality by limiting the infarct size.3-8 Secondly, angiotensin-converting enzyme (ACE) inhibitors attenuated LV dilatation and reduced cardiac morbidity and mortality, especially in patients with LV dysfunction and/or without

Late Cardiac Remodeling After Primary Percutaneous Coronary Intervention

“…A meta-analysis showed that there was no difference in left ventricular dilatation between patients taking ACE inhibitors or placebo in patients treated with thrombolysis. 26 Hence none of these studies looked at the different dilatation patterns, and also these studies used echocardiography and not CMRI. The latter is considered to be the gold-standard for functional imaging and is able to accurately visualize the extent of infarct mass.…”