Abstract

Left ventricular remodelling is a progressive process, which starts immediately after acute myocardial infarction and evolves in the chronic phase of heart failure. It is characterized by left ventricular chamber dilatation and increased wall stress, which results in alteration of the contractile properties of the non-infarct zone and impairment of the systolic and diastolic performances of the left ventricle. Neurohormonal activation and increased sympathetic stimulation are among the factors that have been linked to the development and progression of left ventricular dysfunction after acute myocardial infarction. The present review will address recent insights from new patents and experimental studies of drugs, which ought to prevent left ventricular remodelling. Angiotensin-Converting Enzyme Inhibitors, Angiotensin Receptor Blockers and Beta-Blockers have been proven effective in modulating the process of remodelling and in reducing the occurrence of adverse events. However, in most of the trials high risk patients have been excluded, and uncertainty still exists regarding a number of clinically relevant questions. Data from experimental studies have identified new targets for interventions to prevent reverse left ventricular remodelling, i.e. stem cell transfer, activation of cardiac and leukocyte-dependent oxidant stress pathways, inflammatory pathway activation, matrix-metalloproteinase activation.

Keywords: Acute myocardial infarction, primary coronary angioplasty, left ventricular remodelling, ACE-inhibitors, angiotensin receptor blockers, beta-blockers, aldosterone antagonists, heart failure, left ventricular dysfunction, Angiotensin-Converting Enzyme Inhibitors, matrix-metalloproteinase activation, Reperfusion therapy, systolic and diastolic, autocrine trophic factors, cardiomyocytes, neurohormonal activity, hypertrophy, interstitial fibrosis, metalloproteinases, open-artery hypothesis, optimal reperfusion, captopril, echocardiografic ancillary study, thrombolysis, Losartan, VALIANT, Valsartan, angiotensin-aldosterone system, Candesartan, Carvedilol, nebivolol, Eplerenone, Randomized Aldactone Evaluation Study, Spironolactone, STEM CELL THERAPY, cardiac hypertrophy, nitric oxide, COX-2 selective inhibitors, ibuprofen, indomethacin, interleukin, matrix-metallo-proteinase activation-9, endothelin-1 receptor antagonist, atrial natriuretic peptide