Should angiotensin converting enzyme (ACE) inhibitors be used routinely after infarction? Perspectives from the Survival and Ventricular Enlargement (SAVE) trial.

Left ventricular remodelling after infarction Many factors influence the survival of patients after myocardial infarction, but the single most important clinical determinant is left ventricular function.1-3 Left ventricular function correlates closely with the size of the region of myocyte necrosis in human and in animal infarction models.45 Recently, the cellular processes occurring soon after acute myocardial infarction have become better understood. Viable myocytes adjacent to the necrotic area can remain dysfunctional or stunned for a long time.6 Within the first 72 hours the infarct zone stretches owing to slippage of necrotic myofilaments before the tensile strength of the infarct becomes altered by the deposition of collagen.7 Expansion of the infarction zone results in left ventricular dilatation, increased wall stress, and a fall in ejection fraction.48 Increased wall stress is a potent stimulus for left ventricular hypertrophy. When the hypertrophy is sufficient to normalise the increased wall stress, the left ventricular ejection function is restored towards normal. When the hypertrophy is insufficient to counteract the increased wall stress, however, left ventricular dilatation progresses and further deterioration in contractile function leads to early congestive heart failure and a poor outcome. This combination of left ventricular dilatation, hypertrophy, and alteration in cavity configuration, which has been termed left ventricular remodelling, begins early and may continue for months or even years.8 The impact of raised plasma concentrations of noradrenaline, renin/angiotensin, atrial natriuretic peptide, and a range of other neurohormones on left ventricular remodelling after infarction is currently under intensive investigation.9