[Ischemic cardiomyopathy: remodeling, hypertrophy, subendocardial risk. Can processes be controlled?].

Ischaemic cardiomyopathy reflects the myocardial dysfunction caused by coronary disease. It results from the association of 1. segmental infarction(s) responsible for ventricular "remodelling", i.e. expansion of the necrotic area(s) and hypertrophy-dilatation of the rest of the ventricle, eventually concurring to heart failure; 2. areas which are viable but with a function that is reversibly compromised by severe acute or chronic ischaemia (myocardial sideration or hibernation) affecting mainly the subendocardium. The spontaneous course of cardiomyopathy towards the worst can be arrested by 1. revascularisation of the myocardium at risk by coronary reperfusion performed either as an emergency in case of infarct in the process of formation, or after detection of the viable myocardial areas by isotopic methods; 2. prevention or limitation of ventricular remodelling by coronary reperfusion and improvement of the ventricular load by administration of angiotensin-converting enzyme inhibitors and nitroglycerin. The Survival and Ventricular Enlargement study (SAVE) has been the first to demonstrate the relationship between limitation of ventricular remodelling and improvement of the secondary prognosis of infarction obtained by angiotensin-converting enzyme inhibitors.