[Myocardial viability in acute myocardial infarction and verapamil]

Following prolonged ischemia, if not adequately reperfused, myocardium undergoes necrosis, scarring and thinning. The myocardium tends to dilate in the noninfarcted ventricular area, giving rise to ventricular remodelling. If the ischemic myocardium is adequately reperfused it can be saved and its temporarily depressed functions eventually be recuperated (viable myocardium). The extent of recovery of the postinfarction viable myocardium seems to affect ventricular remodelling. The integrity of the microcirculation of the non-contractile myocardium following prolonged ischemia is fundamental in maintaining a contractile reserve adequate enough for a functional recovery (myocardial viability). Protection of the microcirculation during ischemia-reperfusion is therefore of great importance for the role that the microcirculation plays in ensuring myocardial viability. Experimental studies and initial clinical observations showed that calcium-antagonists exert a beneficial effect in this respect. VAMI is a multicentre, randomized double-blind, placebo-controlled study whose aim is to ascertain the potentiality of verapamil in limiting regional functional damage in patients with acute myocardial infarction and undergoing early thrombolysis.