[Changes in myocardial function and perfusion after acute myocardial infarction].

Rev Esp Cardiol 2003;56(5):433-5 433 Ligation of a coronary artery causes myocardial necrosis. It has been shown in experimental animals1 that the size of the necrotic scar is directly proportional to the time elapsed between ligation and reperfusion. Early reperfusion not only reduces the size of the infarct, but also protects against ventricular dilatation. Although delayed reperfusion is unable to save the damaged myocardium, it has a positive influence on ventricular remodeling. In such cases, the ventricle is more dilated than it is in animals that have undergone early reperfusion, but less so than in animals whose arteries are permanently occluded. When coronary occlusion is permanent, the infarcted zone becomes thinned and expands, but neither occurs when reperfusion takes place early. A thick scar can lead to less systolic thickening and less oxygen demand, since ventricular stress is inversely proportional to the thickness of the wall. This explains why there is less expansion when reperfusion has occurred than when it has not occurred. In 1982, Wackers2 found by using isotope ventriculography that there were important fluctuations in left ventricular ejection fraction over the first 24 hours after an acute myocardial infarction. Between the measurement taken within the first 6 hours and the repeat measurement 24 hours after onset, ejection fraction can increase or decrease substantially. In the first few hours after an infarct, dynamic and apparently unpredictable changes in left ventricular function take place, making it difficult to assess different therapeutic interventions. ED I TO R I A L S