Attempt to quantitate relation between cardiac function and infarct size in acute myocardial infarction

Abstract

In 82 patients with acute myocardial infarction, observed hemodynamic changes were compared with the average maximal serum enzyme rise and the infarction size, as calculated from serial determinations of creatine phosphokinase concentration. For this purpose, patients were divided into 3 groups according to their pulmonary artery end diastolic pressure at the time of admission. There were 19 patients in group I with pulmonary artery end diastolic pressure <12 mmHg; they had an average infarction size of 17g and no impairment of cardiac function. In the 35 patients in group II with pulmonary artery end diastolic pressure 12 to 20 mmHg, the pressure was raised to a mean value of 15.4±0.4 mmHg with a slight decrease of cardiac index (2.5±0.1 l./min per m2) and left ventricular stroke work index (51.4±4.7 g m/m2). Loss of myocardium in group II was 42 g and mortality was 21%. There were 28 patients in group III with pulmonary artery end diastolic pressure >20 mmHg, who had an average infarction size of 99 g. Cardiac index (1.9±0.2 l./min/m2), and stroke work index (27.5±5.7 g m/m2) declined significantly (P < 0.001). Mean end diastolic pressure rose to 28.3 ± 1.1 mmHg. Mortality in group III (60%) was mainly due to cardiogenic shock. It is concluded that the decrease of cardiac function in the acute phase of myocardial infarction must usually be ascribed to the amount of recent myocardial necrosis. Stiffening of the infarction area and normal or increased contractility of the noninfarcted myocardium are regarded as compensatory mechanisms. The combined investigation of hemodynamic and serial enzyme changes is considered to be an appropriate method for the separation of old from recent myocardial necrosis and for providing information predictive of the immediate and the long term prognosis.