Experimental Myocardial Infarction

was studied in dogs 3-5 days after occlusion of the left anterior descending coronary artery. Compliance was assessed from postmortem pressure-volume curves and from pressure-length measurements (mercury-in-silastic segment length gauges) made both in vivo and postmortem. Postmortem pressure-volume curves showed reduced compliance compared to sham-operated animals. Postmortem pressure-length curves of infarcted and adjacent normal myocardium indicated that the diminished total compliance could be attributed to an increase in stiffness of the infarcted area. This was confirmed by in vivo end-diastolic pressure-length changes produced by transient aortic occlusion. The infarcted area was akinetic, showing neither contraction nor aneurysmal bulging. In addition, anesthetized dogs with infarcts, when compared with sham-operated animals, had similar left ventricular end-diastolic volumes (indicator dilution method), but higher left ventricular enddiastolic pressures. Taken with previous observations, which show that systolic aneurysmal bulging is uniformly present at the onset of ischemia, these results indicate that stiffening of the ischemic myocardium occurs during the first 5 days after infarction, and show that elevation of left ventricular filling pressure does not necessarily signify ventricular dilatation. The results also suggest a mechanism whereby ventricular performance may improve during recovery from acute myocardial infarction. Received for publication 8 August 1969 and in revised form 14 January 1970. INTRODUCTION Compromise of left ventricular performance after acute myocardial infarction has been demonstrated in both experimental (1-4) and clinical (5-8) studies. In experimental studies this impairment in ventricular function has been positively correlated with the size of the infarct measured postmortem, suggesting that the defect is directly due to loss of. functioning myocardium (3, 4), or to systolic bulging in the area of infarction (9, 10), or to both. It has furthermore been demonstrated that the acute depression in ventricular function after experimental canine myocardial infarction shows considerable improvement over the 1st week after infarction (11). This finding of time-dependent improvement of ventricular function after infarction has not yet been adequately explained. However, one possible mechanism would be a decrease in compliance of the infarcted muscle, which would prevent bulging, sequestration of blood, and reduction of effective stroke volume during the systolic phase of the cardiac cycle. Accordingly, the following experiments in dogs were carried out to determine whether compliance changes in the ischemic tissue after infarction are observed.