REPERFUSION REDUCES LEFT-VENTRICULAR DILATATION BY PREVENTING INFARCTEXPANSION IN THE ACUTE AND CHRONIC PHASES OF MYOCARDIAL-INFARCTION

Reperfusion reduces left ventricular dilatation in patients with acute myocardial infarction, but it is unclear to what extent this is a pri mary effect or only a consequence of the limiting effect of reperfusio n on infarct size. To address this issue, 56 consecutive patients were examined by means of two-dimensional echocardiography on day 1, on da y 3, before discharge, and at 6 months after an acute myocardial infar ction. From this population two groups of 12 patients each, perfectly matched for site of myocardial infarction, extent of ventricular asyne rgy at two-dimensional echocardiography (akinesis + dyskinesis), and c linical characteristics were identified according to the creatine kina se (CK) time to peak, which was regarded as a marker of spontaneous or induced reperfusion: (1) CK time to peak of 12 hours or less (reperfu sed patients, n = 12), and (2) CK time to peak of more than 12 hours ( nonreperfused patients, n = 12). In these two groups of patients end-d iastolic and end-systolic left ventricular volumes and endocardial len gths of asynergic and normal ventricular segments, imaged in a cross-s ectional view at the level of the papillary muscles, were then compute d. At the first examination end-diastoIic volume, end-systolic volume, and endocardial segment lengths of normal and asynergic segments were similar in the two groups of patients. Patients with late CK time to peak, however, showed a progressive increase in left ventricular systo lic volumes and in asynergic endocardial segment lengths between the f irst and third (predischarge) examinations (p < 0.05 for both), with n o change in systolic length of the normal myocardium. The left ventric ular end-systolic volume and the asynergic endocardial segment length of patients with early CK time to peak, however, did not increase duri ng hospitalization. The increment in end-systolic volume and in systol ic infarct segment length from the first to the third examinations was higher in nonreperfused patients (p = 0.018 and p = 0.04, respectivel y). Changes similar to those detected in systole were found for diasto lic volume and diastolic infarcted and noninfarcted segment length in both groups, but they did not reach statistical significance. After 6 months, an increases in volume and endocardial length were found in bo th groups of patients. Relative to the first examination, however, the increase in systolic volume and in asynergic systolic endocardial len gths remained greater for nonreperfused patients (p = 0.077 and p = 0. 01, respectively). In conclusion, reperfusion after myocardial infarct ion prevents ventricular dilatation by inhibiting infarct expansion du ring the in-hospital phase of the illness, above and beyond its limiti ng effect on infarct size. The difference generated in the acute phase is maintained during the 6-month follow-up period, in which increases in volume and in endocardial segment length affect both reperfused an d nonreperfused patients.