Reperfusion reduces left ventricular dilatation by preventing infarct expansion 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 primary effect or only a consequence of the limiting effect of reperfusion on infarct size. To address this issue, 56 consecutive patients were examined by means of two-dimensional echocardiography on day 1, on day 3, before discharge, and at 6 months after an acute myocardial infarction. From this population two groups of 12 patients each, perfectly matched for site of myocardial infarction, extent of ventricular asynergy at two-dimensional echocardiography (akinesis + dyskinesis), and clinical characteristics were identified according to the creatine kinase (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 (reperfused 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-diastolic and end-systolic left ventricular volumes and endocardial lengths of asynergic and normal ventricular segments, imaged in a cross-sectional view at the level of the papillary muscles, were then computed. At the first examination end-diastolic 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 systolic volumes and in asynergic endocardial segment lengths between the first and third (predischarge) examinations (p < 0.05 for both), with no change in systolic length of the normal myocardium. The left ventricular end-systolic volume and the asynergic endocardial segment length of patients with early CK time to peak, however, did not increase during hospitalization. The increment in end-systolic volume and in systolic infarct segment length from the first to the third examinations was higher in nonreperfused patients (p = 0.018 and p = 0.04, respectively). Changes similar to those detected in systole were found for diastolic 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 both groups of patients. Relative to the first examination, however, the increase in systolic volume and in asynergic systolic endocardial lengths remained greater for nonreperfused patients (p = 0.077 and p = 0.01, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
Golia
G
G
Division of Cardiology, University of Verona, Italy.
Marino
P
P
Rametta
F
F
Nidasio
G P
GP
Prioli
M A
MA
Anselmi
M
M
Destro
G
G
Zardini
P
P
D000328:Adult; D017023:Coronary Angiography; D003402:Creatine Kinase / Q000097:blood; D004108:Dilatation, Pathologic; D004452:Echocardiography; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D013599:Systole / Q000502:physiology; D013997:Time Factors
D003402:Creatine Kinase