ACUTE AND LONG-TERM EFFECTS OF THROMBOLYSIS AFTER ANTERIOR WALL ACUTEMYOCARDIAL-INFARCTION WITH SERIAL ASSESSMENT OF INFARCT EXPANSION ANDLATE VENTRICULAR REMODELING

This study investigates the impact of thrombolysis on infarct expansio n and subsequent left ventricular (LV) remodeling in patients with ant erior wall acute myocardial infarction (AMI). We evaluated 51 consecut ive patients (24 treated with thrombolysis) with anterior wall AMI by 2-dimensional echocardiography in the following sequence: days 1, 2, 3 , and 7, after 3 and 6 weeks, and after 3, 6, and 12 months. LV end-di astolic and end-systolic volume indexes were determined from apical 2- and 4-chamber views using Simpson's biplane formula. Infarct and tota l LV perimeters were determined in the same views and their ratio expr essed as infarct percentage. Infarct expansion was defined as: (1) an increase in infarct percentage and total perimeter >5% on days 2 to 3 in either of the views, or (2) initial infarct percentage >50% with an increase in total perimeter >5% on days 2 to 3. Coronary angiography was performed in 43 patients before discharge, and potency of the infa rct-related artery was assessed using Thrombolysis in Myocardial Infar ction trial criteria. Infarct expansion was detected in 23 patients. I nfarct perimeter steadily decreased in patients with versus without th rombolysis and in patients with patent versus occluded infarct-related arteries. Furthermore, by logistic regression, thrombolysis (p = 0.00 7) and patency of the infarct-related artery (p = 0.02) were strong ne gative predictors of expansion, whereas initial infarct perimeter (p = 0.009) was directly associated with subsequent expansion. End-systoli c volume index was higher in patients with expansion from day 1 (p = 0 .003) through the end of the study (p = 0.021), and end-diastolic volu me index was higher in these patients from day 2 (p = 0.012) through 1 2 months (p = 0.015). Thus thrombolysis, initial infarct size, and inf arct-related artery potency are major predictors of infarct expansion after anterior wall AMI.