Acute and long-term effects of thrombolysis after anterior wall acute myocardial infarction with serial assessment of infarct expansion and late ventricular remodeling.

This study investigates the impact of thrombolysis on infarct expansion and subsequent left ventricular (LV) remodeling in patients with anterior wall acute myocardial infarction (AMI). We evaluated 51 consecutive 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-diastolic and end-systolic volume indexes were determined from apical 2- and 4-chamber views using Simpson's biplane formula. Infarct and total LV perimeters were determined in the same views and their ratio expressed 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 patency of the infarct-related artery was assessed using Thrombolysis in Myocardial Infarction trial criteria. Infarct expansion was detected in 23 patients. Infarct perimeter steadily decreased in patients with versus without thrombolysis and in patients with patent versus occluded infarct-related arteries. Furthermore, by logistic regression, thrombolysis (p = 0.007) and potency of the infarct-related artery (p = 0.02) were strong negative predictors of expansion, whereas initial infarct perimeter (p = 0.009) was directly associated with subsequent expansion. End-systolic 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 volume index was higher in these patients from day 2 (p = 0.012) through 12 months (p = 0.015). Thus thrombolysis, initial infarct size, and infarct-related artery patency are major predictors of infarct expansion after anterior wall AMI.