RESIDUAL EXERTIONAL ISCHEMIA AND UNFAVORABLE LEFT-VENTRICULAR REMODELING IN PATIENTS WITH SYSTOLIC DYSFUNCTION AFTER ANTERIOR MYOCARDIAL-INFARCTION

Objectives. This study investigated whether exercise-induced myocardial ischemia influences left ventricular remodeling after anterior myocardial infarction. Background. The effects of acute and recurrent ischemia on ventricular function are well established. However, to our knowledge the role of exertional ischemia in the remodeling response after infarction has not been investigated. Methods. Ninety one patients with a first anterior Q wave myocardial infarction were studied at 5 weeks by rest echocardiography and exercise scintigraphy. The echocardiographic examination was repeated 6 months later. On the basis of the presence and extent of reversible perfusion defects on exercise scintigraphy, patients were assigned to groups with no exertional ischemia (group 1, n = 20 [22%]), mild to moderate ischemia (group 2, n = 45 [49%]) and severe exertional ischemia (group 3, n = 26 [29%]). Results. Initial left ventricular volumes were similar, and no differences were found among the three groups in the remodeling response over the 6-month period of the study. However, patients in groups 2 and 3 with an ejection fraction less than or equal to 40% showed significant (p < 0.01) ventricular enlargement over time, which was similar between the two groups (end diastolic volume [mean +/- SD] from 74 +/- 13 to 80 +/- 17 ml/m(2) in group 2 and from 72 +/- 11 to 81 +/- 19 ml/m(2) in group 3; regional dilation from 42 +/- 16% to 52 +/- 22% in group 2 and From 38 +/- 18% to 46 +/- 27% in group 3). hi contrast, ventricular dimensions did not change in group 1 patients with an ejection fraction less than or equal to 40% as well as in patients in all three groups with an ejection fraction >40%. Conclusions. Exercise-induced myocardial ischemia may contribute to progressive ventricular enlargement in patients with poor left ventricular function after a large anterior myocardial infarction.