Cardiovascular Death and Left Ventricular Remodeling Two Years After Myocardial Infarction

Abstract

Background We quantified cardiovascular death and/or left ventricular (LV) dilatation in patients from the SAVE trial to determine whether dilatation continued beyond 1 year, whether ACE inhibitor therapy attenuated late LV dilatation, and whether any baseline descriptors predicted late dilatation. Methods and Results Two-dimensional echocardiograms were obtained in 512 patients at 11±3 days and 1 and 2 years postinfarction to assess LV size, percentage of the LV that was akinetic/dyskinetic (%AD), and LV shape index. LV function was assessed by radionuclide ejection fraction. Two hundred sixty-three patients (51.4%) sustained cardiovascular death and/or LV diastolic dilatation; 279 (54.5%) had cardiovascular death and/or systolic dilatation. In 373 patients with serial echocardiograms, LV end-diastolic and end-systolic sizes increased progressively from baseline to 2 years (both P <.01). More patients with LV dilatation had a decrease in ejection fraction: 24.8% versus 6.8% ( P <.001) (diastole) and 25.7% versus 5.3% ( P <.001) (systole). Captopril attenuated diastolic LV dilatation at 2 years ( P =.048), but this effect was carried over from the first year of therapy because changes in LV size with captopril beyond 1 year were similar to those with placebo. Predictors of cardiovascular death and/or dilatation were age ( P =.023), prior infarction ( P <.001), lower ejection fraction ( P <.001), angina ( P =.007), heart failure ( P =.002), LV size ( P <.001), and infarct size (%AD) ( P <.001). Conclusions Cardiovascular death and/or LV dilatation occurred in >50% of patients by 2 years. LV dilatation is progressive, associated with chamber distortion and deteriorating function that is unaffected by captopril beyond 1 year.