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Circulation. 1997;96:3294-3299

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(Circulation. 1997;96:3294-3299.)
© 1997 American Heart Association, Inc.


Articles

Cardiovascular Death and Left Ventricular Remodeling Two Years After Myocardial Infarction

Baseline Predictors and Impact of Long-term Use of Captopril: Information From the Survival and Ventricular Enlargement (SAVE) Trial

Martin St. John Sutton, FRCP; Marc A. Pfeffer, MD, PhD; Lemuel Moye, MD, PhD; Ted Plappert, CVT; Jean L. Rouleau, MD; Gervasio Lamas, MD; Jacques Rouleau, MD; John O. Parker, MD; Malcolm O. Arnold, MD; Bruce Sussex, MD; Eugene Braunwald, MD; ; for the SAVE Investigators

From the Brigham and Women's Hospital, Harvard Medical School, Boston, Mass, and University of Pennsylvania Medical Center (Philadelphia).

Correspondence to M. St. John Sutton, FRCP, Division of Cardiology, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104.

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.


Key Words: remodeling • myocardial infarction • trials




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