Published Online
on May 5, 2003

A more recent version of this article appeared on May 27, 2003

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Submitted on January 16, 2003
Accepted on February 25, 2003

Left Ventricular Remodeling and Ventricular Arrhythmias After Myocardial Infarction

Martin St John Sutton FRCP^*, Douglas Lee MD, PhD, Jean Lucien Rouleau MD, Steven Goldman MD, Ted Plappert CVT, Eugene Braunwald MD, and Marc A. Pfeffer MD, PhD

From Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (M.A.P., E.B.); the University of Toronto, Ontario, Canada (D.L., J.L.R.); the University of Pennsylvania Medical Center, Philadelphia (M.S.J.S., T.P.); and the University of Arizona, Tucson (S.G.).

^* To whom correspondence should be addressed. E-mail: suttonm{at}mail.med.upenn.edu.

Background--The relation between left ventricular (LV) remodeling and ventricular arrhythmias after myocardial infarction is poorly documented. We investigated the relations between LV size, hypertrophy, and function and ventricular arrhythmias in 263 patients from the Survival and Ventricular Enlargement (SAVE) study, using quantitative 2D echocardiography and ambulatory ECG monitoring after myocardial infarction.

Methods and Results--Transthoracic 2D echocardiograms and arrhythmia monitoring were performed at baseline (mean, 11 days) and 1 and 2 years after infarction. LV size, short-axis muscle (mass) area (LVMA), and function were quantified from 2D echocardiograms. The prevalence of ventricular tachycardia (VT) and frequent ventricular ectopy (premature ventricular contractions [PVCs] >10/h) was assessed from ambulatory ECG. VT and PVCs >10/h occurred in 20% and 29% of patients at baseline, in 22% and 35% at 1 year and 23% and 39% at 2 years, respectively. VT and PVCs >10/h at baseline and 1 and 2 years were significantly related to LV size, LVMA, and function. Furthermore, changes in LV size and function from baseline to 2 years predicted both VT and PVCs >10/h. The study was underpowered to detect treatment effect of ACE inhibitors and -adrenergic receptor blockers but did not alter the relations between ventricular arrhythmias, LV size, and function.

Conclusions--Quantitative echocardiographic assessment of LV size, LVMA, and function and changes in these measurements over time predict ventricular arrhythmias after infarction. Altered LV architecture and function during postinfarction LV remodeling provide an important substrate for triggering high-grade ventricular arrhythmias.

Key words: remodeling • arrhythmia • myocardial infarction • echocardiography

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