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(Circulation. 2005;111:3411-3419.)
© 2005 American Heart Association, Inc.

Heart Failure

Changes in Ventricular Size and Function in Patients Treated With Valsartan, Captopril, or Both After Myocardial Infarction

Scott D. Solomon, MD; Hicham Skali, MD; Nagesh S. Anavekar, MD; Mikhail Bourgoun, MD; Stale Barvik, MD; Jalal K. Ghali, MD; J. Wayne Warnica, MD; Margarita Khrakovskaya, MD; J. Malcolm O. Arnold, MD; Yuri Schwartz, MD; Eric J. Velazquez, MD; Robert M. Califf, MD; John V. McMurray, MD; Marc A. Pfeffer, MD, PhD

From the Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (S.D.S., H.S., N.S.A., M.B., M.A.P.); Section of Cardiology, Department of Medicine, Central Hospital in Rogaland, Stavanger, Norway (S.B.); Cardiac Centers of Louisiana, Shreveport (J.K.G.); Foothills Hospital, Calgary, Alberta, Canada (J.W.W.); St George Hospital, St Petersburg, Russia (M.K.); London Health Sciences Center–Victoria Campus, London, Ontario, Canada (J.M.O.A.); University Hospital N3, Saratov, Russia (Y.S.); Duke University Medical Center, Durham, NC (E.J.V., R.M.C.); and Department of Cardiology, Western Infirmary, Glasgow, Scotland (J.V.M.).

Correspondence to Scott D. Solomon, MD, Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis St, Boston, MA 02115. E-mail ssolomon{at}rics.bwh.harvard.edu

Received September 28, 2004; revision received February 22, 2005; accepted March 25, 2005.

Background— Angiotensin-converting enzyme (ACE) inhibitors have been shown to attenuate left ventricular (LV) enlargement in association with reducing mortality after myocardial infarction (MI). Preclinical data suggest that angiotensin receptor blockers (ARBs) may have similar structural and functional effects after MI. The Valsartan in Acute Myocardial Infarction (VALIANT) Echo study was designed to test the hypothesis that the ARB valsartan, either alone or in combination with captopril, could attenuate progressive LV enlargement or improve LV ejection fraction to a greater extent than captopril alone.

Methods and Results— Six hundred ten patients enrolled in the main VALIANT study who experienced MI and evidence of LV dysfunction, heart failure, or both were enrolled in the VALIANT Echo study. Patients were randomized to receive valsartan 160 mg PO BID, captopril 50 mg PO TID, or valsartan 80 mg PO BID plus captopril 50 mg PO TID between 1 and 10 days after MI. Six hundred three patients had echocardiograms of sufficient quality for quantitative analysis. Echocardiograms were digitized, and endocardial borders were traced manually from 2 short-axis and 2 apical views. Ventricular volumes, ejection fractions, combined areas, and infarct segment length were measured, and changes in echocardiographic measures from baseline to 20 months were compared between treatment groups. Baseline clinical and echocardiographic characteristics were similar in the 3 treatment arms. The changes from baseline to 20 months in all echocardiographic parameters were similar in all 3 treatment arms. Baseline echocardiographic measures of ejection fraction, end-diastolic volume, and infarct segment length were highly predictive of outcomes including total mortality, death or hospitalization for heart failure, or death or any cardiovascular event (heart failure, MI, stroke, resuscitated sudden death), even after adjustment for known covariates.

Conclusions— Treatment with the ACE inhibitor captopril, valsartan, or the combination of captopril plus valsartan resulted in similar changes in cardiac volume, ejection fraction, and infarct segment length between baseline and 20 months after MI. Baseline echocardiographic measures were powerfully and independently predictive of all major outcomes.

Key Words: echocardiography • myocardial infarction • remodeling • angiotensin-converting enzyme inhibitors • ventricular function

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