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Circulation. 1995;91:2573-2581

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(Circulation. 1995;91:2573-2581.)
© 1995 American Heart Association, Inc.


Articles

Effects of Long-term Enalapril Therapy on Cardiac Structure and Function in Patients With Left Ventricular Dysfunction

Results of the SOLVD Echocardiography Substudy

Barry Greenberg, MD; Miguel A. Quinones, MD; Chris Koilpillai, MD; Marian Limacher, MD; Daniel Shindler, MD; Claude Benedict, MD; Brent Shelton, PhD; for the SOLVD Investigators

From the Division of Cardiology (B.G.), Oregon Health Sciences University, Portland, Ore; Baylor College School of Medicine (M.A.Q.), Houston, Tex; Dalhousie University School of Medicine (C.K.), Halifax, Nova Scotia, Canada; University of Florida College of Medicine (M.L.) (Gainesville); Robert Wood Johnson School of Medicine (D.S.), Piscataway, NJ; University of Texas School of Medicine (C.B.) (Galveston); and Department of Biostatistics (B.S.), Collaborating Studies Coordinating Center, Chapel Hill, NC.

Correspondence to Barry Greenberg, MD, University of California at San Diego, 200 W Arbor St, San Diego, CA 92103-8411.

Background Studies of Left Ventricular Dysfunction (SOLVD) demonstrated that enalapril therapy significantly improved the clinical course of patients with left ventricular (LV) dysfunction. The goals of this substudy were to evaluate changes in LV structure and function in SOLVD patients and to test the hypothesis that enalapril inhibits remodeling in patients with LV dysfunction.

Methods and Results Patients entering both the prevention and treatment arms of SOLVD from 5 of the 23 clinical centers were recruited for this substudy. The 301 patients who participated underwent Doppler-echocardiographic evaluation according to standard protocol before randomization to either enalapril or placebo and again after 4 and 12 months of therapy. Recorded data were analyzed in a blinded fashion at a central core laboratory. Analysis of baseline clinical characteristics showed that patients enrolled in the substudy were generally representative of the SOLVD population, although prevention arm patients were slightly overrepresented in the substudy group (69.8% compared with 61.9% of remaining SOLVD patients). The enalapril group demonstrated significant reductions in the mitral annular E-wave–to–A-wave velocity ratio (due predominantly to a reduction in E-wave velocity), and this response was different from that seen in the placebo group (P=.030). Changes in the E-to-A ratio in the enalapril group correlated significantly with changes in plasma atrial natriuretic peptide (r=.56; P<=.01). LV end-diastolic and end-systolic volumes increased in placebo but not enalapril-treated patients, and the differences in response between the treatment groups were significant (P=.025 and .019, respectively). LV mass tended to increase in placebo patients and to be reduced in enalapril-treated patients, and the difference in response between the groups was highly significant (P<=.001).

Conclusions These data demonstrate that enalapril attenuates progressive increases in LV dilatation and hypertrophy in patients with LV dysfunction. The results support the possibility that the favorable effects of enalapril reported in the SOLVD trials were related to inhibition of LV remodeling.


Key Words: enalapril • hypertrophy • echocardiography • heart failure • atrial natriuretic peptide




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D. V. Exner, D. L. Dries, M. A. Waclawiw, B. Shelton, and M. J. Domanski
Beta-adrenergic blocking agent use and mortality in patients with asymptomatic and symptomatic left ventricular systolic dysfunction: a post hoc analysis of the studies of left ventricular dysfunction
J. Am. Coll. Cardiol., March 15, 1999; 33(4): 916 - 923.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
J. K. French, D. J. Amos, B. F. Williams, D. B. Cross, J. M. Elliott, H. H. Hart, M. G. Williams, R. M. Norris, N. G. Ashton, R. M. L. Whitlock, et al.
Effects of early captopril administration after thrombolysis on regional wall motion in relation to infarct artery blood flow
J. Am. Coll. Cardiol., January 1, 1999; 33(1): 139 - 145.
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J Am Coll CardiolHome page
D. J. van Veldhuisen, S. Genth-Zotz, J. Brouwer, F. Boomsma, T. Netzer, A. J. Man in 't Veld, Y. M. Pinto, K. I. Lie, and H. J. G. M. Crijns
High- versus low-dose ACE inhibition in chronic heart failure: A double-blind, placebo-controlled study of imidapril
J. Am. Coll. Cardiol., December 1, 1998; 32(7): 1811 - 1818.
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CirculationHome page
A. M. Katz
Regression of Left Ventricular Hypertrophy : New Hope for Dying Hearts
Circulation, August 18, 1998; 98(7): 623 - 624.
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CirculationHome page
M. St. J. Sutton, M. A. Pfeffer, L. Moye, T. Plappert, J. L. Rouleau, G. Lamas, J. Rouleau, J. O. Parker, M. O. Arnold, B. Sussex, et al.
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
Circulation, November 18, 1997; 96(10): 3294 - 3299.
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NEJMHome page
R. S. Vasan, M. G. Larson, E. J. Benjamin, J. C. Evans, and D. Levy
Left Ventricular Dilatation and the Risk of Congestive Heart Failure in People without Myocardial Infarction
N. Engl. J. Med., May 8, 1997; 336(19): 1350 - 1355.
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NEJMHome page
P. A. Poole-Wilson
Prediction of Heart Failure -- An Art Aided by Technology
N. Engl. J. Med., May 8, 1997; 336(19): 1381 - 1382.
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CirculationHome page
E. J. Eichhorn and M. R. Bristow
Medical Therapy Can Improve the Biological Properties of the Chronically Failing Heart: A New Era in the Treatment of Heart Failure
Circulation, November 1, 1996; 94(9): 2285 - 2296.
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CirculationHome page
J. N. Cohn
Structural Basis for Heart Failure : Ventricular Remodeling and Its Pharmacological Inhibition
Circulation, May 15, 1995; 91(10): 2504 - 2507.
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