(Circulation. 1995;91:2573-2581.)
© 1995 American Heart Association, Inc.
Articles |
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-wavetoA-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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J. N. Cohn Structural Basis for Heart Failure : Ventricular Remodeling and Its Pharmacological Inhibition Circulation, May 15, 1995; 91(10): 2504 - 2507. [Full Text] |
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