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J Am Coll Cardiol, 2004; 43:2207-2215, doi:10.1016/j.jacc.2003.11.064 © 2004 by the American College of Cardiology Foundation |



* Heart Failure Research Unit, Donald W. Reynolds Cardiovascular Clinical Research Center, Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA
Division of Cardiology, St. Francis Hospital, Roslyn, New York, USA
Cardiology Section, Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
Division of Cardiology, St. John Hospital and Medical Center and Wayne State University, Detroit, Michigan, USA
|| Division of Epidemiology and Clinical Applications, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA
¶ Department of Biostatistics, University of Washington, Seattle, Washington, USA
# Cardiovascular Health Research Unit, Departments of Medicine and Epidemiology, University of Washington, Seattle, Washington, USA
Manuscript received July 15, 2003; revised manuscript received November 17, 2003, accepted November 24, 2003.
* Reprint requests and correspondence: Dr. Mark H. Drazner, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9047, USA.
mark.drazner{at}utsouthwestern.edu
OBJECTIVES: Our aim in this study was to determine whether increased left ventricular mass (LVM) is a risk factor for the development of a reduced left ventricular ejection fraction (LVEF).
BACKGROUND: Prior studies have shown that increased LVM is a risk factor for heart failure but not whether it is a risk factor for a low LVEF.
METHODS: As part of the Cardiovascular Health Study, a prospective population-based longitudinal study, we performed echocardiograms upon participant enrollment and again at follow-up of 4.9 ± 0.14 years. In the present analysis, we identified 3,042 participants who had at baseline a normal LVEF and an assessment of LVM (either by electrocardiogram or echocardiogram), and at follow-up a measurable LVEF. The frequency of the development of a qualitatively depressed LVEF on two-dimensional echocardiography, corresponding approximately to an LVEF <55%, was analyzed by quartiles of baseline LVM. Multivariable regression determined whether LVM was independently associated with the development of depressed LVEF.
RESULTS: Baseline quartile of echocardiographic LVM indexed to body surface area was associated with development of a depressed LVEF (4.8% in quartile 1, 4.4% in quartile 2, 7.5% in quartile 3, and 14.1% in quartile 4 [p < 0.001]). A similar relationship was seen in the subgroup of participants without myocardial infarction (p < 0.001). In multivariable regression that adjusted for confounders, both baseline echocardiographic (p < 0.001) and electrocardiographic (p < 0.001) LVM remained associated with development of depressed LVEF.
CONCLUSIONS: Increased LVM as assessed by electrocardiography or echocardiography is an independent risk factor for the development of depressed LVEF.
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