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Letter to the Editor |
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215
Address correspondence to: Peter G. Danias, M.D., Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, Massachusetts 02215. E-mail: pdanias{at}bidmc.harvard.edu.
To the editor:
Gates et al. (1) have recently reported on the association between indices of left ventricular structure and adiposity in 113 healthy adult men using M-mode echocardiography. The investigators found that older subjects with higher adiposity, but not their younger counterparts, had increased left ventricular wall thickness and abnormal diastolic function. Left ventricular mass was similar between groups with high and low adiposity, in both the young and older subgroups.
Although provocative, their findings regarding the lack of a significant difference in left ventricular mass between subjects with higher and lower adiposity may be due to their methodology (unidimensional M-mode echocardiography) and inadequate study power for the subgroup analysis. We and others (2, 3) have found that the obese have increased left ventricular mass in comparison with lean controls. A more accurate and reproducible volumetric method such as cardiovascular magnetic resonance imaging is preferable for evaluation of obese subjects because it allows the detection of small differences in cardiac structure and function with a much smaller sample size than with echocardiography (4).
The relative role of adiposity vs. that of other factors mediating age-related cardiac changes cannot be ascertained from this study. The authors recognized that left ventricular changes occurred with advancing age independently of adiposity, presumably due to a variety of mechanisms (hypertension, decreased arterial elasticity, cellular and extracellular myocardial structural changes). Some of these same factors may also be associated with obesity, including findings from our laboratory that demonstrate that obesity is independently associated with decreased elasticity of the abdominal aorta (5). Moreover, as the authors recognized, not only does the presence of high adiposity contribute to structural and functional cardiac changes, but also the duration of high adiposity is likely to be important, although few data are available in this area. Resistance to leptin may also be involved in the pathogenesis of cardiac changes with obesity (6).
Although the authors did not show that the structural and functional cardiac changes in subjects with higher adiposity are associated with a poorer outcome, we agree with the authors suggestion regarding the importance of effective control of excess body adiposity for preserving cardiovascular health. Further investigations into the mechanisms mediating the cardiovascular effects of obesity and the close interplay between the endocrine and cardiovascular systems are needed.
Received November 14, 2003.
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