4.6 Article

Effects of Age and Aerobic Fitness on Myocardial Lipid Content

Journal

CIRCULATION-CARDIOVASCULAR IMAGING
Volume 6, Issue 6, Pages 1048-1055

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCIMAGING.113.000565

Keywords

aging; exercise; ventricular remodeling

Funding

  1. National Institutes of Health [RO1-AG17479]

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Background Aging and sedentary lifestyles lead to cardiac atrophy, ventricular stiffening, and impaired diastolic function. Both conditions are marked by increased adiposity, which can lead to ectopic fat deposition in nonadipocyte tissues including the myocardium. The effect of excess intramyocardial fat on cardiac function in nonobese individuals is unknown. Methods and Results Cardiac lipid content was measured by magnetic resonance spectroscopy in 153 healthy nonobese subjects with varying fitness levels quantified by peak oxygen uptake during treadmill exercise. Cardiac function (echo) and left ventricular (LV) filling pressures (right heart catheterization) were measured under varying preloads. LV stiffness was calculated from a curve fit of the diastolic portion of the pressure-volume curve. The strongest clinical predictors of lipid content were body mass index (=+0.03; 95% confidence interval, 0.001-0.06) and peak oxygen uptake (=-0.02; 95% confidence interval, -0.03 to -0.009; R-2=0.14; P<0.001). Subjects in the highest quintile had smaller LV end-diastolic volumes (6813 versus 58 +/- 12 mL/m(2); P<0.01) and decreased peak early mitral annular and increased peak late mitral inflow velocities. There were no differences in LV stiffness, but a leftward shift in the pressure-volume curve suggested a less distensible ventricle with increasing myocardial lipid levels. After adjusting for age, fitness, and body mass index, echocardiographic and morphometric differences among groups were attenuated and no longer significant. Conclusions Body mass index and fitness levels are the strongest predictors of myocardial lipid content in nonobese humans. Cardiac lipid content is associated with decreased ventricular distensibility, and it may provide a causal mechanism linking changes in LV function related to age and fitness.

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