Adiposity of the heart, revisited.
Obesity is a major risk factor for heart disease. In the face of obesity's growing prevalence, it is important for physicians to be aware of emerging research of novel mechanisms through which adiposity adversely affects the heart. Conventional wisdom suggests that either hemodynamic (that is, increased cardiac output and hypertension) or metabolic (that is, dyslipidemic) derangements associated with obesity may predispose individuals to coronary artery disease and heart failure. The purpose of this review is to highlight a novel mechanism for heart disease in obesity whereby excessive lipid accumulation within the myocardium is directly cardiotoxic and causes left ventricular remodeling and dilated cardiomyopathy. Studies in animal models of obesity reveal that intracellular accumulation of triglyceride renders organs dysfunctional, which leads to several well-recognized clinical syndromes related to obesity (including type 2 diabetes). In these rodent models, excessive lipid accumulation in the myocardium causes left ventricular hypertrophy and nonischemic, dilated cardiomyopathy. Novel magnetic resonance spectroscopy techniques are now available to quantify intracellular lipid content in the myocardium and various other human tissues, which has made it possible to translate these studies into a clinical setting. By using this technology, we have recently begun to study the role of myocardial steatosis in the development of obesity-specific cardiomyopathy in humans. Recent studies in healthy individuals and patients with heart failure reveal that myocardial lipid content increases with the degree of adiposity and may contribute to the adverse structural and functional cardiac adaptations seen in obese persons. These studies parallel the observations in obese animals and provide evidence that myocardial lipid content may be a biomarker and putative therapeutic target for cardiac disease in obese patients.
University of Texas Southwestern Medical Center, Dallas, Texas 75390-8899, USA.
Jonathan M
JM
McGavock
Ronald G
RG
Victor
Roger H
RH
Unger
Lidia S
LS
Szczepaniak
D000818:Animals; D002311:Cardiomyopathy, Dilated / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000378:metabolism; D050356:Lipid Metabolism; D009206:Myocardium / Q000378:metabolism*; D009765:Obesity / Q000150:complications* / Q000378:metabolism*