Adiposity of the heart, revisited

University of Texas Southwestern Medical Center, Dallas, Texas 75390-8899, USA.
Annals of internal medicine (Impact Factor: 17.81). 05/2006; 144(7):517-24.
Source: PubMed


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.

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Available from: Lidia S Szczepaniak,
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    • "Fat is a scarcely elastic tissue [62] [63] and infiltration into the myocardium has to alter the tissue elastic properties, likely impairing distensibility and limiting LV dilatation. Cytosolic accumulation of fatty acid increases the size of cardiomyocytes independently of expression of sarcomeres [30] [64] and, possibly, reduces cell elastance. In addition to promoting reactive fibrosis, overproduction of cytokines from the visceral adipose tissue, namely from the IL6 family, may also contribute to sarcomeric growth in both serial and parallel directions [65e67]. "
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    • "Dynamic cine images were used to quantify left ventricular (LV) volume [16,18,19]. Image analysis was performed by an observer blinded to the subject’s clinical history and treatment, using a commercially available workstation (MASS, Philips Medical Systems). "
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    • "Ectopic lipid deposition in nonadipose tissues is associated with an overstrain of the cellular oxidation capacity. This overstrain leads to insufficient substrate utilization and, consequently, to accumulation of toxic by-products that induce cell damage and organ dysfunction, specifically lipotoxicity (6). However, the precise role of cardiac steatosis in the pathogenesis of myocardial dysfunction remains unclear as yet. "
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