Jonathan M. McGavock, PhD; Ronald G. Victor, MD; Roger H. Unger, MD; Lidia S. Szczepaniak, PhD
*The title Adiposity of the Heart, Revisited was borrowed from an article by Smith and Willius that appeared in Archives of Internal Medicine in 1933.
Grant Support: This work was funded by grants from the Donald W. Reynolds Foundation; National Institutes of Health/National Center for Research Resources (USPHS GCRC grant M01-RR00633); National Heart, Lung, and Blood Institute (K-25 award HL-68736); American Diabetes Association (Innovative Methodologies Award #7-04-IN-21); Veterans Affairs Medical Center, Dallas, Texas; National Institute of Diabetes and Digestive and Kidney Diseases; and by a Target Obesity Postdoctoral Fellowship from the Heart and Stroke Foundation of Canada, the Canadian Institutes of Health Research, and the Canadian Diabetes Association.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Lidia Szczepaniak, PhD, Department of Internal Medicine, Division of Hypertension, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-8899; e-mail, Lidia.email@example.com.
Current Author Addresses: Drs. McGavock and Szczepaniak: University of Texas Southwestern Medical Center at Dallas, Department of Internal Medicine, Division of Hypertension, 5161 Harry Hines Boulevard, CS8.102, Dallas, TX 75390-8899.
Dr. Victor: University of Texas Southwestern Medical Center at Dallas, Department of Internal Medicine, Division of Hypertension, 5323 Harry Hines Boulevard, J4.134, Dallas, TX 75390-8586.
Dr. Unger: University of Texas Southwestern Medical Center at Dallas, Department of Internal Medicine, Touchstone Center for Diabetes, 5323 Harry Hines Boulevard, Y8.128, Dallas, TX 75390-8854.
Author Contributions: Conception and design: R.G. Victor, R.H. Unger, L.S. Szczepaniak.
Analysis and interpretation of the data: J.M. McGavock, L.S. Szczepaniak.
Drafting of the article: J.M. McGavock, L.S. Szczepaniak.
Critical revision of the article for important intellectual content: J.M. McGavock, R.G. Victor, R.H. Unger, L.S. Szczepaniak.
Final approval of the article: R.G. Victor, R.H. Unger, L.S. Szczepaniak.
Statistical expertise: J.M. McGavock.
Obtaining of funding: J.M. McGavock, R.G. Victor, R.H. Unger, L.S. Szczepaniak.
Collection and assembly of data: L.S. Szczepaniak.
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.
McGavock JM, Victor RG, Unger RH, et al. Adiposity of the Heart*, Revisited. Ann Intern Med. 2006;144:517–524. doi: https://doi.org/10.7326/0003-4819-144-7-200604040-00011
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Published: Ann Intern Med. 2006;144(7):517-524.
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