Abstract
Obesity is becoming a worldwide phenomenon. Myocardial changes associated with the obese state are increasingly recognized, independent of hypertension, obstructive sleep apnea and coronary artery disease. The existence of a cardiomyopathy of obesity is supported by a range of evidence: epidemiologic study findings, which have shown an association between obesity and heart failure; clinical studies that have confirmed the association of adiposity with left ventricular dysfunction, independent of hypertension, coronary artery disease and other heart disease; and experimental evidence of structural and functional changes in the myocardium in response to increased adiposity. The most important mechanisms in the development of obesity cardiomyopathy are metabolic disturbances (insulin resistance, increased free fatty acid levels, and also increased levels of adipokines), activation of the renin–angiotensin–aldosterone and sympathetic nervous systems, myocardial remodeling, and small-vessel disease (both microangiopathy and endothelial dysfunction). In the first part of this two-part Review, we seek to evaluate the emerging evidence for the existence of a cardiomyopathy of obesity and clarify the responsible mechanisms.
Key Points
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The existence of a cardiomyopathy of obesity is increasingly recognized and supported by many experimental models and epidemiological and clinical studies
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These myocardial changes cannot be ascribed to hypertension, diabetes, obstructive sleep apnea or coronary artery disease
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Obesity cardiomyopathy involves both left and right ventricular structure, and systolic and diastolic function
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Metabolic factors (insulin resistance, lipotoxicity, increased free fatty acids, and adipokines), renin–angiotensin–aldosterone and sympathetic nervous systems, myocardial remodeling and small vessel disease can all contribute
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Acknowledgements
The authors gratefully acknowledge the support of the National Health and Medical Research Council, Canberra, Australia (Centers of Clinical Research Excellence Award and postgraduate research scholarship).
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C Wong declared he has no competing interests.
TH Marwick receives grant support from GE Healthcare and Philips Medical Systems, but unrelated to this topic.
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Wong, C., Marwick, T. Obesity cardiomyopathy: pathogenesis and pathophysiology. Nat Rev Cardiol 4, 436–443 (2007). https://doi.org/10.1038/ncpcardio0943
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DOI: https://doi.org/10.1038/ncpcardio0943
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