Correction: The Relative Contribution of Metabolic and Structural Abnormalities to Diastolic Dysfunction in Obesity.

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The relative contribution of metabolic and structural abnormalities to diastolic dysfunction in obesity.

BACKGROUND: Obesity causes diastolic dysfunction, and is one of the leading causes of heart failure with preserved ejection fraction. Myocardial relaxation is determined by both active metabolic processes such as impaired energetic status and steatosis, as well as intrinsic myocardial remodelling. However, the relative contribution of each to diastolic dysfunction in obesity is currently unknown. METHODS: Eighty adult subjects (48 male) with no cardiovascular risk factors across a wide range of body mass indices (18.4-53.0 kg m-2) underwent magnetic resonance imaging for abdominal visceral fat, left ventricular geometry (LV mass:volume ratio) and diastolic function (peak diastolic strain rate), and magnetic resonance spectroscopy for PCr/ATP and myocardial triglyceride content. RESULTS: Increasing visceral obesity was related to diastolic dysfunction (peak diastolic strain rate, r=-0.46, P=0.001). Myocardial triglyceride content (ß=-0.2, P=0.008), PCr/ATP (ß=-0.22, P=0.04) and LV mass:volume ratio (ß=-0.61, P=0.04) all independently predicted peak diastolic strain rate (model R2 0.36, P<0.001). Moderated multiple regression confirmed the full mediating roles of PCr/ATP, myocardial triglyceride content and LV mass:volume ratio in the relationship between visceral fat and peak diastolic strain rate. Of the negative effect of visceral fat on diastolic function, 40% was explained by increased myocardial triglycerides, 39% by reduced PCr/ATP and 21% by LV concentric remodelling. CONCLUSIONS: Myocardial energetics and steatosis are more important in determining LV diastolic function than concentric hypertrophy, accounting for more of the negative effect of obesity on diastolic function than LV geometric remodelling. Targeting these metabolic processes is an attractive strategy to treat diastolic dysfunction in obesity.

The paradox of obesity cardiomyopathy and the potential for weight loss as a therapy.

Obesity is an independent risk factor for developing heart failure and the combination of the two disease states will prove to be a significant health burden over the coming years. Obesity is likely to contribute to the development of heart failure through a variety of mechanisms, including structural and functional changes, lipotoxicity and steatosis and altered substrate selection. However, once heart failure has developed, it seems that obesity confers a beneficial influence on prognosis in what has been termed the 'obesity paradox'. This may be a statistical phenomenon, but it should be considered that there is truly a protective state in the physiology of obesity. There is little evidence regarding the impact of weight loss in obese heart failure and whether or not this is beneficial. There have been small studies regarding the cardiovascular effects of both dietary weight loss and bariatric surgery, but few in heart failure. This is an important and increasingly relevant clinical question which must be addressed.