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(Hypertension. 2009;54:1209.)
© 2009 American Heart Association, Inc.
Editorial Commentaries |
From the Division of Cardiology (W.C.S.), Department of Medicine, University of Maryland School of Medicine, Baltimore, Md; Pauley Heart Center (K.B.S.), Medical College of Virginia Hospitals, Virginia Commonwealth University, Richmond, Va; Department of Physiological Sciences (M.F.S.), Stellenbosch University, Stellenbosch, South Africa.
Correspondence to William C. Stanley, Division of Cardiology, Department of Medicine, University of Maryland-Baltimore, 20 Penn St, HSF2, Room S022, Baltimore, MD 21201. E-mail wstanley@medicine.umaryland.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Experimental and clinic studies show that chronic hypertension leads to myocardial pathology and systolic and diastolic dysfunctions that frequently progress to heart failure.1 Elevated afterload causes cardiomyocyte hypertrophy, which alters myocardial energy metabolism by increasing glucose metabolism and impairing mitochondrial oxidative capacity, increasing the production of reactive oxygen species and oxidative damage, and triggering remodeling of the myocardial extracellular matrix and the left ventricle (see Figure).2 Obesity is also a strong risk factor for both hypertension and heart failure and has been increasing at epidemic proportions worldwide.3,4 The increase in obesity in Western societies over the last century is associated with greater consumption of highly processed carbohydrates (eg, sugar, white flour, and white potatoes) and saturated fats.5 At present, there is little information regarding the effects of dietary fat and carbohydrate composition on cardiac function and the development of heart failure in hypertension.
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In the present issue of Hypertension, Majane et al6 present the novel finding that consuming a diet that is high in sugar and saturated fat results in relative modest obesity (
10% increase in body mass) compared with a sugar-free, low-fat diet but greatly accelerates left ventricular dysfunction in a rat model of essential hypertension. Importantly, this effect occurred in the
Related Article:
Hypertension 2009 54: 1376-1383.
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