Type 2 diabetes mellitus substantially increases the lifetime risk of both developing and dying from heart failure. While this appears to be explained in part by the well-known association of diabetes with hypertension, dyslipidemia, and coronary atherosclerosis, additional pathophysiologic mechanisms linking type 2 diabetes and heart failure have recently been suggested. These include the potentially adverse effects of hyperglycemia on endothelial function and redox state, effects of excess circulating glucose and fatty acids on cardiomyocyte ultrastructure, intracellular signaling and gene expression, and the possibility that diabetes may impair recruitment of the myocardial insulin-responsive glucose transport system in response to ischemia. Because many of these putative pathophysiologic mechanisms should be amenable to normalization of the diabetic metabolic milieu, strategies designed to more carefully control circulating levels of glucose and fatty acids might conceivably delay or prevent the development of heart failure.
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http://dx.doi.org/10.1111/j.1527-5299.2002.00901.x | DOI Listing |
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