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J Am Coll Cardiol, 2004; 43:315, doi:10.1016/j.jacc.2003.11.003
© 2004 by the American College of Cardiology Foundation
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SPECIAL SECTION: LETTER TO THE EDITOR

Heart disease in diabetes—resist the beginnings

Heinrich Taegtmeyer, MD, DPhil, FACCa and Peter Razeghi, MDa

a The University of Texas Houston Medical School, Department of Internal Medicine, Division of Cardiology, 6431 Fannin, MSB 1.246, Houston, TX 77030, USA

Heinrich.Taegtmeyer{at}uth.tmc.edu

The study by Fang et al. (1), together with the accompanying editorial by Picano (2), draws attention to early functional changes of the heart in diabetes. It is tempting to take the story one step further: to consider the consequences of changes in energy substrate supply to the heart. Diabetes is as much a disorder of dysregulated fatty acid metabolism as it is a disorder of dysregulated glucose metabolism (3), and, in the blood of diabetic patients, fatty acid levels are elevated along with glucose levels. We have found substantial changes in the metabolic gene expression profile of hearts from diabetic animals before the onset of functional abnormalities (4,5). This is one end of the spectrum. At the other end of the spectrum, the transcriptional profile of diabetic patients with heart failure reveals a severe downregulation of the myocyte enhancer factor-2 (MEF2C) and its target genes (6) contributing to more severe contractile dysfunction. We proposed that metabolic remodeling in diabetes precedes, causes, and sustains the functional and structural remodeling of the heart (7,8). Consequently, early detection and correction of the metabolic abnormalities should also prevent the heart's functional decline later on. When used early enough, new pharmacological agents directed at metabolic targets may prevent a significant amount of cardiovascular disease (9). The Romans used to have a term for this: Principiis obsta—"Resist the beginnings."


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 References
 

  1. Fang ZY, Najos-Valencia O, Leano R, Marwick TH. Patients with early diabetic heart disease demonstrate a normal myocardial response to dobutamine. J Am Coll Cardiol. 2003;42:446–453[Abstract/Free Full Text]
  2. Picano E. Diabetic cardiomyopathy: the importance of being earliest. J Am Coll Cardiol. 2003;42:454–457[Free Full Text]
  3. McGarry JD. What if Minkowski had been ageusic? An alternative angle on diabetes. Science. 1992;258:766–770[Abstract/Free Full Text]
  4. Depre C, Young ME, Ying J, et al. Streptozocin-induced changes in cardiac gene expression in the absence of severe contractile dysfunction. J Mol Cell Cardiol. 2000;32:985–996[CrossRef][Medline]
  5. Young ME, Wilson CR, Razeghi P, Guthrie P, Taegtmeyer H. Alterations of the circadian clock in the heart by streptozocin-induced diabetes. J Mol Cell Cardiol. 2002;34:223–231[CrossRef][Medline]
  6. Razeghi P, Young ME, Cockrill TC, Frazier OH, Taegtmeyer H. Downregulation of myocardial myocyte enhancer factor 2C and myocyte enhancer factor 2C regulated gene expression in diabetic patients with non-ischemic heart failure. Circulation. 2002;106:407–411[Abstract/Free Full Text]
  7. Taegtmeyer H, McNulty P, Young ME. Adaptation and maladaptation of the heart in diabetes: part I: general concepts. Circulation. 2002;105:1727–1733[Free Full Text]
  8. Young ME, McNulty P, Taegtmeyer H. Adaptation and maladaptation of the heart in diabetes: part II: potential mechanisms. Circulation. 2002;105:1861–1870[Free Full Text]
  9. Russell JC. Reduction and prevention of the cardiovascular sequelae of the insulin resistance syndrome. Curr Drug Targets Cardiovasc Haematol Disord. 2001;1:107–120[CrossRef][Medline]



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