4.7 Article

Chronic Hyperglycemia and Subclinical Myocardial Injury

Journal

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 59, Issue 5, Pages 484-489

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2011.10.875

Keywords

diabetes mellitus; epidemiology; hyperglycemia

Funding

  1. National Heart, Lung, and Blood Institute (NHLBI) [N01-HC-55015, N01-HC-55022, 5T32HL007024]
  2. NIH/NIDDK [R21 DK080294, K01 DK076595, R01-DK-076770]
  3. Roche

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Objectives The purpose of this study was to examine the association between hyperglycemia and subclinical myocardial injury in persons without clinically evident coronary heart disease (CHD). Background Hyperglycemia is associated with an increased risk of cardiac events, but limited information is available on its relationship to subclinical myocardial damage. Elevated cardiac troponin T even below traditional detection levels can be detected by a novel high-sensitivity assay. Methods We examined the association between baseline glycated hemoglobin (HbA1c) and high-sensitivity cardiac troponin T (hs-cTnT) in 9,661 participants free of CHD and heart failure in the ARIC (Atherosclerosis Risk in Communities) study. Multivariable logistic regression models characterized the association between clinical categories of HbA1c (<5.7%, 5.7% to 6.4%, and >= 6.5%) and our primary outcome of elevated hs-cTnT (>= 14 ng/l). Results Higher baseline values of HbA1c were associated in a graded fashion with elevated hs-cTnT (p for trend < 0.001). After adjusting for traditional risk factors, compared to persons with HbA1c <5.7%, the odds ratios of elevated hs-cTnT for persons with HbA1c 5.7% to 6.4% and >= 6.5% were 1.26 (95% confidence interval: 1.01 to 1.56) and 1.97 (95% confidence interval: 1.44 to 2.70), respectively. Conclusions Higher HbA1c is associated with elevated hs-cTnT among persons without clinically evident CHD, suggesting that hyperglycemia contributes to myocardial injury beyond its effects on development of clinical atherosclerotic coronary disease. (J Am Coll Cardiol 2012; 59: 484-9) (C) 2012 by the American College of Cardiology Foundation

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