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  Vol. 165 No. 16, September 12, 2005 TABLE OF CONTENTS
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Glycemic Control and Coronary Heart Disease Risk in Persons With and Without Diabetes

The Atherosclerosis Risk in Communities Study

Elizabeth Selvin, PhD, MPH; Josef Coresh, MD, PhD; Sherita H. Golden, MD, MHS; Frederick L. Brancati, MD, MHS; Aaron R. Folsom, MD; Michael W. Steffes, MD, PhD

Arch Intern Med. 2005;165:1910-1916.

Background  Chronic hyperglycemia has been hypothesized to contribute to coronary heart disease (CHD), but the extent to which hemoglobin A1c (HbA1c) level, a marker of long-term glycemic control, is independently related to CHD risk is uncertain.

Methods  We conducted a prospective case-cohort study of 1321 adults without diabetes and a cohort study of 1626 adults with diabetes from the Atherosclerosis Risk in Communities Study. Using proportional hazards models, we assessed the relation between HbA1c level and incident CHD during 8 to 10 years of follow-up.

Results  In adults with diabetes, the relative risk (RR) of CHD was 2.37 (95% confidence interval [CI], 1.50-3.72) for the highest quintile of HbA1c level compared with the lowest after adjustment for CHD risk factors. In persons without diabetes, the adjusted RR of CHD in the highest quintile of HbA1c level was 1.41 (95% CI, 0.90-2.30); however, there was evidence of a nonlinear relationship in this group. In nondiabetic adults, HbA1c level was not related to CHD risk below a level of 4.6% but was significantly related to risk above that level (P<.001). In diabetic adults, the risk of CHD increased throughout the range of HbA1c levels. In the adjusted model, the RR of CHD for a 1–percentage point increase in HbA1c level was 2.36 (95% CI, 1.43-3.90) in persons without diabetes but with an HbA1c level greater than 4.6%. In diabetic adults, the RR was 1.14 (95% CI, 1.07-1.21) per 1–percentage point increase in HbA1c across the full range of HbA1c values.

Conclusion  Elevated HbA1c level is an independent risk factor for CHD in persons with and without diabetes.


Author Affiliations: Department of Epidemiology and Welch Center for Prevention, Epidemiology, and Clinical Research (Drs Selvin, Coresh, Golden, and Brancati), Johns Hopkins Bloomberg School of Public Health, Baltimore, Md; Johns Hopkins School of Medicine, Baltimore (Drs Coresh, Golden, and Brancati); and Division of Epidemiology and Community Health, School of Public Health (Dr Folsom) and Department of Laboratory Medicine and Pathology, Medical School (Dr Steffes), University of Minnesota, Minneapolis.



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