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Volume 86, Issue 1, Pages 67-73 (October 2009)


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Association of glucose measures with total and coronary heart disease mortality: Does the effect change with time? The Rancho Bernardo Study

Beth E. CohenabCorresponding Author Informationemail address, Elizabeth Barrett-Connorc, Christina L. Wasselc, Alka M. Kanayabd

Received 22 January 2009; received in revised form 25 June 2009; accepted 14 July 2009. published online 11 August 2009.

Abstract 

Aims

To compare the associations of three glucose measures with coronary heart disease (CHD) and total mortality and to examine how these associations changed over time.

Methods

Prospective study of 1774 adults (median age 68 years, 56% female). Fasting plasma glucose (FPG), 2h post-challenge glucose (2hPG), and glycohemoglobin (GHb) were obtained in 1984–1987. Mortality data was obtained for all participants. Multivariable Cox models examined the association of baseline glucose measures with mortality during sequential periods of follow-up (0–6, 7–12, and 13–18 years), adjusting for age, sex, blood pressure, LDL-cholesterol, smoking, exercise, and aspirin use.

Results

854 (48%) participants died during follow-up. In adjusted models, only GHb was associated with total mortality over the entire 18 years (p=0.007). In analyses of mortality in successive six year time intervals, the association of GHb and total mortality was only significant in years 0–6. For each 1% increase in GHb, the hazard ratio for death in years 0–6 was 1.14 (95% CI 1.01–1.30, p=0.04) and the hazard ratio for CHD death was 1.26 (95% CI 1.03–1.55, p=0.02). Stratification by sex and exclusion of participants with diabetes did not change our results.

Conclusions

Higher levels of GHb were associated with increased total and CHD mortality within the first six years independent of cardiac risk factors. Though further research is needed, this supports the hypothesis that early glycemic control may affect mortality outcomes.

a General Internal Medicine Section, Department of Veterans Affairs Medical Center, San Francisco, United States

b Department of Medicine, University of California, San Francisco, United States

c Department of Family and Preventive Medicine, Division of Epidemiology, University of California, San Diego, United States

d Division of General Internal Medicine, University of California, San Francisco, United States

Corresponding Author InformationCorresponding author at: VA Medical Center, General Internal Medicine Section (111A1), 4150 Clement Street; San Francisco, CA 94121-1598. Tel.: +1 415 221 4810x4851; fax: +1 415 379 5573.

PII: S0168-8227(09)00308-8

doi:10.1016/j.diabres.2009.07.006


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