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Volume 20, Issue 1, Pages 15-21 (January 2010)


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Glycosylated hemoglobin and the risk of death and cardiovascular mortality in the elderly

M. ChoncholaCorresponding Author Informationemail address, R. Katzb, L.F. Friedcf, M.J. Sarnakd, D.S. Siscovicke, A.B. Newmanf, E.S. Strotmeyerf, A. Bertonig, M.G. Shlipakh

Received 8 October 2008; received in revised form 6 February 2009; accepted 17 February 2009. published online 13 April 2009.

Abstract 

Background and aims

Glycosylated hemoglobin (HbA1c) has been associated with incident cardiovascular disease (CVD), but the findings are inconsistent. We tested the hypothesis that HbA1c may be associated with an increased risk of death and cardiovascular mortality in older adults.

Methods and results

We evaluated the association between HbA1c with all-cause and cardiovascular mortality in 810 participants without a history of diabetes in a sub-study of the Cardiovascular Health Study (CHS), a community cohort study of individuals ≥65years of age. Glycosylated hemoglobin was measured at baseline and all-cause and cardiovascular mortality was assessed during the follow-up period. The relation between baseline HbA1c and death was evaluated with multivariate Cox proportional hazards regression models. After a median follow-up of 14.2years, 416 deaths were observed. The crude incidence rates of all-cause mortality across HbA1c groups were: 4.4% per year, 4.3% per year and 4.6% per year for tertile 1 (≤5.6%), tertile 2 (5.61–6.20%) and tertile 3 (≥6.21%), respectively. In unadjusted and fully adjusted analyses, baseline HbA1c was not associated with all-cause mortality and cardiovascular mortality (hazard ratio: 1.16 [95% confidence interval 0.91–1.47] and hazard ratio: 1.31 [95% confidence interval 0.90–1.93], respectively for the highest HbA1c tertile compared with the lowest).

Conclusion

These results suggest that HbA1c does not significantly predict all-cause and cardiovascular mortality in non-diabetic community-dwelling older adults.

a University of Colorado Health Sciences Center, Division of Renal Diseases and Hypertension, Box C-280, Denver, CO 80262, USA

b Collaborative Health Studies Coordinating Center, University of Washington, Seattle, WA, USA

c Veterans Affairs Pittsburgh Healthcare System, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA

d Department of Medicine, Tufts Medical Center, Boston, MA, USA

e University of Washington, Departments of Medicine and Epidemiology, Cardiovascular Health Research Unit, Seattle, WA, USA

f University of Pittsburgh Graduate School of Public Health, Department of Epidemiology, Pittsburgh, PA, USA

g Division of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, USA

h University of California San Francisco, General Internal Medicine Section, Veterans Affairs Medical Center, University of California, San Francisco, CA, USA

Corresponding Author InformationCorresponding author. Tel.: +1 303 399 6997; fax: +1 303 399 3131.

PII: S0939-4753(09)00041-6

doi:10.1016/j.numecd.2009.02.007


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