Similarity of the Impact of Type 1 and Type 2 Diabetes on Cardiovascular Mortality in Middle-Aged Subjects
- Auni Juutilainen, MD12,
- Seppo Lehto, MD12,
- Tapani Rönnemaa, MD34,
- Kalevi Pyörälä, MD2 and
- Markku Laakso, MD12
- 1Kuopio University Hospital, Kuopio, Finland
- 2Department of Medicine, University of Kuopio, Kuopio, Finland
- 3Turku University Central Hospital, Turku, Finland
- 4Department of Medicine, University of Turku, Turku, Finland
- Address correspondence and reprint requests to Markku Laakso, Academy Professor, University of Kuopio and Kuopio University Hospital, 70210 Kuopio, Finland. E-mail: markku.laakso{at}kuh.fi
Abstract
OBJECTIVE—To compare the risk of cardiovascular disease (CVD) death and the impact of hyperglycemia on the risk of CVD mortality associated with type 1 diabetes to that associated with type 2 diabetes.
RESEARCH DESIGN AND METHODS—The study comprised 173 participants with type 1 diabetes, 834 participants with type 2 diabetes, and 1,294 nondiabetic participants, aged 45–64 years at baseline and free of CVD. The age of onset of diabetes was >30 years in both diabetic groups.
RESULTS—During an 18-year follow-up, 86 participants with type 1 diabetes, 567 participants with type 2 diabetes, and 252 nondiabetic participants died. CVD mortality rates per 1,000 person-years were 23.1 (95% CI 16.9–31.9) in type 1 diabetic, 35.3 (30.8–40.4) in type 2 diabetic, and 4.6 (3.8–5.7) in nondiabetic participants. Adjusted hazard ratios for CVD mortality in participants with type 1 diabetes versus no diabetes was 3.6 (95% CI 2.2–5.7) in men and 13.3 (6.9–22.5) in women and in participants with type 2 diabetes versus no diabetes 3.3 (2.5–4.5) in men and 10.1 (6.7–17.4) in women. An increment of 1 unit (%) of GHb increased CVD mortality by 52.5% (95% CI 28.4–81.3) in type 1 diabetic subjects and by 7.5% (4.3–10.8) in type 2 diabetic participants.
CONCLUSIONS—The impact of type 1 and type 2 diabetes on CVD mortality was similar. The effect of increasing hyperglycemia on the risk of CVD mortality was more profound in type 1 than in type 2 diabetic subjects.
Footnotes
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Published ahead of print at http://care.diabetesjournals.org on 14 December 2007. DOI: 10.2337/dc07-2124.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C Section 1734 solely to indicate this fact.
See accompanying editorial, p. 830.
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- Accepted December 8, 2007.
- Received November 4, 2007.
- DIABETES CARE
