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The impact of dyslipidaemia on cardiovascular mortality in individuals without a prior history of diabetes in the DECODE Study
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2009 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 206, no 1, 298-302 p.Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: To evaluate the impact of dyslipidaemia on cardiovascular disease (CVD) mortality in relation to fasting (FPG) and 2-h (2hPG) plasma glucose levels in individuals without a prior history of diabetes. METHODS: Data from 14 European population-based prospective studies of 9132 men and 8631 women aged 25-89 years were jointly analysed. A total of 871 CVD deaths occurred during the average 10 years of follow-up. Subjects were classified into normoglycaemia, isolated fasting hyperglycaemia (IFH, FPG>/=6.10mmol/l and 2hPG<7.80mmol/l), isolated post-load hyperglycaemia (IPH, FPG<6.10mmol/l and 2hPG>/=7.80mmol/l) and combined fasting and post-load hyperglycaemia (CH, FPG>/=6.10mmol/l and 2hPG>/=7.80mmol/l). Multivariate-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for CVD mortality were estimated using Cox proportional hazard analysis. RESULTS: Multivariate-adjusted HRs (95% CIs) for high-density lipoprotein cholesterol (HDL-C) were 0.84 (0.75-0.94), 0.66 (0.48-0.92), 1.03 (0.84-1.27) and 0.67 (0.51-0.89) in individuals with normoglycaemia, IFH, IPH and CH, respectively. For total cholesterol (TC) to HDL-C ratio they were 1.14 (1.03-1.27), 1.44 (1.13-1.84), 0.94 (0.77-1.15) and 1.26 (1.05-1.50), respectively. HRs for TC and triglycerides (TG) were not significant in most of the glucose categories except for TG in those with CH [HR 1.12 (1.00-1.27)]. CONCLUSIONS: Low HDL-C and high TC/HDL-C increase CVD mortality in either diabetic or non-diabetic individuals defined based on the fasting glucose criteria, but not the 2-h criteria. TG is a significant CVD risk predictor only in the presence of combined hyperglycaemia or diabetes. The difference between fasting and post-load hyperglycaemia with regard to the lipid-CVD relation may suggest a different pathophysiology underlying these two prediabetic states.

Place, publisher, year, edition, pages
2009. Vol. 206, no 1, 298-302 p.
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Medical and Health Sciences
URN: urn:nbn:se:uu:diva-102725DOI: 10.1016/j.atherosclerosis.2008.12.043ISI: 000270002000048PubMedID: 19303072OAI: oai:DiVA.org:uu-102725DiVA: diva2:216650
Group Author: DECODE Study Group Available from: 2009-05-11 Created: 2009-05-11 Last updated: 2010-10-18Bibliographically approved

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