A progressive increase in cardiovascular risk assessed by coronary angiography in non-diabetic patients at sub-diabetic glucose levelsReport as inadecuate

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Cardiovascular Diabetology

, 10:56

First Online: 24 June 2011Received: 24 May 2011Accepted: 24 June 2011


ObjectiveDiabetes mellitus type 2 DM2 is a risk factor for coronary heart disease CHD. While there is a clear correlation of fasting blood glucose FBG and 2 h post-challenge blood glucose values 2h-BG with microvascular complications, the risk for CHD conferred by glucose dysregulation antecedent to DM2 is less clear. Therefore, we investigated associations of FBG and 2h-BG values with the prevalence of CHD assessed by coronary angiography as the most sensitive diagnostic tool.

Research Design and MethodsCoronary angiography was performed in 1394 patients without known DM. Capillary blood glucose was analyzed before and 2 h after an oral glucose tolerance test. Associations between FBG as well as 2h-BG levels and the risk for CHD were assessed by logistic regression analysis.

Results1064 75% of patients were diagnosed with CHD. 204 15% were diagnosed with so far unknown DM2, 274 20% with isolated impaired fasting glucose IFG, 188 13% with isolated impaired glucose tolerance IGT and 282 20% with both, IGT and IFG. We found a continuous increase in the risk for CHD with fasting and post-challenge blood glucose values even in the subdiabetic range. This correlation did however not suggest clear cut-off values. The increase in risk for CHD reached statistical significance at FBG levels of > 120 mg-dl Odds Ratio of 2.7 1.3-5.6 and 2h-BG levels > 140 mg-dl 141-160 mg-dl OR 1.8 1.1-2.9, which was however lost after adjusting for age, sex and BMI.

ConclusionsIn our study population we found a continuous increased risk for CHD at fasting and 2h-BG levels in the sub-diabetic glucose range, but no clear cut-off values for cardiovascular risk.

Keywordsimpaired glucose tolerance impaired fasting glucose diabetes mellitus oral glucose tolerance test cardiovascular disease Electronic supplementary materialThe online version of this article doi:10.1186-1475-2840-10-56 contains supplementary material, which is available to authorized users.

Sven Schinner, Reiner Füth, Kerstin Kempf contributed equally to this work.

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Author: Sven Schinner - Reiner Füth - Kerstin Kempf - Stephan Martin - Holger S Willenberg - Matthias Schott - Wilfried Dinh - We

Source: https://link.springer.com/article/10.1186/1475-2840-10-56

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