Impact of glucose intolerance on coronary calcified lesions evaluated using multislice computed tomography

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Abstract

Metabolic syndrome has the unique concept that the common occurrence of individual disease components increases the risk of coronary artery disease (CAD). However, some studies suggest that the burden of different CAD risk factors is not equal, and focusing on the whole set of risk factors might neglect the impact of individual factors that could be useful targets for prophylactic therapies. The purpose of this study was to investigate the effect of glucose intolerance on CAD using multislice computed tomography (MSCT). Ninety-eight consecutive patients with at least one traditional CAD risk factor who visited a municipal hospital were enrolled in this study. The risk factors were impaired glucose tolerance (fasting glucose ≧ 110 mg/dl or patients with diabetes), low high-density lipoprotein cholesterol (HDL-C, < 40 mg/dl for men and ↽ 50 mg/dl for women), hypertriglycemia (triglyceride ≧ 150 mg/dl), hypertension (blood pressure ≧ 130/85 mmHg), and obesity (body mass index, > 25 kg/m2 for men and > 23 kg/m2 for women). CAD was determined by the presence of either stenoses, non-calcified plaques or calcified lesions. The following risk factors were significantly related in univariate logistic models: glucose intolerance and coronary calcified lesions (p = 0.001), and hypertriglycemia and non-calcified plaque lesions (p = 0.048). Multivariate models showed that glucose intolerance was significantly associated with calcified lesions, even after adjustment for gender, age, low HDL-C, hypertriglycemia, hypertension, and obesity (p = 0.018). Our results suggest that glucose intolerance might be closely related to the presence of coronary calcified lesions among traditional CAD risk factors. © 2007 Tohoku University Medical Press.

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Nomura, K., Yamanouchi, T., Kim, G. U., Ohwaki, K., & Yano, E. (2007). Impact of glucose intolerance on coronary calcified lesions evaluated using multislice computed tomography. Tohoku Journal of Experimental Medicine, 212(2), 107–113. https://doi.org/10.1620/tjem.212.107

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