E Lukich1, Z Matas, M Boaz, M Shargorodsky. 1. Department of Medicine, Wolfson Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Abstract
AIM: Glucose intolerance produces structural and functional changes in the arterial wall. The present study investigated association between glucose tolerance status and arterial stiffness in subjects with normal and impaired glucose regulation (IGR). METHODS: The study group consisted of 284 subjects, including 111 subjects with normal fasting glucose (NFG), 61 subjects classed as impaired fasting glucose (IFG) according of the new fasting blood glucose (FBG) cut-off point of 100 mg/dL and 112 patients with diabetes mellitus (DM). All patients were evaluated for glucose, HbA1C, insulin, lipids, C-reactive protein (CRP) and homeostasis model assessment-insulin resistance. Pulse wave velocity (PWV) and augmentation index (AI) were performed as a noninvasive recording of the two artery sites pressure waveform using SphygmoCor (version 7.1, AtCor Medical, Sydney, Australia). RESULTS: Pulse wave velocity, augmentation index and central arterial pressure increased consistently with deterioration of glucose tolerance. PWV was significantly higher in subjects with diabetes than in the normal and IFG groups (p < 0.0001 and p = 0.007, respectively). IFG subjects had marginally higher PWV than normal subjects (p = 0.050). Compared to normal subjects, IFG and diabetes groups were associated with increased AI (p = 0.003 and p < 0.0001, respectively). Arterial stiffness parameters remained significantly higher in both IFG and diabetes groups compared to normal after adjustment for cardiovascular risk factors and concomitant medications. Positive correlations between FBG, HbA1C and arterial stiffness parameters were detected. CONCLUSIONS: Arterial stiffness parameters varied significantly across subgroups of patients with different degrees of impaired glucose regulation, such that increasingly deranged glucose homeostasis was associated with increased arterial stiffness. Early adverse vascular changes were detected in subjects with IFG. Copyright (c) 2010 John Wiley & Sons, Ltd.
AIM: Glucose intolerance produces structural and functional changes in the arterial wall. The present study investigated association between glucose tolerance status and arterial stiffness in subjects with normal and impaired glucose regulation (IGR). METHODS: The study group consisted of 284 subjects, including 111 subjects with normal fasting glucose (NFG), 61 subjects classed as impaired fasting glucose (IFG) according of the new fasting blood glucose (FBG) cut-off point of 100 mg/dL and 112 patients with diabetes mellitus (DM). All patients were evaluated for glucose, HbA1C, insulin, lipids, C-reactive protein (CRP) and homeostasis model assessment-insulin resistance. Pulse wave velocity (PWV) and augmentation index (AI) were performed as a noninvasive recording of the two artery sites pressure waveform using SphygmoCor (version 7.1, AtCor Medical, Sydney, Australia). RESULTS: Pulse wave velocity, augmentation index and central arterial pressure increased consistently with deterioration of glucose tolerance. PWV was significantly higher in subjects with diabetes than in the normal and IFG groups (p < 0.0001 and p = 0.007, respectively). IFG subjects had marginally higher PWV than normal subjects (p = 0.050). Compared to normal subjects, IFG and diabetes groups were associated with increased AI (p = 0.003 and p < 0.0001, respectively). Arterial stiffness parameters remained significantly higher in both IFG and diabetes groups compared to normal after adjustment for cardiovascular risk factors and concomitant medications. Positive correlations between FBG, HbA1C and arterial stiffness parameters were detected. CONCLUSIONS: Arterial stiffness parameters varied significantly across subgroups of patients with different degrees of impaired glucose regulation, such that increasingly deranged glucose homeostasis was associated with increased arterial stiffness. Early adverse vascular changes were detected in subjects with IFG. Copyright (c) 2010 John Wiley & Sons, Ltd.
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