BACKGROUND: The QT interval reflects the duration of the intracellular action potential. Little is known on the interval QT duration in non diabetic insulin-resistant subjects. OBJECTIVE: The aims of the current study were to evaluate the QTc interval in three groups of non diabetic insulin-resistant subjects and the possible correlation between QTc and the autonomic nervous system's activity. DESIGN:90 subjects were divided in subjects with impaired fasting glycaemia (IFG) and, by the results of OGTT, according to the criteria of ADA, in subjects with normal glucose regulation (NGR) and impaired glucose tolerance (IGT). Insulin resistance was evaluated by the homeostasis model assessment-index (HOMA-I). Heart rate variability and Qtc were calculated. RESULTS:QTc interval is correlated with SDNN, LF n.u. and LF/HF. CONCLUSION: We have observed that the QTc interval is prolonged in insulin-resistant subjects with associated impaired glucose metabolism, while no difference was reported between insulin-resistant and non insulin-resistant subjects with normal glucose regulation. We hypothesize that hyperglycaemia could play a major role than hyperinsulinemia on the QTc prolongation. 2009 Elsevier B.V. All rights reserved.
RCT Entities:
BACKGROUND: The QT interval reflects the duration of the intracellular action potential. Little is known on the interval QT duration in non diabetic insulin-resistant subjects. OBJECTIVE: The aims of the current study were to evaluate the QTc interval in three groups of non diabetic insulin-resistant subjects and the possible correlation between QTc and the autonomic nervous system's activity. DESIGN: 90 subjects were divided in subjects with impaired fasting glycaemia (IFG) and, by the results of OGTT, according to the criteria of ADA, in subjects with normal glucose regulation (NGR) and impaired glucose tolerance (IGT). Insulin resistance was evaluated by the homeostasis model assessment-index (HOMA-I). Heart rate variability and Qtc were calculated. RESULTS:QTc interval is correlated with SDNN, LF n.u. and LF/HF. CONCLUSION: We have observed that the QTc interval is prolonged in insulin-resistant subjects with associated impaired glucose metabolism, while no difference was reported between insulin-resistant and non insulin-resistant subjects with normal glucose regulation. We hypothesize that hyperglycaemia could play a major role than hyperinsulinemia on the QTc prolongation. 2009 Elsevier B.V. All rights reserved.
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