Hyperglycemia and QT interval: time for re-evaluation.
Among the many mechanisms proposed to explain the relationship between glucose levels and subsequent cardiovascular events, a prolonged QT interval, ie the time interval between the start of activation of the ventricle and completion of its repolarization, seems noteworthy. In Type 2 diabetic patients, for example, the prevalence of QTc (corrected QT interval) prolongation is as high as 26% and is associated with heart disease. The mechanism by which hyperglycemia may produce ventricular instability, as manifested in QTc prolongation, may be increased sympathetic activity, increased cytosolic calcium content in myocytes, or both. By raising the production of free radicals, high glucose may reduce nitric oxide (NO) availability to target cells inducing a state of increased vasomotor tone and ventricular instability. Reduction of Na+/K+-ATPase activity, inhibition of Ca2+-ATPase activity, depressed Na+/Ca2+ exchanger activity, and activation of Na+/H+ antiport may all be implicated. Further studies are urgently needed to characterize in full the effect of hyperglycemia on vascular cells, in order to find therapeutic approaches that lessen the burden of cardiovascular morbidity and mortality in human diabetes.
Marfella
R
R
Rossi
F
F
Giugliano
D
D
D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000503:physiopathology*; D004562:Electrocardiography; D006331:Heart Diseases / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000503:physiopathology*; D008133:Long QT Syndrome / Q000453:epidemiology / Q000209:etiology*; D015995:Prevalence; D012307:Risk Factors