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Titolo:
Hyperglycemia and QT interval: Time for re-evaluation
Autore:
Marfella, R; Rossi, F; Giugliano, D;
Indirizzi:
Univ Naples 2, Dept Geriatr & Metab Dis, Naples, Italy Univ Naples 2 Naples Italy s 2, Dept Geriatr & Metab Dis, Naples, Italy Univ Naples 2, Dept Expt Med, Naples, Italy Univ Naples 2 Naples ItalyUniv Naples 2, Dept Expt Med, Naples, Italy
Titolo Testata:
DIABETES NUTRITION & METABOLISM
fascicolo: 2, volume: 14, anno: 2001,
pagine: 63 - 65
SICI:
0394-3402(200104)14:2<63:HAQITF>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORONARY HEART-DISEASE; DIABETIC-PATIENTS; NITRIC-OXIDE; CARDIOVASCULAR MORTALITY; MYOCARDIAL-INFARCTION; AUTONOMIC NEUROPATHY; SMOOTH-MUSCLE; RISK FACTOR; GLUCOSE; PROLONGATION;
Keywords:
QT interval; diabetes; hyperglycemia;
Tipo documento:
Editorial Material
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Giugliano, D Via Emilia 1, I-80021 Afragola, NA, Italy Via Emilia 1 Afragola NA Italy I-80021 1 Afragola, NA, Italy
Citazione:
R. Marfella et al., "Hyperglycemia and QT interval: Time for re-evaluation", DIABET NUTR, 14(2), 2001, pp. 63-65

Abstract

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 cytosoliccalcium 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. (C) 2001, Editrice Kurtis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 03:20:38