Improvement of Repolarization Abnormalities by a K+ Channel Opener in the LQT1 Form of Congenital Long-QT Syndrome

摘要: Background —This study used monophasic action potential (MAP) to examine the effect of nicorandil, a K + channel opener, on repolarization abnormalities induced by epinephrine in LQT1 form congenital long-QT syndrome which KvLQT1 mutation underlies defect responsible for slowly activating component delayed rectifier potassium current. Methods and Results —MAPs were recorded simultaneously from two or three sites right ventricular left endocardium 6 patients with (17 sites) 8 control (24 sites). In patients, infusion prolonged QT interval 90% MAP duration (MAPD 90 ) increased dispersion MAPD . Epinephrine also early afterdepolarizations (EADs) as well premature complexes (VPCs) 2 patients. Nicorandil during abbreviated , decreased abolished EADs VPCs 1 patient. Addition propranolol completely reversed prolonging increasing eliminated another that additional nicorandil parameters much less than Conclusions —Our results suggest improves defect.