کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474947 | 1550437 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mechanisms underlying the development of the electrocardiographic and arrhythmic manifestations of early repolarization syndrome
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کلمات کلیدی
BRSJ wave syndromeTransmural dispersion of repolarizationKATPTDRERSEDRICAEarly repolarization - repolarization در اوایلVT/VF - VT / VFACh - آهAcetylcholine - استیل کولینElectrophysiology - الکتروفیزیولوژیITO - اینright ventricle - بطن راستleft ventricle - بطن چپventricular tachycardia/ventricular fibrillation - تاکیکاردی بطنی / فیبریلاسیون بطنیParasympathetic tone - تن پارازیمپاتیکTransient outward current - جریان مداوم بیرونTransient outward potassium current - جریان پتاسیم بیرون گذراBrugada syndrome - سندرم بروگاداEarly repolarization syndrome - سندرم رپولاریزاسیون اولیهVentricular fibrillation - فیبریلاسیون بطنیIdiopathic ventricular fibrillation - فیبریلاسیون بطنی ایدیوپاتیکIVF - لقاح مصنوعی action potential - پتانسیل عمل ATP-sensitive potassium channel - کانال پتاسیم حساس به ATP
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Early repolarization pattern in the ECG has been associated with increased risk for ventricular tachycardia/fibrillation (VT/VF), particularly when manifest in inferior leads. This study examines the mechanisms underlying VT/VF in early repolarization syndrome (ERS). Transmembrane action potentials (APs) were simultaneously recorded from 2 epicardial sites and 1 endocardial site of coronary-perfused canine left-ventricular (LV) wedge preparations, together with a pseudo-ECG. Transient outward current (Ito) was recorded from epicardial myocytes isolated from the inferior and lateral LV of the same heart. J wave area (pseudo-ECG), epicardial AP notch magnitude and index were larger in inferior vs. lateral wall preparations at baseline and after exposure to provocative agents (NS5806 + verapamil + acetylcholine (ACh)). Ito density was greater in myocytes from inferior vs. lateral wall (18.4 ± 2.3pA/pF vs. 11.6 ± 2.0pA/pF; p < 0.05). A combination of NS5806 (7 μM) and verapamil (3 μM) or pinacidil (4 μM), used to pharmacologically model the genetic defects responsible for ERS, resulted in prominent J-point and ST-segment elevation. ACh (3 μM), simulating increased vagal tone, precipitated phase-2-reentry-induced polymorphic VT/VF. Using identical protocols, inducibility of arrhythmias was 3-fold higher in inferior vs. lateral wedges. Quinidine (10 μM) or isoproterenol (1 μM) restored homogeneity and suppressed VT/VF. Our data support the hypothesis that 1) ERS is caused by a preferential accentuation of the AP notch in the LV epicardium; 2) this repolarization defect is accentuated by elevated vagal tone; 3) higher intrinsic levels of Ito account for the greater sensitivity of the inferior LV wall to development of VT/VF; and 4) quinidine and isoproterenol exert ameliorative effects by reversing the repolarization abnormality.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 68, March 2014, Pages 20-28
Journal: Journal of Molecular and Cellular Cardiology - Volume 68, March 2014, Pages 20-28
نویسندگان
István Koncz, Zsolt Gurabi, Bence Patocskai, Brian K. Panama, Tamás Szél, Dan Hu, Hector Barajas-MartÃnez, Charles Antzelevitch,