Apamin-Sensitive Potassium Current Modulates Action Potential Duration Restitution and Arrhythmogenesis of Failing Rabbit Ventricles

• DOI: 10.1161/circep.111.000152
• Publication Date: 2013-02-19T13:39:29Z
• Authors: Yu-Cheng Hsieh; Po-Cheng Chang; Chia-Hsiang Hsueh; Young Soo Lee; Changyu Shen; James N. Weiss; Zhenhui Chen; Tomohiko Ai; Shien-Fong Lin; Peng-Sheng Chen
• Keywords: Apamin

Background— Apamin-sensitive K currents ( I KAS ) are upregulated in heart failure. We hypothesize that apamin can flatten action potential duration restitution (APDR) curve and reduce ventricular fibrillation failing ventricles. Methods Results— simultaneously mapped membrane intracellular Ca (Ca i 7 rabbit hearts with pacing-induced failure normal hearts. A dynamic pacing protocol was used to determine APDR at baseline after (100 nmol/L) infusion. Apamin did not change APD 80 ventricles, but prolonged ventricles either long (≥300 ms) or short (≤170 cycle length, intermediate length. The maximal slope of 2.03 (95% confidence interval, 1.73–2.32) 1.26 1.13–1.40) P =0.002). After administration, the decreased 1.43 1.01–1.84; =0.018), whereas no significant changes were observed During number phase singularities (baseline versus apamin, 4.0 2.5), dominant frequency (13.0 10.0 Hz), (160 s) all significantly <0.05) by apamin. Conclusions— prolongs short, length upregulation may be antiarrhythmic preserving repolarization reserve slow rate, is proarrhythmic steepening curve, which promotes generation maintenance fibrillation.