title: Verapamil reduces incidence of reentry during ventricular fibrillation in pigs.
abstract: The characteristics of reentrant circuits during short duration ventricular fibrillation (SDVF; 20 s in duration) and the role of Ca(++) and rapid-activating delayed rectifier potassium currents during long duration ventricular fibrillation (LDVF; up to 10 min in duration) were investigated using verapamil and sotalol. Activation mapping of the LV epicardium with a 21 × 24 electrode plaque was performed in 12 open-chest pigs. Pigs were given either verapamil (0.136 mg/kg) or sotalol (1.5 mg/kg) and verapamil. Reentry patterns were quantified for SDVF, and, for LDVF, activation patterns were compared with our previously reported control LDVF data. Verapamil significantly increased conduction velocity around the reentrant core by 10% and reduced the reentrant cycle length by 15%, with a net reduction in reentry incidence of 70%. Sotolol had an opposite effect of decreasing the conduction velocity around the core by 6% but increasing the reentrant cycle length by 13%, with a net reduction of reentry incidence of 50%. After 200 s of VF, verapamil significantly slowed wavefront conduction velocity and activation rate compared with control data. Verapamil decreased the incidence of reentry in SDVF by accelerating conduction velocity to increase the likelihood of conduction block, possibly through increased sympathetic tone. The drug slowed activation rate and conduction velocity after 200 s of VF, suggesting that L-type Ca(++) channels remain active and may be important in the maintenance of LDVF. Sotalol in addition to verapamil caused no additional antiarrhythmic effect.
authors.affiliation: Department of Cardiology, Shanghai Rui Jin Hospital, Jiao Tong University School of Medicine, Shanghai, People's Rebublic of China;
authors.forename: Qi
authors.initials: Q
authors.lastname: Jin
authors.affiliation: Department of Internal Medicine, Comprehensive Arrhythmia Research and Management Center, University of Utah, Salt Lake City, Utah;
authors.forename: Derek J
authors.initials: DJ
authors.lastname: Dosdall
authors.affiliation: Department of Internal Medicine, Comprehensive Arrhythmia Research and Management Center, University of Utah, Salt Lake City, Utah;
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.affiliation: Cardiac Rhythm Management Laboratory, Department of Biomedical Engineering, University of Alabama at Birmingham, Alabama;
authors.forename: Jack M
authors.initials: JM
authors.lastname: Rogers
authors.affiliation: Cardiac Rhythm Management Laboratory, Department of Biomedical Engineering, University of Alabama at Birmingham, Alabama; Department of Medicine, University of Alabama at Birmingham, Alabama; and Department of Physiology, University of Alabama at Birmingham, Alabama.
authors.forename: Raymond E
authors.initials: RE
authors.lastname: Ideker
authors.affiliation: Department of Medicine, University of Alabama at Birmingham, Alabama; and jh@crml.uab.edu.
authors.forename: Jian
authors.initials: J
authors.lastname: Huang
mesh_terms: D000200:Action Potentials; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D006339:Heart Rate; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology; D013015:Sotalol / Q000494:pharmacology; D013552:Swine; D014693:Ventricular Fibrillation / Q000503:physiopathology*; D016276:Ventricular Function / Q000187:drug effects*; D014700:Verapamil / Q000494:pharmacology*
chemical_list: D000889:Anti-Arrhythmia Agents; D013015:Sotalol; D014700:Verapamil
keywords: reentry; ventricular fibrillation; verapamil