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Electrophysiologic effects of intravenous and oral sotalol for sustained ventricular tachycardia secondary to coronary artery disease

Authors
Journal
The American Journal of Cardiology
0002-9149
Publisher
Elsevier
Publication Date
Volume
61
Issue
13
Identifiers
DOI: 10.1016/0002-9149(88)90116-6
Keywords
  • Arrhythmias And Conduction Disturbances
Disciplines
  • Biology
  • Medicine
  • Pharmacology

Abstract

Abstract The electrophysiologic effects of intravenous sotalol (1.5 mg/kg load followed by 0.008 mg/kg maintenance, mean dose 150 ± 23 mg) and oral sotalol (mean dose 583 ± 204 mg daily) were prospectively evaluated in 16 patients undergoing electrophysiologic evvaluation for sustained ventricular tachycardia (VT) secondary to coronary artery disease. Electrocardiographic intervals, indexes of sinus and atrioventricular node function and indexes of atrial and ventricular function were assessed. Inducibility or noninducibility of sustained VT and characteristics of the induced arrhythmia were also evaluated. Intravenous and oral sotalol exerted similar β-blocking effects, which included significant prolongation of sinus cycle length (baseline 820 ± 165 ms, intravenous sotalol 1,077 ± 206 ms, oral sotalol 1,141 ± 306 ms), AH interval (baseline 126 ± 43, intravenous sotalol 169 ± 42, oral sotalol 197 ± 55 ms) and Wenckebach cycle length (baseline 375 ± 70, intravenous sotalol 460 ± 84, oral sotalol 449 ± 68 ms). Both intravenous and oral sotalol also prolonged repolarization and refractoriness including significant increases in QT interval (baseline 338 ± 47, intravenous sotalol 417 ± 35, oral sotalol 450 ± 70 ms), atrial effective refractory period (baseline 240 ± 38, intravenous sotalol 330 ± 71, oral sotalol 299 ± 26 ms) and right ventricular effective refractory period (baseline 241 ± 16, intravenous sotalol 289 ± 35, oral sotalol 291 ± 22 ms). Both intravenous and oral sotalol significantly slowed the cycle length of induced VT (baseline 265 ± 53, intravenous sotalol 351 ± 31, oral sotalol 331 ± 64 ms) and increased the mean arterial pressure during VT (baseline 45 ± 14 mm Hg, intravenous sotalol 78 ± 13 mm Hg, oral sotalol 65 ± 25 mm Hg). Intravenous and oral sotalol prevented induction of sustained VT in a similar percentage of patients (intravenous sotalol 2 of 9, 22%, oral sotalol 2 of 11, 18%). The observed electropharmacologic effects of intravenous and oral sotalol did not correlate with plasma concentration. Intravenous and oral sotalol have similar qualitative electrophysiologic effects but the specific quantitative effects observed may vary among individual patients.

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