Long-term results of electrophysiologically guided sotalol therapy for life-threatening ventricular arrhythmias

We describe postoperative refractory ventricular tachycardia (VT) in a patient following aortic and mitral valve replacement. Following an uneventful separation from cardiopulmonary bypass with dobutamine, the patient developed recurrent VT, 4 hours into the postoperative period. The VT did not respond to standard doses of xylocard, magnesium and amiodarone. Electrolyte and acid base parameters were normal. Multiple cardioversions failed to revert back to a stable rhythm. Intra-aortic balloon pumping was instituted and overdrive right ventricular pacing was unsuccessful. Following intravenous sotalol 80 mg, the VT came under control and reverted to a nodal rhythm, which required atrial pacing for the next 8 hours. Oral sotalol therapy was continued at 40 mg daily. The VT did not recur.

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“…Although the incidence of side-effects is high, patients appear to tolerate sotalol therapy well. [7] …”

Section: Discussionmentioning

confidence: 99%

Sotalol: A rescue drug in the face of life-threatening refractory ventricular tachycardia

Kandasamy¹,

Arumugham²,

Krupanandha³

et al. 2014

Ann Card Anaesth

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“…Sotalol (dl-sotalol) is an effective antiarrhythmic drug for life-threatening ventricular arrhythmias that occur after myocardial infarction Nademanee and Singh, 1990;Kus et al, 1992;Mason, 1993;Lee, 1996;Bocker et al, 1996;Kuhlkamp Kovoor et al, 1999]. Sotalol produces a prolongation of cardiac action potential duration and effective refractory periods (ERPs) by a block of the delayed rectifier current of the potassium channel and b-blocking action, thereby reducing the reentrant arrhythmias [Singh et al, 1970;Strauss, 1970;Carmeliet et al, 1985;Echt et al, 1982;Singh and Nademanee, 1985].…”

Section: Introductionmentioning

confidence: 99%

“…Sotalol (dl-sotalol) is an effective antiarrhythmic drug for life-threatening ventricular arrhythmias that occur after myocardial infarction Nademanee and Singh, 1990;Kus et al, 1992;Mason, 1993;Lee, 1996;Bocker et al, 1996;Kuhlkamp DDR n Correspondence to: Hisakuni Hashimoto, Department of Hospital Pharmacy, Hamamatsu University School of Medicine, Handayama 1-20-1, Hamamatsu, 431-3192 Japan. E-mail: hhashi@tm.hama-med.ac.jp Kovoor et al, 1999].…”

Section: Introductionmentioning

confidence: 99%

Differences in coupling interval‐dependent effects of sotalol on infarcted and noninfarcted areas of dog hearts after myocardial infarction

Hashimoto

Ohmura

Nakamura

et al. 2003

Drug Development Research

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We examined the coupling interval-dependence of the effects of sotalol (dl-sotalol) on effective refractory periods (ERPs) and epicardial activation in ventricles of dog hearts after myocardial infarction, and clarified their differences between infarcted and noninfarcted areas. Myocardial infarction was produced by the two-stage ligation of left anterior descending coronary artery in dogs. At 7 to 9 days after ligation, bipolar electrodes were sutured on the ventricular surface of the noninfarcted and the infarcted areas. Single (S1) or double (S1/S2) electrical stimulations with various coupling intervals were applied on the ventricle during atrial pacing. S1 was triggered by a prior R wave of pacing rhythm with coupling interval of 300 ms (S1[300]) or 180 ms (S1 [180]). Coupling intervals of S1 and S2 were between 250 and 130 ms. ERPs, activation delay, and functional refractory periods (FREPs) in ventricles were measured after S1(180) or S1(300). Ventricular activation delay was a time interval from the artifact of S1 or S2 to the most delayed measurable wave. The coupling interval of S1-S2 was 170 or 160 ms. RT intervals were measured in the bipolar ECGs after S1(300) or S1(180). Sotalol was administered intravenously in dosages of 2, 4, and 8 mg/kg. Sotalol prolonged the ERPs in noninfarcted areas in a lesser extent after S1(180) than after S1(300), whereas in infarcted areas the ERP prolongation was in a similar extent after S1(180) and S1(300). Sotalol prolonged the RT intervals in a lesser extent after S1(180) than after S1(300) in noninfarcted areas, but in a similar extent after S1(180) and after S1(300) in infarcted areas. FERPs were also prolonged by sotalol in infarcted areas in a similar extent after S1(180) and after S1(300). Sotalol prolonged ventricular activation delay after S1/S2 in the infarcted areas, which was greater after S1/S2(180/170) than after (300/170). Delayed activation was blocked more frequently after the S1/S2(180/ 160) than after S1/S2(300/160). These results indicate that the effects of sotalol on ventricular activation delay are reverse-use dependent in noninfarcted areas but use-dependent in infarcted areas, which may contribute to suppression of ventricular tachyarrhythmias in patients with coronary heart disease. Drug Dev. Res. 58:258-267, 2003.

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There Should Never Be Another Antiarrhythmics Versus Implantable Defibrillator (AVID) Trial

Singer

Nisam

1997

The American Journal of Cardiology

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Long-term results of electrophysiologically guided sotalol therapy for life-threatening ventricular arrhythmias

Cited by 6 publications

References 13 publications

Sotalol: A rescue drug in the face of life-threatening refractory ventricular tachycardia

Sotalol: A rescue drug in the face of life-threatening refractory ventricular tachycardia

Differences in coupling interval‐dependent effects of sotalol on infarcted and noninfarcted areas of dog hearts after myocardial infarction

There Should Never Be Another Antiarrhythmics Versus Implantable Defibrillator (AVID) Trial

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