Sotalol for refractory sustained ventricular tachycardia and nonfatal cardiac arrest

Singh, Steven; Cohen, Andrew I.; Chen, Yiwang; Wish, Marc; Thoben-O'grady, Laura; Peralba, Jose; Gottdiener, John S.; Fletcher, Ross D.

doi:10.1016/0002-9149(88)90966-6

Cited by 35 publications

(4 citation statements)

References 13 publications

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“…Surprisingly, sotalol produced a comparatively weak negative inotropic response, reducing peak LV dP/ dt by 13 f 3% in the present study, this being similar to findings reported in humans (Singh et al 1988). The fall in contractility associated with sotalol injection appears to be predominantly due to its @-adrenoceptor blocking effects as after autonomic blockade, peak LV dP/dt did not change significantly after sotalol injection (Fig.…”

Section: Discussionsupporting

confidence: 90%

“…Although early clinical experience suggested a more favourable haemodynamic profile (Anderson et al 1981), more recent studies have substantiated concerns regarding the potential for adverse haemodynamic effects with flecainide (De Paola et al 1987). Sotalol shares with amiodarone the effect of prolonging action potential duration and has been reported to be well tolerated, even in patients with impaired ventricular function (Singh et al 1988). By the lengthening of the action potential duration, amiodarone and sotalol may delay inactivation of the slow inward calcium current and augment contractility in isolated preparations (Tande & Refsum 1988.…”

Section: Introductionmentioning

confidence: 99%

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Comparative Haemodynamic Effects of Verapamil, Flecainide, Amiodarone and Sotalol in the Conscious Rabbit

Twidale

Roberts‐Thomson

McRitchie

et al. 1994

Clin Exp Pharma Physio

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1. The effect of intravenous boluses of verapamil (0.15 mg/kg), flecainide (2 mg/kg), amiodarone (5 mg/kg), and sotalol (1.5 mg/kg) on mean arterial pressure, heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), and peak rate of change of left ventricular pressure (LV dP/dt) were assessed in the conscious rabbit. 2. All four drugs had negative inotropic effects: verapamil reduced peak LV dP/dt by 19 +/- 4% (mean +/- s.e.m.; P < 0.01), flecainide by 27 +/- 9% (P < 0.001), amiodarone by 11 +/- 2% (P < 0.01) and sotalol by 13 +/- 3% (P < 0.01). 3. The drugs had different effects on CO as a result of differences in their actions on peripheral blood vessels: verapamil and amiodarone produced, respectively, a 12 +/- 4% (P < 0.03) and 16 +/- 6% (P < 0.01) increase in CO associated with a substantial vasodilatory effect (TPR reduced 15 +/- 7% [P < 0.05] and 20 +/- 5% [P < 0.01], respectively). Flecainide caused only a small (6 +/- 1%; P < 0.01) increase in CO and sotalol had no effect on either CO or TPR. 4. Bolus intravenous injections of verapamil, flecainide and amiodarone produced an increase in HR, while sotalol reduced HR by 10 +/- 2% (P < 0.01). The increase in HR and cardiac output seen with verapamil, flecainide and amiodarone was in part secondary to reflex increase in sympathetic tone and these changes were abolished after total cardiac autonomic blockade. 5. The modest reduction in cardiac performance associated with sotalol was abolished by cardiac autonomic blockade, suggesting that the predominant effect of sotalol on contractility was mediated through its beta-adrenoceptor blocking effect.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Comparative Haemodynamic Effects of Verapamil, Flecainide, Amiodarone and Sotalol in the Conscious Rabbit

Twidale

Roberts‐Thomson

McRitchie

et al. 1994

Clin Exp Pharma Physio

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“…The limited clinical information on the hemodynamic effects of D-sotalol in humans suggests that a marked cardiodepressive effect was not observed in humans without severely depressed left ventricular function. However, with regard to recent data on DL-sotalol in humans [25,28], this finding does not rule out druginduced heart failure in patients with considerably compromised left ventricular function.…”

Section: Discussionmentioning

confidence: 64%

Hemodynamic effects of the D- and L-isomers of sotalol on normal myocardium

Hoffmeister

Beyer

Seipel

1991

Cardiovasc Drug Ther

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This study investigated the hemodynamic effects of the D-isomer of sotalol in open-chest rats and compared this to the action of the L-isomer and the racemic DL-sotalol. Hemodynamic and additional isovolumic maximum measurements were registered at the end and 5 minutes after an intravenous infusion period of 7 minutes. DL- (1 and 2 mg/kg) and L-sotalol (2 mg/kg) caused a significant reduction in the heart rate and in the indices of contractility during and after infusion. D-sotalol (2, 4, and 8 mg/kg), however, decreased the contractility only transiently after very high doses at high plasma concentrations. Thus, while the effects of the beta-blocking L-isomer were comparable to those of DL-sotalol, only a slight and transient hemodynamic action of comparable doses of D-sotalol was found. These findings may be of significance for the proposed use of the D-isomer as a class-III antiarrhythmic agent.

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“…The average effectiveness for preventing reinducibility of VT/VF for most class I agents has been reported to be about 20% (67)(68)(69)(70)(71)(72). The use of triple extrastimuli reported by Singh et al (65) in a multicenter study comparing sotalol and procainamide gave the response rates of 30% for sotalol and 20% for procainamide. Nademanee et al (16) found a reasonably concordant predictive accuracy of Holter monitoring and PES.…”

Section: Sotalol In the Post-myocardial Infarction Patientmentioning

confidence: 99%

Review : Sotalol: Current Status and Expanding Indications

Singh

1999

J Cardiovasc Pharmacol Ther

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BACKGROUND: The role of antiarrhythmic drug therapy continues to undergo major changes. The change is necessitated by the advent of invasive interventional procedures, such as catheter ablation of arrhythmias and the use of implantable devices for sensing and terminating life-threatening ventricular arrhythmias and symptomatically traublesome supraventricular arrhythmias. Many conventional and time-honored drugs, such as sodium channel blockers, have been found either to be ineffective or to have the potential to produce serious proarrhythmic reactions. Attention is therefore focused on compounds that prolong repolarization and reduce sympathetic stimulation. Two compounds, amiodarone and sotalol, have emerged as prototypes of drugs of the future. METHODS AND RESULTS: This review focuses on sotalol for controlling supraventricular and ventricular tachyarrhythmias. Sotalol is a major antiarrhythmic agent that combines potent class III action with nonselective beta-blocking properties. The drug's pharmacokinetics is simple. Its elimination half-life is 10-15 hours, the drug being excreted almost exclusively by the kidneys. Sotalol's pharmacokinetics allows development of optimal dosing for initiation of therapy relative to changes in creatinine clearance with further dose adjustment by monitoring the QT interval on the surface electrocardiogram. The compound exerts broad-spectrum antiarrhythmic actions in supraventricular and ventricular arrhythmias. It prevents inducible ventricular tachycardia (VT) and ventricular fibrillation (VF) in approximately 30% of patients with a higher figure for the suppression of spontaneously occurring arrhythmias documented on Holter recordings. CONCLUSIONS: The major role of sotalol is in the management of VT/VF often in conjunction with an implantable cardioverter/defibrillator, in which context it lowere the defibrillation threshold. Sotalol is superior to class I agents, especially in VT/VF and in survivors of cardiac arrest. Sotalol has emerged as a major antifibrillatory compound for the control of life-threatening ventricular arrhythmias as the main indication. Data have indicated its potential for the maintenance of stability of sinus rhythm in patients with atrial fibrillation and flutter after electrical conversion and in preventing their occurrence in a variety of clinical settings.

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Sotalol for refractory sustained ventricular tachycardia and nonfatal cardiac arrest

Cited by 35 publications

References 13 publications

Comparative Haemodynamic Effects of Verapamil, Flecainide, Amiodarone and Sotalol in the Conscious Rabbit

Comparative Haemodynamic Effects of Verapamil, Flecainide, Amiodarone and Sotalol in the Conscious Rabbit

Hemodynamic effects of the D- and L-isomers of sotalol on normal myocardium

Review : Sotalol: Current Status and Expanding Indications

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