Sotalol drug interactions

Sotalol is well absorbed orally with bioavailability of approximately 100%. It is not metabolized in the liver and is not bound to plasma proteins. Excretion is predominantly by the kidneys in the unchanged form with a half-life of approximately 12 hours. Because of its relatively simple pharmacokinetics, solatol exhibits few direct drug interactions. Its most significant cardiac adverse effect is an extension of its pharmacologic action a dose-related incidence of torsade de pointes that approaches 6% at the highest recommended daily dose. Patients with overt heart failure may experience further depression of left ventricular function during treatment with sotalol. 

In a Prescription-Event Monitoring study in 3085 patients, mean age 65 years, there were 11 possible drug interactions. Nine involved beta-blockers, with eight reports of bradycardia and one of syncope. One patient developed palpitation and dyspnea while also taking digoxin and sotalol. 

Drug/Food interactions Food enhances the bioavailability of metoprolol and propranolol this effect is not noted with nadolol, bisoprolol, or pindolol. The rate of carteolol and penbutolol absorption is slowed by the presence of food however, extent of absorption is not appreciably affected. Sotalol absorption is reduced approximately 20% by a standard meal. 

Hypotension, bradycardia, ventricular fibrillation and asystole have been seen in a few patients given amiodarone with propranolol, metoprolol or sotalol (for sotalol, see also Drugs that prolong the QT interval + Other drugs that prolong the QT interval , p.2S7). However, analysis of clinical trials su ests that the combination can be beneficial. Amiodarone may inhibit the metabolism of beta blockers metabolised by CYP2D6, such as metoprolol, which might be a factor in the interaction. 

A 71-year-old woman with a history of atrial fibrillation was successfully treated with sotalol 80 mg twice daily. She started to take terfenadine 60 mg twice daily, and 8 days later she developed repeated self-limiting episodes of torsade de pointes arrhythmia. On one oeeasion she required resuscitation. Both drugs were stopped and no further episodes of arrhythmia occurred 72 hours after temporary pacing was discontinued. It seems likely that what happened resulted from the additive effects of both drugs on the QT interval, which can lead to the development of torsade de pointes. This case confirms a previous mention of the possibility of this interaction. ... 

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