Sotalol depression with

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. 

As with some other quinolones, moxifloxadn also prolongs the QTC interval [265], although the prolongation time of 4—6 ms (i.e., 1.4—1.6% of the starting interval) is relatively minimal. For safety reasons, the treatment of patients with QT interval prolongation and certain cardiac diseases is therefore contraindicated. Other medicaments with a potential for prolonging the QT interval may not be administered simultaneously with moxifloxacin. These indude anti-arrhythmic drugs of class IA (e.g., quinidine, hydroquinidine, disopyramide) and III (e.g., amiodarone, sotalol, dofetilide, ibutilide), intravenous erythromydn, tricyclic anti-depressives, and cisapride etc. 

All beta-blockers cause an increase in atrioventricular conduction time this is most pronounced with drugs that have potent membrane-depressant properties and no partial agonist activity. Sotalol differs from other beta-blockers in that it increases the duration of the action potential in the cardiac Purkinje fibers and ventricular muscle at therapeutic doses. This is a class III antidysr-hythmic effect, and because of this, sotalol has been used to treat ventricular (54-56) and supraventricular dysrhythmias (57). The main serious adverse effect of sotalol is that it is prodysrhythmic in certain circumstances, and can cause torsade de pointes (58,59). 

Sotalol prolongs the QT interval and can predispose to torsade de pointes (3), sustained ventricular tachycardia, and cardiac arrest, especially in those taking 160mg/day or more (SEDA-16, 191). Torsade de pointes has been reported in 1.2% of those exposed (data on file, Bristol-Myers Squibb, Princeton, New Jersey). In a review it was concluded that torsade de pointes is also more hkely in patients with depressed left ventricular function and a history of sustained ventricular tachydysrhythmias (4). 

The combined use of flecainide and beta blockers may have additive cardiac depressant effects. An isolated case of bradycardia and fatal AV block has been reported during the use of flecainide with sotalol, and bradycardia has been reported in a patient taking flecainide who was given timolol eye drops. 

Clonidine may potentiate the effects of alcohol, sedatives and CNS depressants (102 ). High doses of clonidine combined with high doses of propranolol were in several cases associated with the development of nightmares, delusion and marked drowsiness (8 ). The combination of clonidine with the 3-adrenergic blocker Sotalol gave rise to an antagonistic effect, comprising a marked rise of blood pressure in 3 out of 6 cases so treated (103 ). 

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