Sotalol Flecainide

This occurs in otherwise healthy individuals, who possess an anomalous (accessory) atrioventricular pathway they often experience attacks of paroxj mal AV re-entrant tachycardia or atrial fibrillation. Drugs that both suppress the initiating ectopic beats and delay conduction through the accessory pathway are used to prevent attacks e.g. flecainide, sotalol or amiodarone. Verapamil and digoxin may increase conduction through the anomalous pathway and should not be used. Electrical conversion may be needed to restore sinus rhythm when the ventricular rate is very rapid. Radiofrequency ablation of aberrant pathways will almost certainly provide a cure. 

Ventricular fibrillation should be terminated by electrical defibrillation. Alternatively, lidocaine can be injected intravenously. In cases with lower frequency, ventricular tachyarrhythmia class I diugs such as aj marine, flecainide or propafenone are more effective as a result of the use-dependence of lidocaine. For prophylaxis treatment, amiodarone or sotalol may be helpful or the implantation of a cardioverter-defibrillator system. Acute amiodarone (i.v. in higher doses) can also terminate ventricular tachyarrhythmias. This action, however, seems to be mediated by its INa-blocking side effects and not (or less) by its class III like effects. 

AF often recurs after initial cardioversion because most patients have irreversible underlying heart or lung disease. A metaanalysis confirmed that quinidine maintained sinus rhythm better than placebo however, 50% of patients had recurrent AF within 1 year, and more importantly, quinidine increased mortality, presumably due in part to proarrhythmia. Type Ic (e.g., flecainide, propafenone) and type III (e.g., amiodarone, sotalol, dofetilide) antiarrhythmic agents may be alternatives to quinidine however, these agents are also associated with proarrhythmia. Consequently, chronic antiarrhythmic drugs should be reserved for patients with recurrent paroxysmal AF associated with intolerable symptoms during episodes of AF. 

Deneer VHM, Drese GB, Roemele PEH, Verhoef JC, Lie-A-Huen L, Kingma JH, Brouwers JRBJ, Junginger HE (2002) Buccal transport of flecainide and sotalol Effect of a bile salt and ionization state. Int J Pharm 241 127-134... 

Classes I, III, and IV all involve transmembrane ion channels Classes I and III involve Na+ channels. Class I compounds are designed to block cardiac Na channels in a voltage-dependent manner, similar to local anesthetics. Not surprisingly, many of these Class I agents are either local anesthetics or are structurally based on local anesthetics. Class I compounds include procainamide (7.15), disopyramide (7.16), amiodarone (7.17), lido-caine (7.5), tocainide (7.18), mexiletine (7.19), and flecainide (7.20). The majority of these compounds possess two or three of the fundamental structural building blocks found within local anesthetics. Propranolol (7.21) is the prototypic Class II agent. Class III compounds include molecules that block outward K channels, such as sotalol (7.22) and dofetilide (7.23), and molecules that enhance an inward Na current, such as... 

Of 26 fetuses with hydrops fetalis and supraventricular tachycardias, 25 received transplacental drug therapy prenatal conversion occurred in 15 (82). Nine fetuses were converted to sinus rhythm using either flecainide (n = 7) or amiodarone (n = 2) as first-line therapy, while digoxin either alone or in association with sotalol failed to restore sinus rhythm in all cases. After first-line therapy, supraventricular tachycardia persisted in 10 fetuses, nine of whom received amiodarone alone or in association with digoxin as second-line therapy, and five of whom converted to sinus rhythm. Of 11 neonates who received amiodarone in utero, two developed raised thyroid stimulating hormone concentrations on postnatal days 3-4 they received thyroid hormone and had normal outcomes. 

A systematic review of randomized controlled trials in patients with newly detected AF identified a number of antiarrhythmic drugs for which there was statistically significant evidence of benefit (I). In a limited number of comparative studies, flecainide was more effective than propafenone and procainamide, propafenone was superior to amiodarone, amiodarone was superior to quinidine, and quinidine was superior to sotalol. 

Intravenous sotalol appears to be less effective than intravenous flecainide or ibutilide (47). 

Reisinger J, et al, Prospective comparison of flecainide versus sotalol for immediate cardioversion of atrial fibrillation. Am J Cardiol 1998 81 (12) I450-I454. 

Antidysrhythmic dmgs can themselves cause cardiac dysrhythmias, their major adverse effect. The risk of antidysrhythmic-induced cardiac dysrhythmias (prodys-rhythmic effects) has been estimated at about 11-13% in non-invasive studies (18,19) and at up to 20% in invasive electrophysiological studies. However, the risk varies from dmg to drug and is particularly low with class III drugs. In one study the quoted risks of dysrhythmias were flecainide 30%, quinidine 18%, propafenone 7%, sotalol 6%, and amiodar-one 0% (20). However, amiodarone does cause dysrhythmias, especially when the QT interval is over 600 ms. 

At 30 weeks of gestation in a 41-year-old woman the fetus had hydrops, ascites, a pericardial effusion, and bilateral hydroceles. A supraventricular tachycardia with 1 1 conduction was treated by giving the mother oral flecainide 150 mg bd. However, during the next few weeks the mother developed evidence of hepatic cholestasis. The dosage of flecainide was reduced to 50 mg bd and the liver damage resolved. The child was born healthy but later required sotalol for a re-entry tachycardia. 

Clinically important, potentially hazardous interactions with amiodarone, bepridil, cisapride, disopyramide, droperidol, erythromycin, flecainide, levodopa, pentamidine, procainamide, quinidine, sotalol, sparfloxacin, terfenadine, thioridazine... 

Note LQTS can be provoked by potassium channel blockers (e.g., quinidine, sotalol), and Brugada syndrome can be provoked by potent sodium channel blockers (e.g., cocaine, flecainide). LQTS3 and Brugada may coexist. 

Amiodarone Bretylium Diltiazem Flecainide Fluoxetine Lidocaine Nitroglycerin Propranolol Sotalol Verapamil... 

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. 

Warren R, Vohra J, Hunt D, Hamer A Serious interactions of sotalol with amiodarcne and flecainide. 1990) 152, 277. 

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