Antiarrhythmics proarrhythmia with

Hohnloser SH. Proarrhythmia with class III antiarrhythmic drugs Types, risks, and management. Am J Cardiol 1997 80(8A) 82G-89G. 

Albrecht CA. Proarrhythmia with non-antiarrhythmics. A review. Cardiology. 2004 102 122-139. 

Wolbrette DL. Risk of proarrhythmia with class III antiarrhythmic agents Sex-based differences and other issues. Am J Cardiol 2003 91 39D-44D. 

Proarrhythmia refers to development of a significant new arrhythmia (such as VT, ventricular fibrillation [VF], or TdP) or worsening of an existing arrhythmia. Proarrhythmia results from the same mechanisms that cause other arrhythmias or from an alteration in the underlying substrate due to the antiarrhythmic agent. TdP is a rapid form of polymorphic VT associated with evidence of delayed ventricular repolarization due to blockade of potassium conductance. TdP may be hereditary or acquired. Acquired forms are associated with many clinical conditions and drugs, especially type la and type III IKr blockers. 

The use of antiarrhythmic drugs in the United States is declining because of major trials that showed increased mortality with their use in several clinical situations, the realization of proarrhythmia as a significant side effect, and the advancing technology of nondrug therapies such as ablation and the implantable cardioverter-defibrillator (ICD). 

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. 

The typical form of proarrhythmia caused by the type Ic antiarrhythmic drugs is a rapid, sustained, monomorphic VT with a characteristic sinusoidal QRS pattern that is often resistant to resuscitation with cardioversion or overdrive pacing. Some clinicians have had success with IV lidocaine (competes for the sodium channel receptor) or sodium bicarbonate (reverses the excessive sodium channel blockade). 

Proarrhythmia Like other antiarrhythmic agents, sotalol can provoke new or worsened ventricular arrhythmias in some patients, including sustained ventricular tachycardia or ventricular fibrillation, with potentially fatal consequences. Because of its effect on cardiac repolarization, is the most common form of proarrhythmia associated with sotalol, occurring in approximately 4% of high-risk patients. 

Quinidine Quinidex) was one of the first clinically used antiarrhythmic agents. Because of the high incidence of ventricular proarrhythmia associated with its use and numerous other equally efficacious agents, quinidine is now used sparingly. Quinidine shares all of the pharmacological properties of quinine, including an-timalarial, antipyretic, oxytocic, and skeletal muscle relaxant actions. 

The Cardiac Arrhythmia Suppression Trial (CAST) highlighted the importance and awareness of proarrhythmia. The main finding of CAST was that, despite elimination of complex ventricular ectopy after myocardial infarction, mortality was significantly higher in patients treated with encainide or flecainide. Others have reported that the overall risk of cardiac mortality is higher, presumably due to proarrhythmia, in patients treated with Type la antiarrhythmics for atrial fibrillation who have con-... 

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