Symposium on the management of ventricular dysrhythmias. Antifibrillatory versus antiectopic therapy.
The concept of antifibrillatory action distinct from antiarrhythmic effect has recently been recognized. An antiarrhythmic (antiectopic) action leads to a decrease in the frequency of ventricular ectopic beats. In contrast, an antifibrillatory drug action increases myocardial electric stability, decreasing the propensity for ventricular fibrillation. Agents with predominant antiarrhythmic action (designated class I) include lidocaine, quinidine, procainamide and disopyramide. Bretylium is an agent with predominant antifibrillatory action (class III). Amiodarone and sotalol are experimental class III drugs. The beta-blockers (class II) also possess antifibrillatory action, particularly in ischemic heart disease. The rationale for the use of agents with antiarrhythmic (antiectopic) effects is the reduction of triggering events for more complex ventricular tachyarrhythmias. These agents act by slowing conduction, decreasing abnormal automaticity and affecting phase IV depolarization. In contrast, agents with antifibrillatory action may exert little effect on cardiac conduction and automaticity. However, they raise the energy threshold required for premature electrical discharge to initiate ventricular fibrillation (ventricular fibrillation threshold). The inhomogeneity of electrophysiologic properties and adrenergic tone in different portions of the heart may be reduced or eliminated. Direct electrophysiologic effects of agents such as bretylium include a general lengthening of the refractory period and the action potential duration in the heart and a diminution in the disparity of their durations between normal and abnormal myocardium. Clinical studies are incomplete, but they support the concept of antifibrillatory therapy. In postmyocardial infarction patients at intermediate risk of sudden death, the broad use of oral antiarrhythmic agents has not decreased the incidence of sudden death, whereas high-dose beta-blocker therapy, which exerts experimental antifibrillatory effects, may reduce sudden death by 30 to 70%.(ABSTRACT TRUNCATED AT 250 WORDS)
D000284:Administration, Oral; D000319:Adrenergic beta-Antagonists / Q000145:classification / Q000502:physiology / Q000627:therapeutic use; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000145:classification / Q000494:pharmacology / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000209:etiology; D001949:Bretylium Compounds / Q000502:physiology; D002121:Calcium Channel Blockers / Q000145:classification / Q000502:physiology / Q000627:therapeutic use; D003327:Coronary Disease / Q000150:complications; D003645:Death, Sudden / Q000209:etiology; D004195:Disease Models, Animal; D004594:Electrophysiology / Q000187:drug effects; D006321:Heart / Q000187:drug effects; D006329:Heart Conduction System / Q000187:drug effects; D006801:Humans; D011674:Pulse / Q000187:drug effects; D013610:Tachycardia / Q000188:drug therapy / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control
D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents; D001949:Bretylium Compounds; D002121:Calcium Channel Blockers