Rationale of therapy in the patient with acute myocardial infarction and life-threatening arrhythmias: A focus on bretylium
Lucchesi, Benedict Robert
1984-07-30
Citation
Lucchesi, Benedict R. (1984/07/30)."Rationale of therapy in the patient with acute myocardial infarction and life-threatening arrhythmias: A focus on bretylium." The American Journal of Cardiology 54(2): A14-A19. <http://hdl.handle.net/2027.42/24751>
Abstract
Experimental evidence suggests a number of pathologic and electrophysiologic mechanisms that may help initiate ventricular arrhythmias accompanying myocardial ischemia and infarction. Early and late phase events are associated with reentry or an enhancement of focal mechanisms, or both. These can initiate ventricular tachycardia (VT) or ventricular fibrillation (VF), or both. The presence of distinct mechanisms that may initiate and maintain life-threatening dysrhythmias early in myocardial ischemia suggest different pharmacologic approaches for their prevention or suppression. Another consideration concerns patients subjected to coronary artery angioplasty or thrombolytic therapy and the development of arrhythmias associated with reperfusion of the once ischemic myocardium. The electrophysiologic mechanisms associated with reperfusion arrhythmias are unknown, and little is known about appropriate therapy for each episode of cardiac dysrhythmia.Ventricular extrasystoles or VT usually precedes VF. These premonitory arrhythmias are poor criteria for the institution of antiarrhythmic drug therapy, because VF develops within 1 to 10 minutes after the appearance of the rhythmic disturbances. Some authorities suggest that all patients with acute myocardial infarction should receive prophylactic antiarrhythmic therapy, because warning arrhythmias either do not occur at all or provide insufficient time to intervene pharmacologically.Many of the new class 1 antiarrhythmic agents effectively reduce the frequency of premature ventricular depolarizations, but lack specific antiflbrillatory activity. However, the recent introduction of bretylium into clinical cardiology opens a new approach to preventing life-threatening ventricular dysrhythmias. Along with other members of class III, bretylium exerts different cardiac electrophysiologic effects than do the other 3 classes of drugs. Bretylium has been designated as class III because it increases the action potential duration and prolongs the effective refractory period. The other class III drugs, including amiodarone, sotalol, clofilium and pranolium, experimentally prevent the establishment of a reentry pathway that can initiate VF. Bretylium along with these other class III agents is primarily antifibrillatory rather than antiarrhythmic. Thus, antiarrhythmic agents that reduce the frequency and complexity of premature ventricular depolarizations are not necessarily antifibrillatory. It is necessary to reorient our thinking about how pharmacologic interventions may influence the course of events in patients at risk of developing life-threatening ventricular arrhythmias. Because the lethal event is most often associated with VF, it may be sufficient to have an agent that protects against this electrophysiologic disorder even though it does not completely prevent or suppress other ventricular arrhythmias.Publisher
Elsevier
Types
Article
URI
http://www.sciencedirect.com/science/article/B6T10-4BYB026-H7/2/8c48e2bec86f6d8c5ef575ec8886e530Metadata
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