Clinical Suppression of Refractory Ventricular Tachycardia with Oral Bretylium Not Predicted by Electrophysiologic Drug Testing: Ventricular pacing

9 Feb

Clinical Suppression of Refractory Ventricular Tachycardia with Oral Bretylium Not Predicted by Electrophysiologic Drug Testing: Ventricular pacingA second dose of oral bethanidine (750 mg) was given four hours after the initial dose. The same sustained VT was induced from the right ventricular outflow tract during ventricular pacing at 500 ms with double ventricular extrastimuli. The patient received two more 500-mg oral doses of bethanidine at six-hour intervals, but sustained VT developed. Bretylium was restarted, and VT was again suppressed. Bethanidine was increased to 1,000 mg by mouth every six hours for eight doses, but VT recurred within eight hours of terminating the bretylium. Similar observations were noted with bethanidine (1,500 mg by mouth every six hours) but was very difficult to terminate with DC cardioversion. Bethanidine was discontinued, and the patient was again stabilized on intravenous bretylium. After a period of one week, a second trial of bethanadine was attempted, with identical results. alphagan eye drops

Oral bretylium (Dupont Critical Care) was started at 1,000 mg by mouth every six hours but nonsustained VT occurred. At a dose of 1,600 mg by mouth every six hours, VT was suppressed, and nearly all ventricular ectopic complexes were eliminated. Electrophysiologic drug testing was performed after one week of therapy with oral bretylium. Sustained VT was induced during ventricular pacing at a 400-ms cycle length with triple extrastimuli to the right ventricular outflow tract (Fig 1B). The VT morphology was of left bundle-branch block with left axis deviation with a cycle length of 260 ms. Attempts to lower the oral dosage of bretylium resulted in reappearance of episodes of nonsustained VT. As a precaution, an automatic implantable cardio-verter-defibrillator was implanted prior to discharge from the hospital. On oral therapy with bretylium, the patient has remained free of arrhythmias for nine months and has not required use of his defibrillator.
This case illustrates the beneficial effect of both intravenous and oral bretylium as therapy for sustained VT. Two other Vaughn-Williams class 3 antiarrhythmic drugs, amio-darone and bethanidine, failed to suppress VT and demonstrated proarrhythmic effects. Upon removal of each of these agents, episodes of VT subsided, only to reappear on rechallenge. An average of 11 percent of ventricular arrhythmias are aggravated by antiarrhythmic agents. Aggravation of ventricular arrhythmias by bretylium is rare, and amio-darone has only a 2 to 6 percent incidence of proarrhythmic effects. Bethanidine is investigational but has not previously been shown to be proarrhythmic. In this case, failure of one class 3 agent did not predict the success of another, despite the fact that bethanidine is an oral congener of bretylium.
Although sustained VT was easily induced in the electrophysiology laboratory on therapy with both bethanidine and bretylium, bretylium successfully prevented any further episodes of VT. Further studies will be necessary to determine whether inducibility of VT on bretylium accurately predicts subsequent clinical recurrences.