VALUE OF ELECTROPHYSIOLOGIC STUDIES IN HYPERTROPHIC CARDIOMYOPATHY TREATED WITH AMIODARONE

The relation of electrophysiologic effects of amiodarone to long-term outcome was studied in 35 patients with hypertrophic cardiomyopathy (HC). Indications for electrophysiologic studies were: cardiac arrest (n = 3), syncope/presyncope (n = 27) and asymptomatic ventricular tachycardia (VT) (n = 5). Twenty-eight patients (80%) had VT, 3 (9%) atrial tachycardia and 3 (9%) paroxysmal atrial fibrillation during 24-hour Holter monitoring. The studies were repeated after a total amiodarone dose of 58 +/- 122 g and during a maintenance median daily dose of 400 mg. Amiodarone abolished paroxysmal atrial arrhythmias in all 6 patients. However, it caused marked atrioventricular nodal conduction abnormality in 3 patients and heart block or marked HV interval prolongation (to greater-than-or-equal-to 100 ms) in 4 patients. Sustained VT was induced in 26 patients (74%) at baseline study and in 23 patients (66%) taking amiodarone therapy. With amiodarone, VT was no longer inducible or was more difficult to induce in 11 patients (31%), and the drug abolished VT during Holter monitoring in all patients. However, VT was easier to induce with amiodarone or was induced only with amiodarone in 18 (51%) patients. Amiodarone significantly slowed the rate of induced VT (from 248 +/- 29 to 214 +/- 37 beats/min, p < 0.001). This was associated with a change in its morphology from polymorphic to monomorphic VT in 7 patients. During a follow up of 18 +/- 14 months (range 2 to 56), amiodarone was discontinued because of adverse effects in 8 patients (23%). Additionally, 4 of 18 patients in whom amiodarone facilitated induction of VT either died (n = 2) or received appropriate electric shocks from an implanted defibrillator device compared with none of the remaining 17 patients taking amiodarone in whom VT induction was not possible, unchanged or more difficult (1-year event-free rates: 71 vs 100%, p < 0.05). All 4 patients had presented with syncope or cardiac arrest. Thus, although amiodarone effectively suppresses atrial arrhythmias and reduces or prevents VT induction in about one-third of patients with HC, it causes important conduction abnormalities in about 20% of patients and facilitates induction of VT in about half of patients. This latter group of patients may be prone to malignant VT and amiodarone, and cannot be identified by Holter recordings. Electrophysiologic studies are therefore necessary when initiating amiodarone, because the results identify patients with HC who should receive a pacemaker with the drug, as well as those in whom amiodarone should be discontinued because of serious proarrhythmic effects.