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Hemodynamic and electrophysiologic effects of encainide in patients with bundle branch block
Insights
Encainide significantly prolonged the His-Purkinje (H-Q) interval in patients with bundle branch block, increasing the risk of adverse cardiac events, including sudden death and new arrhythmias.
Area of Science:
- Clinical Electrophysiology
- Pharmacology
- Cardiology
Background:
- Bundle branch block and organic heart disease are associated with increased risk of ventricular arrhythmias.
- Encainide is an antiarrhythmic drug whose effects on electrophysiology in these patients require investigation.
Purpose of the Study:
- To evaluate the electrophysiologic effects of encainide in patients with bundle branch block and organic heart disease.
- To assess the safety and efficacy of encainide in this patient population.
Main Methods:
- Electrophysiologic studies were conducted in 6 patients before and after intravenous encainide.
- Three patients also received oral encainide, and programmed ventricular stimulation was performed.
- His-ventricular intervals (H-Q) and ventricular tachycardia inducibility were assessed.
Main Results:
- Intravenous encainide increased the mean H-Q interval by 14% (p <= .05).
- Oral encainide increased the mean H-Q interval by 56% (p <= .05) in 3 patients.
- Ventricular tachycardia inducibility was altered by encainide in some patients, and all patients on chronic oral encainide experienced adverse outcomes.
Conclusions:
- Encainide significantly prolongs the H-Q interval in patients with bundle branch block and organic heart disease.
- The drug was associated with a high rate of major adverse outcomes, including sudden death and new arrhythmias.
- These findings raise concerns about the use of encainide in this specific patient group.
Abstract:
Electrophysiologic studies were performed in 6 consecutive patients with bundle branch block and organic heart disease. All were studied after intravenous (0.9 mg/kg) encainide and 3 of the 6 after 36-72 hours of oral encainide (50 mg every 6 hours). After intravenous encainide, mean H-Q increased from 51 +/- 20 msec to 58 +/- 25 msec (14% p less than or equal to .05). After oral encainide (3 patients) H-Q increased to 90 +/- 39 msec (56% p less than or equal to .05, compared to baseline). Programmed ventricular stimulation was performed in 5. In 1 patient without spontaneous ventricular tachycardia, tachycardia was non-inducible before and after encainide. Of 5 patients with spontaneous arrhythmia, 3 had ventricular tachycardia induced before and after intravenous encainide at mean cycle lengths of 287 +/- 130 msec and 407 +/- 261 msec, (not significant) respectively, while 1 had ventricular tachycardia induced only after encainide. Four patients began chronic treatment with oral encainide (2 patients with inducible rapid ventricular tachycardia after encainide were excluded). All suffered major adverse outcomes. One died suddenly after an electrophysiology study demonstrated inducible ventricular tachycardia, which occurred only after encainide. One experienced new syncope after baseline H-Q increased 75% after encainide. Two patients developed new sustained atrial tachycardias and 1 patient developed persistent ventricular tachycardia on encainide.(ABSTRACT TRUNCATED AT 250 WORDS)