Hypertonic sodium bicarbonate (HSB) has been reported to reduce the toxicity of Class IC antiarrhythmic agents in rats and, anecdotally, in patients. A pilot study was conducted of the safety and efficacy of HSB for reversing the electrocardiographic effects of therapeutic doses of encainide or flecainide in ten patients taking these drugs for chronic ventricular arrhythmias. Patients had a mean drug-induced QRS prolongation before treatment of 27.6 +/- 8.8%. Each patient received a single dose of HSB 100 mEq or normal saline IV over 5 minutes on two separate occasions. The administration of treatments was blinded and balanced. There were no important side effects of HSB. Venous blood pH, CO2 content and sodium concentration were all significantly increased by HSB in comparison to saline. No differences were found during the 2-hour observation period in the primary endpoint, QRS duration, the PR or QT intervals, or the frequency of premature ventricular beats. It was concluded that HSB 100 mEq does not reduce QRS duration in patients taking therapeutic doses of flecainide or encainide. Because HSB was well tolerated, investigation of its use in higher doses or in patients with overt toxicity due to Class IC drugs is feasible.
Although there are many reports of the short-term effectiveness of antiarrhythmic drugs for suppression of ventricular ectopic depolarizations, there are less data available on the long-term use of these drugs. We treated 122 patients for up to 2 years with antiarrhythmic drugs for suppression of frequent ventricular ectopic depolarizations. The percent suppression of ventricular ectopic depolarizations and nonsustained ventricular tachycardia for each drug was determined at 1, 3, 6, 12, 18, and 24 months of therapy. Among 33 patients treated with flecainide, the mean suppression of ventricular ectopic depolarizations (average of all data during 24 months) was 93 +/- 17% and of nonsustained ventricular tachycardia was 97 +/- 7%. In 27 patients treated with encainide, the mean suppression of ventricular ectopic depolarizations was 88 +/- 18% and of ventricular tachycardia was 95 +/- 16%. Among 26 patients treated with propafenone, the mean suppression of ventricular ectopic depolarizations was 77 +/- 32% and of ventricular tachycardia was 93 +/- 15%. For the 20 patients treated with moricizine, the mean suppression of ventricular ectopic depolarizations was 62 +/- 35% and of ventricular tachycardia was 90 +/- 14%. Among 16 patients treated with amiodarone, the mean suppression of ventricular ectopic depolarizations was 92 +/- 14% and of nonsustained ventricular tachycardia was 99 +/- 3%. In 54 of the 122 patients (44%), the study drug was stopped during 2 years of therapy because of death (2 sudden, 2 unwitnessed and 6 noncardiac), side effects (21 patients), lack or of loss of efficacy (13 patients), and noncompliance (10 patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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