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Antiarrhythmic effects of intravenous timolol in supraventricular arrhythmias
Insights
Timolol effectively treats supraventricular arrhythmias by converting them to sinus rhythm or reducing heart rate. This study found timolol significantly outperformed placebo in restoring normal heart rhythm.
Area of Science:
- Cardiology
- Clinical Pharmacology
Background:
- Supraventricular arrhythmias pose a significant clinical challenge.
- Effective antiarrhythmic agents are crucial for patient management.
Purpose of the Study:
- To evaluate the antiarrhythmic efficacy of timolol in patients with supraventricular arrhythmias.
- To compare the effects of timolol versus placebo in a randomized, double-blind study.
Main Methods:
- 160 subjects with supraventricular arrhythmias participated.
- Intravenous timolol (1 mg) or placebo was administered, with optional repeat doses.
- Responders were transitioned to oral timolol (10 mg twice daily).
Main Results:
- Timolol demonstrated a mean heart rate decrease of 44 bpm versus 7 bpm for placebo.
- Overall responder rates were 68% for timolol and 7% for placebo.
- Significantly higher response rates were observed for paroxysmal supraventricular tachycardia, atrial fibrillation, and atrial flutter with timolol.
Conclusions:
- Timolol is an effective intravenous agent for managing supraventricular arrhythmias.
- Common adverse effects included bradycardia and hypotension.
Abstract:
The antiarrhythmic effect of timolol was investigated in 160 subjects with supraventricular arrhythmias. In our double-blind, randomized, parallel, multiclinic study, subjects received timolol, 1 mg iv, or matching placebo as a starting dose, followed by a second and third dose of 1 mg each (or matching placebo) at 20-min intervals if the arrhythmia did not convert to sinus rhythm. Subjects in whom the sinus rhythm returned or the ventricular rate decreased to less than 100 bpm were transferred to a dosing regimen of timolol in 10-mg tablets twice a day by mouth, 1 hr after the last intravenous dose. Data indicated that the mean decrease in heart rate was 44 bpm after timolol and 7 bpm after placebo. The overall proportion of responders (either conversion to sinus rhythm or a decrease in ventricular rate to less than 100 bpm) was 68% after timolol and 7% after placebo. The proportions of responders after timolol were significantly higher than the proportions after placebo for paroxysmal supraventricular tachycardia (26 of 32 subjects and two of 38 subjects), atrial fibrillation (17 of 29 subjects and three of 32 subjects), and atrial flutter (seven of 11 subjects and one of nine subjects). The most common adverse effects were bradycardia and hypotension.