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Antiarrhythmic effects of indecainide in a drug-resistant population with ventricular tachycardia at programmed
Insights
Indecainide, a new antiarrhythmic drug, was studied in patients with ventricular tachycardia. While it slowed tachycardia rates, it was less effective than procainamide in preventing induction.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Ventricular tachycardia (VT) and cardiac arrest are life-threatening arrhythmias.
- Effective antiarrhythmic therapy is crucial for managing these conditions.
- Class IC antiarrhythmic agents represent a therapeutic option for VT.
Purpose of the Study:
- To evaluate the antiarrhythmic properties of indecainide in patients with inducible VT.
- To compare the efficacy of indecainide with procainamide in preventing VT induction.
- To assess the effect of indecainide on VT rate in patients who remain inducible.
Main Methods:
- Fifteen patients with a history of cardiac arrest or VT underwent programmed electrical stimulation.
- Patients were tested with intravenous procainamide (1000 mg) and then intravenous indecainide (1 mg/kg).
- Inducibility of VT, VT rate, and electrocardiographic intervals (PR, QRS, QTc) were assessed.
Main Results:
- Indecainide significantly prolonged PR and QRS intervals but did not alter heart rate, blood pressure, or QTc interval.
- Procainamide prevented VT induction in 5 of 15 patients, while indecainide did not prevent induction in 12 of 15 patients.
- In inducible patients, indecainide slowed VT rate from 281 bpm to 224 bpm; procainamide slowed it to 215 bpm.
Conclusions:
- Indecainide exhibits antiarrhythmic effects by slowing VT rate, similar to procainamide.
- Indecainide appears less effective than procainamide in preventing VT induction in this patient cohort.
- Further research is warranted to define the role of indecainide in managing life-threatening tachyarrhythmias.
Abstract:
The antiarrhythmic properties of indecainide were studied in 15 patients with a history of a cardiac arrest or ventricular tachycardia. Programmed electrical stimulation studies were performed in nine men and six women with a mean age of 68 +/- 2 years and a mean left ventricular ejection fraction of 41 +/- 4%. All patients had inducible ventricular tachycardia by programmed electrical stimulation while off all antiarrhythmic therapy. Patients were then tested on procainamide, 1000 mg, administered intravenously, and ventricular tachycardia could be provoked in 10 of 15 patients. Indecainide was given intravenously, 1 mg/kg. Indecainide did not significantly change the baseline heart rate, blood pressure, and QTc interval from control values. The PR and QRS intervals were significantly prolonged. Twelve of 15 patients were still inducible for ventricular tachycardia on indecainide. Procainamide protected 5 of 15 patients against ventricular tachycardia induction. In patients still inducible on indecainide therapy, the ventricular tachycardia rate was significantly slowed, from 281 bpm to 224 bpm on indecainide and to 215 bpm on procainamide. The effects of this new class IC antiarrhythmic agent appears similar to procainamide in patients with serious life-threatening tachyarrhythmias.