Propafenone is an antiarrhythmic agent that falls under subgroup 1C. It shares structural similarities with propranolol and has weak β-blocking activity. Primarily used for treating supraventricular arrhythmias, propafenone has a mechanism of action similar to that of quinidine but with some distinct differences. This article will explore the mechanism of action, adverse effects, and therapeutic uses of propafenone.
Mechanism of Action
- Weak β-Blocking Activity: Unlike many other antiarrhythmic agents, propafenone possesses weak β-blocking activity due to its structural similarities to propranolol.
- Sodium Channel-Blocking Kinetics: Propafenone’s sodium channel-blocking kinetics are similar to those of flecainide.
- No Action Potential Prolongation: Unlike quinidine, propafenone does not prolong the action potential.
- Metabolism and Half-Life: Propafenone is metabolized in the liver and has an average half-life of 5–7 hours.
- Dosage: The usual daily dosage of propafenone ranges from 450–900 mg, administered in three divided doses.
- Supraventricular Arrhythmias: Propafenone is primarily used for treating supraventricular arrhythmias, similar to flecainide.
- Metallic Taste and Constipation: The most common adverse effects of propafenone include a metallic taste and constipation.
- Arrhythmia Exacerbation: Like flecainide, propafenone can also exacerbate existing arrhythmias.
Propafenone is a versatile antiarrhythmic agent with a unique profile that includes weak β-blocking activity. It is primarily used for treating supraventricular arrhythmias and has a similar mechanism of action to that of quinidine and flecainide. However, its use is associated with some adverse effects, including a metallic taste and constipation, as well as the potential for exacerbating existing arrhythmias. Therefore, propafenone should be used cautiously and under close medical supervision.