General Characteristics and Limitations
The mechanism of action of this drug group is based on the blockade of sodium channels. Like representatives of subclass IA, they act predominantly on the ventricles and cardiac pacemakers.
The main feature of Class IC is its narrow clinical niche. They are used exclusively to terminate life-threatening ventricular arrhythmias when other agents have proven ineffective.
Such caution is due to serious limiting factors:
- Proarrhythmic effect: drugs frequently provoke rhythm disorders themselves.
- Cardiodepression: most of them depress myocardial contractility.
- Conduction blockade: marked suppression of atrioventricular (AV) conduction.
Propafenone and Flecainide
Propafenone has a complex mechanism: in addition to primary sodium channel blockade, it moderately blocks calcium channels and exhibits $\beta$-adrenoreceptor blocking activity. It is well absorbed orally, but due to an intense "first-pass" hepatic effect, its bioavailability varies widely (from 4% to 40%). Side effects include dyspepsia, sleep disturbances, bradycardia, and bronchospasm (a consequence of $\beta$-blockade).
Flecainide (administered as acetate) strongly depresses conduction in the AV node and the His-Purkinje system, but has almost no effect on the effective refractory period of the ventricles. Unlike propafenone, it does not undergo significant first-pass hepatic metabolism, and peak plasma concentrations are reached in 3–4 hours. It frequently causes neurological disturbances (dizziness, visual disturbances) and proarrhythmic effects (in 5–15% of cases).
Phenothiazine Derivatives: Moracizine and Etacizine
Moracizine (ethmozine) is unique in combining the properties of all three sodium channel blocker subclasses (IA, IB, and IC). It depresses impulse propagation in the AV node and Purkinje fibers, but has a mild effect on the sinus node. Despite potential efficacy in supraventricular arrhythmias, in practice it is used only for resistant ventricular arrhythmias due to the high risk of arrhythmogenicity. Its elimination half-life is only 2 hours.
Its chemical analogue, etacizine, additionally blocks calcium channels. However, its safety profile is inferior: adverse reactions occur more frequently and are more severe, especially with intravenous administration.
Herbal Agent: Lappaconitine Hydrobromide
Lappaconitine hydrobromide (allapinin) is derived from the alkaloid of Aconitum leucostomum. It is a drug with a "mild" hemodynamic profile that stands out among the Class IC agents.
Its key advantages include:
- Practically does not depress AV conduction (slows only intra-atrial and intraventricular conduction).
- Inotropic neutrality (does not reduce myocardial contractility).
- Does not lower blood pressure.
Due to the absence of cardiodepressive effects, it is the only drug among those reviewed that can be used during myocardial infarction to treat both ventricular and supraventricular extrasystoles. Notable side effects involve the central nervous system (diplopia, dizziness, headache) because the drug crosses the blood-brain barrier. These phenomena are dose-dependent and disappear upon dose reduction.