[Cardiac side effects of anti-arrhythmia agents]

Antiarrhythmic drugs have typical cardiac side effects. These effects are due to their electrophysiological action on the one hand and to the negative inotropy on the other. These electrophysiological effects can cause a depression of sinus node function and/or AV conduction leading to severe bradycardia or asystole. However, the proarrhythmic effects of these drugs are clinically more important, especially the induction of ventricular tachycardia and "torsades". The incidence of these proarrhythmic effects is at least 5% of all patients treated. Patients with reduced ventricular function, "malignant" ventricular arrhythmias, and QT prolongation are especially endangered. Proarrhythmic effects may occur after the first dose. However, in most instances the risk is increased with higher dosage. The hemodynamic effects of antiarrhythmic drugs are especially important in patients with reduced cardiac function. The negative inotropy of antiarrhythmic drugs is often counterbalanced by the simultaneous decrease in blood pressure leading to an afterload reduction. Antiarrhythmic drugs causing an increase in systemic resistance may have a more pronounced depressive effect on cardiac function. However, if the acute treatment of severely ill patients in the CCU is excluded, the negative inotropy of antiarrhythmic drugs is not such an important problem as the proarrhythmic effect. As a consequence, antiarrhythmic treatment should be restricted to severely symptomatic patients on the one hand and to those with arrhythmias of prognostic importance on the other. In addition, the patient's treatment should be carefully controlled, especially during the early phase of treatment with antiarrhythmic drugs.