Pharmacotherapy in Ventricular Arrhythmias.

Background: Ventricular ectopy is observed in most of the population ranging from isolated premature ventricular contractions to rapid hemodynamically unstable ventricular tachyarrhythmias like ventricular tachycardia and ventricular fibrillation. Multiple mechanisms exist for ventricular arrhythmias such as triggered activity, reentry, and automaticity. Scar-based reentry forms the basis of most malignant VA that can lead to sudden cardiac death. Many antiarrhythmic drugs have been utilized for the suppression of ventricular arrhythmia. They are commonly classified using the Vaughan Williams Singh classification which distinguishes them based on the predominant action on different phases of the cardiac action potential. Class Ic agents are widely used in premature ventricular contraction suppression but are contraindicated in patients with prior myocardial infarction or ischemic scar and heart failure. β-Blockers continue to be a mainstay in the treatment of most symptomatic VA and are well tolerated, relatively safe, and have additional benefits in symptomatic coronary heart disease and left ventricular systolic dysfunction. Amiodarone continues to be used for the management of most cases of serious VA especially in the acute setting when accompanied by hemodynamic perturbations but has the disadvantage of having a poor toxicity profile for long-term use.

Summary: Historically used for long-term ventricular arrhythmia suppression and prevention of sudden cardiac death, antiarrhythmics are now used to reduce implantable defibrillator shocks and symptoms. They still have a role in premature ventricular complex suppression in patients with failed catheter ablation or those who are not candidates for invasive therapy. Newer concepts in cardiac imaging and the use of artificial intelligence may help further delineate sudden cardiac risk and identify patients that may benefit from pharmacological management.

Key Message: Anti-arrhythmic agents continue to perform an important role in the suppression of ventricular arrhythmias especially channelopathies, polymorphic VT, and idiopathic ventricular fibrillation. Judicious use of these agents while recognizing side effects can help reduce the long-term effects of ventricular arrhythmias on cardiac function.