Implantable cardiac defibrillators (ICD) are the foundation of therapy for the prevention of sudden cardiac death. While ICDs prevent SCD, they do not prevent the occurrence of ventricular arrhythmias which are usually symptomatic. Though catheter ablation has been successful in substrate modification of ventricular tachycardia in patients with ischemic cardiomyopathy, there is much less evidence to support its use in non-ischemic cardiomyopathy. Therefore, anti-arrhythmic drugs (AADs) are an essential adjunctive therapy for secondary prevention of ventricular arrhythmias in patients with non-ischemic cardiomyopathy. In patients with hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM), the prevalence of ventricular arrhythmias correlates with the volume of scar as characterized by late gadolinium enhancement. Beta-blockers forms the cornerstone of treatment to prevent ventricular arrhythmias in both HCM and DCM. Disopyramide is an important therapeutic option in HCM as it provides both negative inotropy which reduces obstruction as well as lass I anti-arrhythmic action. In DCM sotalol, through is combined beta-blocking and class III AD effects, significantly reduces the burden of ventricular arrhythmias. Though amiodarone is efficacious in the prevention of ventricular arrhythmias in both HCM and DCM, its use is limited by its side-effects profile. Evidence for AAD therapy for arrhythmogenic right ventricular dysplasia (ARVD) is limited by its low prevalence and lack of studies. ICDs have been shown to reduce SCD regardless of whether patients are receiving AAD therapy.
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