Etiology and management of sustained ventricular tachycardia.

Abstract

Ventricular tachyarrhythmias secondary to a variety of underlying cardiovascular problems pose a therapeutic challenge to the clinician. The initial presentation may be as sudden cardiac death, which underlies its public health problem. The underlying conditions predisposing to this arrhythmia include ischemic heart disease, dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmiogenic right ventricle dysplasia and certain postoperative states including corrective surgery for tetralogy of Fallot and valve replacement. Other causes include prolonged QT syndrome, idiopathic right and left ventricle tachycardia and bundle branch re-entry tachycardia. Ischaemic heart disease is the most common cause of ventricular tachycardia and therapy has evolved considerably over the past two decades. The development of and refinements in the implantable cardioverter-defibrillator (ICD) have introduced a new dimension in therapeutic options and markedly improved survival in these patients. Insights in the dichotomy between arrhythmia suppression and total mortality have reoriented drug therapy with a decrease in the use of sodium channel blockers. beta-blockers have emerged as antiarrhythmic drugs in their own right and their synergistic effects with amiodarone have strengthened the antiarrhythmic drug arm. The role of these drugs in patients with hemodynamically stable ventricular tachycardia, especially in relatively preserved ventricles needs to be explored. Catheter ablation techniques have provided curative therapy in patients with idiopathic and bundle branch reentry tachycardia. Further advances in radiofrequency ablation, including use of newer mapping techniques, promise a greater role for ablation of ischemic ventricular tachycardia in the future. A hybrid approach consisting of drugs, catheter ablation and/ or ICD may provide effective therapeutic approach in some situations. Further innovations and technologic developments promise a further reorientation in therapy towards identification and treatment of the underlying arrhythmogenic substrate.