Catheter ablation of idiopathic ventricular tachycardia: pathophysiological insights and electroanatomical mapping.

Abstract

The term ``idiopathic ventricular tachycardia'' summarizes a variety of pathophysiologically different arrhythmogenic mechanisms. These tachycardias have in common that clinical investigations do not reveal a structural heart disease. About 80% of these arrhythmias originate from the right ventricle, most often from the right ventricular out ow tract. In the remaining 20%, idiopathic ventricular tachycardia originates from the left ventricle, most often from the inferoposterior region. Irrespective of the anatomic origin, idiopathic ventricular tachycardias have been classi®ed according to their response to pharmacological agents. The response to adenosine, verapamil, or propranolol differentiates nearly all forms of these arrhythmias. The electrophysiological mechanisms ± triggered activity, automatic, or reentry ± is in uenced by catecholamines. Adenosine-sensitive ventricular tachycardia is believed to be due to a catecholamine-induced cyclic-AMP-mediated increase in intracellulur calcium resulting in delayed afterdepolarizations and triggered activity [1]. The clinical diagnosis of triggered activity is supported by termination of ventricular tachycardia either with adenosine, verapamil and betablockade or with valsalva maneuvers. The response to stimulation techniques is suggestive but not necessarily diagnostic of clinical triggered activity. Adenosine-sensitive tachycardia can be initiated and terminated by means of programmed ventricular or atrial stimulation. Its onset is usually provoked by isoproterenol although it can be inconsistently induced and terminated with programmed electrical stimulation during isoproterenol infusion. The arrhythmogenic area is most often located in the right ventricular out ow tract, only in a small number of patients in the anterobasal region of the left ventricle. Automatic, monomorphic or polymorphic, propranololsensitive idiopathic ventricular tachycardia can arise from either the right or left ventricle. It is often exercise-dependent and in general occurs in patients under 50 years of age. The tachycardia can be transiently suppressed but not terminated by adenosine. Mapping and ablation studies of adenosine-, and propanolol-sensitive idiopathic right ventricular tachycardia showed that pacemapping during sinus rhythm was a better predictor of success as compared to earliest endocardial activation [2,3]. Verapamil-sensitive ventricular tachycardia usually originates from the left ventricle and is suggested to be due to left posterior intrafascicular reentry. Only rarely triggered activity is found to be the electrophysiological mechanism [4±6]. Left ventricular tachycardia can be induced with stimulation techniques, even with atrial pacing [4,7]. Mapping studies revealed that in the inferoposterior region of the left ventricle a Purkinje potential preceding the QRS-complex can be recorded [8]. In the present issue of the Journal, Yano et al. [9] report on one patient with idiopathic left ventricular tachycardia, in whom catheter ablation at several sites with earliest ventricular activation around the postero-apical portion of the interventricular septum had failed. However, ablation at the site of earliest Purkinje potential preceding the onset of the QRS complex, which was at least 1,5 cm distant from any of the earliest endocardial activation sites in the midseptal portion of the ventricle, was successful. This is in accordance with the results of Nakagawa et al. [10] who described catheter ablation of idiopathic verapamil-sensitive ventricular tachycardia in 8 patients. The earliest endocar-