[Catheter ablation in ventricular tachycardia]

The basis for management of ventricular tachycardia (VT) is pharmacologic treatment which is effective, however, in only about 20 to 30% of the patients. With respect to this problem, alternative therapeutic modes have been developed which include, in addition to antitachycardia stimulation, electrical, palliative therapy such as the implantable automatic defibrillator, definitive measures such as map-guided antitachycardia surgery and catheter ablation. The goal of catheter ablation is the selective destruction of heart structures which are the morphologic correlate for initiation of propagation of VT. Catheter ablation was discovered by chance by Fontaine after a defibrillation during an electrophysiologic study in which a defibrillating electrode in the proximity of a catheter at the His bundle induced complete AV-block. This effect of destruction in the AV-conduction system by direct current as a therapeutic measure was further developed by Gallagher and Scheinman. The mechanism held responsible is coagulation by the electrode of neighboring tissue and barotrauma. The technique, which was initially used for ablation of the His bundle in supraventricular tachycardia, can also be used for ablation of accessory pathways or the site of origin of VT which generally lies endocardially in marginal regions of myocardial infarctions. CATHETER MAPPING: In sinus rhythm and induced VT, endocavity catheter mapping is carried out after heparinization with electrocardiograms recorded from at least six to ten sites in the right and left ventricles. At the site of early activation, detailed mapping is used for identification of the site of earliest activation, then pace-mapping is performed during sinus rhythm and VT. The morphology of the stimulated QRS complexes is compared with that of the spontaneous VT. In patients in whom VT cannot be induced, localization is carried out by pace-mapping alone. CATHETER ABLATION: After localization, in intubation narcosis and with continuously monitored arterial blood pressure, the suspected site of origin of the VT is subjected to an initial shock during sinus rhythm by means of a distal electrode of a catheter in stable contact with the endocardium. For mapping and ablation, the same catheter is used. After each subsequent shock, assessment is performed to determine if the distal electrode pair still conducts local ventricular signals and if ventricular stimulation is possible. The shock energy delivered is 100, 200 or 400 Joules. At the time of shock discharge, the remaining electrodes or catheters are disconnected. In the case of bradycardia or tachycardia after the shock, immediate connection to an external stimulation generator is established. At the time of the shocks, relaxation is provided by succinylcholine. All shocks are delivered from the anode. The integrity of the catheter is tested after each shock, no catheter is used more than three or four times. At the earliest, ten minutes after shock delivery, induction of clinical VT is attempted with programmed stimulation and if induction is possible, at the same site a maximum of two more shocks are delivered or, after renewed mapping, another shock is delivered to a different site. Induced non-clinical VT is not subjected to ablation.(ABSTRACT TRUNCATED AT 400 WORDS)