• Diogo Cavaco, Pedro Adragão, Francisco Morgado, Katya Reis-Santos, António Pinheiro Vieira, Dipali Chotalal, Daniel Bonhorst, and Ricardo Seabra-Gomes.
• Serviço de Cardiologia, Hospital de Santa Cruz, Carnaxide, Portugal.
• Rev Port Cardiol. 2005 May 1; 24 (5): 715-21.

IntroductionPatients with coronary heart disease and left ventricular dysfunction are at increased risk for the development of ventricular tachycardia (VT) related to areas of myocardial fibrosis. Although the mechanism and the circuit of this arrhythmia are well understood, little is known about the triggers that precipitate VT episodes. Purkinje fiber potentials may be responsible for idiopathic VT, and recent studies have related them to polymorphic VT and ventricular fibrillation.MethodsBetween January 2002 and December 2003, we performed ablation in 10 patients with coronary heart disease, left ventricular systolic dysfunction and VT refractory to pharmacological therapy. All patients had implantable cardioverter-defibrillators. Electroanatomical activation and voltage mapping (CARTO) and electrophysiological criteria (premature activation during VT, pace mapping, and presence of diastolic potentials) were used to define scar regions, slow conduction areas and the reentry circuit isthmuses.ResultsSpike potentials were recorded in the scars of three patients. These potentials were almost fused with the ventricular electrogram during sinus rhythm, and were more premature during VT, probably reflecting local activation of Purkinje fibers. During ablation, we were able to dissociate the spike from the ventricular electrogram, thus terminating the VT. In the cases with conduction recovery, ventricular; ectopic beats recurred, preceded by a spike and degenerating into short runs of VT. The ablation strategy was not modified since persistence of the VT required the isthmus.ConclusionThe results suggest that residual Purkinje fibers may be present in scar regions and that the activity of these fibers may trigger VT in pre-established circuits.

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