BACKGROUND: The mechanisms by which ventricular fibrillation (VF) is initiated in the infarcted human heart have not been defined. METHODS AND RESULTS: Left ventricular noncontact mapping of 8 episodes of pacing-induced VF in 6 patients (age 64.8+/-7.9 years, with previous myocardial infraction and left ventricular ejection fraction of 36+/-4%) undergoing ventricular tachycardia (VT) ablation revealed a consistent mechanism of VF induction. Whether during VT or sinus rhythm, the first of a train of paced extrastimuli to capture the LV produced an arc or arcs of functional block at regions bordering scar. With subsequent extrastimuli, the arcs elongated to circumscribe an enlarging area of increasingly late activation, with reentry through part of this functional (unidirectional) block leading to wavefront fragmentation and VF. These regions had longer fibrillation intervals (263+/-63 ms) than remote LV regions (209+/-23.4 ms; P<0.0001), implying longer refractory periods, and in 6 of the 8 VF episodes, these regions correlated with VT exit sites. In each of the 2 patients with 2 episodes of VF, both episodes formed arcs of functional block in the same location, despite pacing from different sites. CONCLUSIONS: Pacing-induced VF in the infarcted human heart is initiated by the development of functional lines of block dictated by the properties of a particular region of myocardium characterized by longer refractory periods, at or near VT circuit exit sites. Identification of these characteristic properties may help stratify risk of arrhythmic death and explain the potential for VT ablation to modify risk of VF in the infarcted heart.
BACKGROUND: The mechanisms by which ventricular fibrillation (VF) is initiated in the infarctedhuman heart have not been defined. METHODS AND RESULTS: Left ventricular noncontact mapping of 8 episodes of pacing-induced VF in 6 patients (age 64.8+/-7.9 years, with previous myocardial infraction and left ventricular ejection fraction of 36+/-4%) undergoing ventricular tachycardia (VT) ablation revealed a consistent mechanism of VF induction. Whether during VT or sinus rhythm, the first of a train of paced extrastimuli to capture the LV produced an arc or arcs of functional block at regions bordering scar. With subsequent extrastimuli, the arcs elongated to circumscribe an enlarging area of increasingly late activation, with reentry through part of this functional (unidirectional) block leading to wavefront fragmentation and VF. These regions had longer fibrillation intervals (263+/-63 ms) than remote LV regions (209+/-23.4 ms; P<0.0001), implying longer refractory periods, and in 6 of the 8 VF episodes, these regions correlated with VT exit sites. In each of the 2 patients with 2 episodes of VF, both episodes formed arcs of functional block in the same location, despite pacing from different sites. CONCLUSIONS: Pacing-induced VF in the infarctedhuman heart is initiated by the development of functional lines of block dictated by the properties of a particular region of myocardium characterized by longer refractory periods, at or near VT circuit exit sites. Identification of these characteristic properties may help stratify risk of arrhythmic death and explain the potential for VT ablation to modify risk of VF in the infarcted heart.