Layered activation of epicardial scar in arrhythmogenic right ventricular dysplasia: possible substrate for confined epicardial circuits.

BACKGROUND: Ventricular tachycardia ablation in arrhythmogenic right ventricular dysplasia (ARVD) is more successful when including epicardial ablation. Scarring may cause independent, layered epicardial activation and promote epicardially confined ventricular tachycardia circuits. We aimed to characterize transmural right ventricular activation in ARVD patients and to compare this with reference patients without structural heart disease. METHODS AND RESULTS: Eighteen ARVD patients underwent detailed endocardial and epicardial sinus rhythm electroanatomic mapping. Bipolar activation was annotated at the sharpest intrinsic deflection including late potentials and compared with 6 patients with normal hearts. Total scar area was larger on the epicardium (97±78 cm(2)) than the endocardium (57±44 cm(2); P=0.04), with significantly more isolated potentials. Total epicardial activation time was longer than endocardial (172±54 versus 99±27 ms; P<0.01), and both were longer than in reference patients. Earliest endocardial site was the right ventricular anteroseptum in 17 of 18 ARVD patients versus 5 of 6 controls (P=0.446), and latest endocardial site was in the outflow tract in 13 of 18 ARVD patients versus 4 of 6 controls and tricuspid annulus in 5 of 18 ARVD patients versus 2 of 6 controls (P=1.00). In reference patients, epicardial activation directly opposite endocardial sites occurred in 5.2±1.9 ms, suggesting direct transmural activation. In contrast, ARVD patients had major activation delay to the epicardium with laminar central scar activation from the scar border, not by direct transmural spread from the endocardium. CONCLUSIONS: Transmural right ventricular activation is modified by ARVD scarring with a delayed epicardial activation sequence suggestive of independent rather than direct transmural activation. This may predispose ventricular tachycardia circuits contained entirely within the epicardium in ARVD and explains observations on the need for direct epicardial ablation to eliminate ventricular tachycardia.

Mechanism of complex fractionated electrograms recorded during atrial fibrillation in a canine model.

BACKGROUND: Complex fractionated atrial electrograms (CFEs) have been described as a target during atrial fibrillation (AF) ablation; however, the mechanism leading to CFEs is poorly understood. We used noncontact mapping in a canine model of AF to determine the activation patterns in areas of CFEs. METHODS: Sustained AF was induced in 10 canines with 10-12 weeks of atrial tachy-pacing at 440 ppm. A roving mapping catheter and noncontact multielectrode array (MEA) were deployed in the left atrium (LA). NavX software was used to construct a contact bipolar CFE LA map. The MEA was then used to reconstruct wavefront propagation in proximity to CFE regions. Wavefront propagation was assessed during three separate recording segments for each site. RESULTS: There were 34 CFE regions identified (3.4/dog) and 102 noncontact CFE regional activation sequences studied. The CFE regions were stereotypically located at the junctions of (1) the left pulmonary vein (PV)/posterior LA, (2) right inferior PV/posterior LA, (3) right superior PV/anterior LA, and (4) the LA roof. The majority (47%) of CFE recordings were characterized by wavefront collision, usually between circulating LA wavefronts and entry/exit from the PVs. Thirty-eight (38%) CFE recordings were noted to be the central functional barrier of a reentrant wavefront. Ablation through CFE regions due to reentry led to AF termination and noninducibility in 3/5 animals. CONCLUSIONS: In this pacing-induced AF model, common causes of CFEs include: (1) wavefront collision, (2) conduction through channels of functional block, (3) reentry. The vast majority of these CFE regions were caused by wavefront collision rather than true "drivers" of AF.