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Background Ultra-high-density mapping enables detailed mechanistic analysis of atrial reentrant tachycardia but has yet to be used to assess circuit conduction velocity (CV) patterns in adults with congenital heart disease. Methods and Results Circuit pathways and central isthmus CVs were calculated from consecutive ultra-high-density isochronal maps at 2 tertiary centers over a 3-year period. Circuits using anatomic versus surgical obstacles were considered separately and pathway length <50th percentile identified small circuits. CV analysis was used to derive a novel index for prediction of postablation conduction block. A total of 136 supraventricular tachycardias were studied (60% intra-atrial reentrant, 14% multiple loop). Circuits with anatomic versus surgical obstacles featured longer pathway length (119 mm; interquartile range [IQR], 80-150 versus 78 mm; IQR, 63-95; P <0.001), faster central isthmus CV (0.1 m/s; IQR, 0.06-0.25 versus 0.07 m/s; IQR, 0.05-0.10; P =0.016), faster non-isthmus CV (0.52 m/s; IQR, 0.33-0.71 versus 0.38 m/s; IQR, 0.27-0.46; P =0.009), and fewer slow isochrones (4; IQR, 2.3-6.8 versus 6; IQR 5-7; P =0.008). Both central isthmus ( R 2 =0.45; P <0.001) and non-isthmus CV ( R 2 =0.71; P <0.001) correlated with pathway length, whereas central isthmus CV <0.15 m/s was ubiquitous for small circuits. Non-isthmus CV in tachycardia correlated with CV during block validation ( R 2 =0.94; P <0.001) and a validation map to tachycardia conduction time ratio >85% predicted isthmus block in all cases. Over >1 year of follow-up, arrhythmia-free survival was better for homogeneous CV patterns (90% versus 57%; P =0.04). Conclusions Ultra-high-density mapping-guided CV analysis distinguishes atrial reentrant patterns in adults with congenital heart disease with surgical obstacles producing slower and smaller circuits. Very slow central isthmus CV may be essential for atrial tachycardia maintenance in small circuits, and non-isthmus conduction time in tachycardia appears to be useful for rapid assessment of postablation conduction block.

Background Patients with Eisenmenger syndrome are known to have a high incidence of sudden cardiac death (SCD), yet the underlying causes are not well understood. We sought to define the predictors of SCD in this population. Methods and Results A retrospective analysis of all patients with Eisenmenger syndrome from 2 large tertiary referral centers was performed. ECGs, prolonged ambulatory recordings, echocardiograms, and clinical histories were reviewed; and the cause of death was identified. A total of 246 patients (85 [34.6%] men) with a mean age of 37.3 (±14.2) years were followed up for a median of 7 years. Over the study period, 136 patients died, with 40 experiencing SCD and 74 experiencing cardiac death (sudden and nonsudden). Age, atrial fibrillation, prolonged QRS duration, complete heart block, right atrial enlargement, right bundle branch block, increased right atrial pressure, impaired biventricular function, and the presence of a pacemaker were associated with increased risk of SCD, whereas advanced pulmonary hypertension therapies were protective. Atrial fibrillation (11.45-fold increased risk; P <0.001) and QRS duration ≥120 ms (2.06-fold increased risk; P =0.034) remained significant predictors of SCD in the multivariate analysis, whereas advanced pulmonary hypertension therapies were strongly protective against SCD ( P <0.001). Conclusions Atrial arrhythmias, impaired ventricular function, and conduction system disease were associated with increased risk of SCD in this cohort of patients with Eisenmenger syndrome, providing an opportunity for early risk stratification and potential intervention. Clinical heart failure symptoms (New York Heart Association class ≥II) were predictive of increased mortality but not of SCD, suggesting a potential arrhythmic cause behind SCD.