Heart rhythm · 2026
Invasive and non-invasive mapping of the cardiac electromechanical substrate in pulmonary arterial hypertension.
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Reddy S Ashwin, De Bie Eckart Mdd, Nethercott Sarah L, Polwarth Gary J, Bullock Kat, Patel Kiran H K, Bajaj Nikesh, Statton Ben K, Zahra Syeda Anum, Ehnesh Mahmoud, Roney Caroline H, Jackson Nicola, Ng Fu Siong, Rothman Alexander M K, Taboada Dolores, Bunclark Katherine, Cannon John E, Sheares Karen S, Pepke-Zaba Joanna, Martin Claire A, Toshner Mark R
Аннотация
BACKGROUND: Pulmonary hypertension (PH) is associated with right atrial (RA) and ventricular remodeling, predisposing patients to arrhythmias and adverse outcomes. Mechanistic insights into atrial and ventricular electrophysiology in PH may inform arrhythmia risk stratification and therapeutic strategies.
OBJECTIVES: To determine myocardial conduction characteristics in Patients with and to correlate these with structural, functional, and clinical outcomes.
METHODS: Adult patients with pulmonary arterial hypertension (PAH) or chronic thromboembolic PH (CTEPH) were studied using non-invasive electrocardiographic imaging (n = 30) or invasive RA electroanatomical mapping during ablation (n = 10). Electrical parameters were quantified and correlated with structural and functional measures, such as chamber size, scar burden, and strain. Patients were prospectively followed for arrhythmias and clinical worsening events.
RESULTS: In non-invasive mapping, PAH patients exhibited prolonged atrial and ventricular depolarization and repolarization versus matched controls (atrial activation time 72 ± 17 ms vs 46 ± 12 ms, P = .001; ventricular activation time 41 ± 13 ms vs 31 ± 6 ms, P = .009; ventricular repolarization time 127 ± 51 ms vs 87 ± 25 ms, P = .007; ventricular activation-recovery interval 292 ± 30 ms vs 246 ± 25 ms, P = .001). RA dilatation correlated with slower atrial conduction (R = 0.51, P = .01) and prolonged repolarization (R = 0.40, P = .02). Invasive mapping showed that RA volume was strongly correlated with atrial conduction velocity (R = -0.64, P = .05) and atrioventricular (AV) nodal effective refractory period (R = 0.82, P = .03).
CONCLUSION: RA dilatation in PAH and CTEPH is associated with slowed conduction, prolonged repolarization, and increased AV nodal refractoriness, providing a mechanistic substrate for atrial arrhythmias and conduction disease. These findings highlight structural-electrophysiological correlations that may guide arrhythmia risk assessment and targeted interventions in PH.
OBJECTIVES: To determine myocardial conduction characteristics in Patients with and to correlate these with structural, functional, and clinical outcomes.
METHODS: Adult patients with pulmonary arterial hypertension (PAH) or chronic thromboembolic PH (CTEPH) were studied using non-invasive electrocardiographic imaging (n = 30) or invasive RA electroanatomical mapping during ablation (n = 10). Electrical parameters were quantified and correlated with structural and functional measures, such as chamber size, scar burden, and strain. Patients were prospectively followed for arrhythmias and clinical worsening events.
RESULTS: In non-invasive mapping, PAH patients exhibited prolonged atrial and ventricular depolarization and repolarization versus matched controls (atrial activation time 72 ± 17 ms vs 46 ± 12 ms, P = .001; ventricular activation time 41 ± 13 ms vs 31 ± 6 ms, P = .009; ventricular repolarization time 127 ± 51 ms vs 87 ± 25 ms, P = .007; ventricular activation-recovery interval 292 ± 30 ms vs 246 ± 25 ms, P = .001). RA dilatation correlated with slower atrial conduction (R = 0.51, P = .01) and prolonged repolarization (R = 0.40, P = .02). Invasive mapping showed that RA volume was strongly correlated with atrial conduction velocity (R = -0.64, P = .05) and atrioventricular (AV) nodal effective refractory period (R = 0.82, P = .03).
CONCLUSION: RA dilatation in PAH and CTEPH is associated with slowed conduction, prolonged repolarization, and increased AV nodal refractoriness, providing a mechanistic substrate for atrial arrhythmias and conduction disease. These findings highlight structural-electrophysiological correlations that may guide arrhythmia risk assessment and targeted interventions in PH.