Key result
Pulmonary arterial hypertension is linked to ~26 ms longer atrial activation time versus matched controls.
Why the study?
Pulmonary hypertension is associated with right atrial and ventricular remodeling that predisposes to arrhythmias, but mechanistic insights into atrial and ventricular electrophysiology in PH are needed to inform risk stratification and therapy.
Does pulmonary arterial hypertension alter atrial and ventricular electrophysiological conduction characteristics compared to matched controls?
Observational (n=40)
Does pulmonary arterial hypertension alter atrial and ventricular electrophysiological conduction characteristics compared to matched controls?
Absolute Event Rate: 72% vs 46%
p-value: p=0.001
Right atrial dilatation in pulmonary hypertension is associated with slowed electrical conduction and prolonged repolarization, providing a mechanistic substrate for increased arrhythmia risk.
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.
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Reddy et al. (2026) conducted an observational in Pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension (n=40). Pulmonary arterial hypertension vs. Matched controls was evaluated on Atrial activation time (ms) (p=0.001). Patients with pulmonary arterial hypertension exhibited significantly prolonged atrial activation time compared to matched controls (72 vs 46 ms; P=0.001).
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