Citation

BibTex format

@article{Reddy:2026:10.1016/j.hrthm.2026.08.036,
author = {Reddy, SA and De, Bie EM and Nethercott, SL and Polwarth, GJ and Bullock, K and Patel, KHK and Bajaj, N and Statton, BK and Zahra, SA and Ehnesh, M and Roney, CH and Jackson, N and Ng, FS and Rothman, AMK and Taboada, D and Bunclark, K and Cannon, JE and Sheares, KS and Pepke-Zaba, J and Martin, CA and Toshner, MR},
doi = {10.1016/j.hrthm.2026.08.036},
journal = {Heart Rhythm},
title = {Invasive and non-invasive mapping of the cardiac electromechanical substrate in pulmonary arterial hypertension.},
url = {http://dx.doi.org/10.1016/j.hrthm.2026.08.036},
year = {2026}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - BACKGROUND: Pulmonary hypertension (PH) is associated with right atrial (RA) and ventricular remodelling, 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 PH patients and correlate this 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 (ECGi) (n=30) or invasive right atrial 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±17ms vs 46±12ms, p=0.001; ventricular activation time 41±13ms vs 31±6ms, p=0.009; ventricular repolarisation time 127±51ms vs 87±25ms, p=0.007; ventricular activation-recovery interval 292±30ms vs 246±25ms, p=0.001). RA dilatation correlated with slower atrial conduction (R=0.51, p=0.01) and prolonged repolarization (R=0.40, p=0.02). Invasive mapping showed RA volume strongly correlated with atrial conduction velocity (R=-0.64, p=0.05) and AV nodal effective refractory period (R=0.82, p=0.03). CONCLUSIONS: 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 assessm
AU - Reddy,SA
AU - De,Bie EM
AU - Nethercott,SL
AU - Polwarth,GJ
AU - Bullock,K
AU - Patel,KHK
AU - Bajaj,N
AU - Statton,BK
AU - Zahra,SA
AU - Ehnesh,M
AU - Roney,CH
AU - Jackson,N
AU - Ng,FS
AU - Rothman,AMK
AU - Taboada,D
AU - Bunclark,K
AU - Cannon,JE
AU - Sheares,KS
AU - Pepke-Zaba,J
AU - Martin,CA
AU - Toshner,MR
DO - 10.1016/j.hrthm.2026.08.036
PY - 2026///
TI - Invasive and non-invasive mapping of the cardiac electromechanical substrate in pulmonary arterial hypertension.
T2 - Heart Rhythm
UR - http://dx.doi.org/10.1016/j.hrthm.2026.08.036
UR - https://www.ncbi.nlm.nih.gov/pubmed/42660261
ER -

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