TY - JOUR
T1 - Assessing the arrhythmogenic propensity of fibrotic substrate using digital twins to inform a mechanisms-based atrial fibrillation ablation strategy
AU - Sakata, Kensuke
AU - Bradley, Ryan P.
AU - Prakosa, Adityo
AU - Yamamoto, Carolyna A.P.
AU - Ali, Syed Yusuf
AU - Loeffler, Shane
AU - Tice, Brock M.
AU - Boyle, Patrick M.
AU - Kholmovski, Eugene G.
AU - Yadav, Ritu
AU - Sinha, Sunil Kumar
AU - Marine, Joseph E.
AU - Calkins, Hugh
AU - Spragg, David D.
AU - Trayanova, Natalia A.
N1 - Publisher Copyright:
© The Author(s) 2024.
PY - 2024/7
Y1 - 2024/7
N2 - Atrial fibrillation (AF), the most common heart rhythm disorder, may cause stroke and heart failure. For patients with persistent AF with fibrosis proliferation, the standard AF treatment—pulmonary vein isolation—has poor outcomes, necessitating redo procedures, owing to insufficient understanding of what constitutes good targets in fibrotic substrates. Here we present a prospective clinical and personalized digital twin study that characterizes the arrhythmogenic properties of persistent AF substrates and uncovers locations possessing rotor-attracting capabilities. Among these, a portion needs to be ablated to render the substrate not inducible for rotors, but the rest (37%) lose rotor-attracting capabilities when another location is ablated. Leveraging digital twin mechanistic insights, we suggest ablation targets that eliminate arrhythmia propensity with minimum lesions while also minimizing the risk of iatrogenic tachycardia and AF recurrence. Our findings provide further evidence regarding the appropriate substrate ablation targets in persistent AF, opening the door for effective strategies to mitigate patients’ AF burden.
AB - Atrial fibrillation (AF), the most common heart rhythm disorder, may cause stroke and heart failure. For patients with persistent AF with fibrosis proliferation, the standard AF treatment—pulmonary vein isolation—has poor outcomes, necessitating redo procedures, owing to insufficient understanding of what constitutes good targets in fibrotic substrates. Here we present a prospective clinical and personalized digital twin study that characterizes the arrhythmogenic properties of persistent AF substrates and uncovers locations possessing rotor-attracting capabilities. Among these, a portion needs to be ablated to render the substrate not inducible for rotors, but the rest (37%) lose rotor-attracting capabilities when another location is ablated. Leveraging digital twin mechanistic insights, we suggest ablation targets that eliminate arrhythmia propensity with minimum lesions while also minimizing the risk of iatrogenic tachycardia and AF recurrence. Our findings provide further evidence regarding the appropriate substrate ablation targets in persistent AF, opening the door for effective strategies to mitigate patients’ AF burden.
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U2 - 10.1038/s44161-024-00489-x
DO - 10.1038/s44161-024-00489-x
M3 - Article
C2 - 39157719
AN - SCOPUS:85196306264
SN - 2731-0590
VL - 3
SP - 857
EP - 868
JO - Nature Cardiovascular Research
JF - Nature Cardiovascular Research
IS - 7
ER -