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Towards Ensuring Longterm Safety and Mechanisms of Clinical Cardioneuroablation

Award Number: R01HL186501
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/15/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2028

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Towards Ensuring Longterm Safety and Mechanisms of Clinical Cardioneuroablation - PROJECT SUMMARY/ABSTRACT Vasovagal syncope (VVS) is a debilitating condition with limited therapeutic options. VVS is commonly caused by vagally-mediated bradyarrhythmias, including sinoatrial (SA) node arrest and functional atrioventricular (AV) block. These events are driven by hypervagotonia via the intrinsic cardiac nervous system (ICNS), a network of ganglionated plexi (GPs) that mediate pre- to post-ganglionic vagal signaling to the heart. Cardioneural ablation (CNA) is an emerging interventional therapy that targets excessive vagal tone. CNA involves percutaneous identification and radiofrequency ablation of epicardial GPs, aiming to prevent reflex bradyarrhythmias by disrupting vagal input. However, while vagal tone is physiologically cardioprotective, autonomic imbalance favoring sympathetic dominance is a known driver of cardiovascular pathology. Therapies such as vagus nerve stimulation demonstrate benefit in heart failure, supported by strong preclinical data, whereas preclinical models of vagal denervation suggest increased risk of ventricular arrhythmias. Our laboratory recently developed the first chronic large-animal model of clinical CNA. We demonstrated that biatrial CNA increases susceptibility to ischemia-induced ventricular tachycardia and fibrillation (VT/VF), likely through autonomic dysregulation. These findings raise critical concerns that CNA’s therapeutic benefits may be offset by proarrhythmic risk. The overall objective of this proposal is to define mechanisms of CNA-associated ventricular arrhythmogenesis to enable safer and more effective application of CNA a therapy with significant potential for patients with vagally mediated bradyarrhythmias. We hypothesize that extensive CNA disrupts coordinated ICNS activity, leading to excessive and spatially heterogeneous release of adrenergic neurotransmitters (norepinephrine and neuropeptide), which serve as both substrate and trigger for VT/VF. We will test this hypothesis through three specific aims in pigs and in human hearts. In Aim 1, we test the hypothesis that excessive and spatially heterogeneous NE/NPY release in ventricular myocardium underlies arrhythmia susceptibility following CNA, while in Aim 2 we test the hypothesis that CNA induces structural and functional remodeling in ventricular GPs, contributing to autonomic dysreflexia Aim 3 will test the hypothesis that focused CNA can achieve therapeutic vagal denervation while minimizing proarrhythmic risk. Successful completion of these aims will clarify the contribution of ICNS disruption to post-CNA arrhythmogenesis and define parameters for safer, targeted CNA. These insights will support refinement of clinical protocols and inform future neuromodulation strategies, addressing an unmet need in the treatment of vagally mediated bradyarrhythmias.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $1,567,702 )
2026	2026	UNIVERSITY OF CALIFORNIA, LOS ANGELES	10889 WILSHIRE BLVD STE 700	LOS ANGELES	CA	90024	LOS ANGELES	USA	Cardiovascular Diseases Research	000	1	7/7/2026	NEW	$1,567,702
														Subtotal = $1,567,702

Grand Total All Awards = $1,567,702

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Towards Ensuring Longterm Safety and Mechanisms of Clinical Cardioneuroablation

Award Number: R01HL186501

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 07/15/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2028

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