AB-452675-4 CORONARY ARTERIAL SPASM DURING CAVO-TRICUSPID ISTHMUS ABLATION WITH A NOVEL FOCAL PULSED FIELD ABLATION CATHETER: FINDINGS FROM CORONARY ANGIOGRAPHY AND FRACTIONAL FLOW RESERVE MEASUREMENTS

Abstract

Pulsed field ablation (PFA) has been shown to avoid esophageal damage, PV stenosis and permanent phrenic nerve paralysis. But not studied in these trials was ablation of the cavo-tricuspid isthmus (CTI), a not uncommon adjunct target for ablation during pulmonary vein isolation (PVI) procedures. Indeed, recent studies demonstrated that when PFA is performed adjacent to a coronary artery, there is a susceptibility for vasospasm: in a study of right coronary artery (RCA) angiography during PFA of the cavo-tricuspid isthmus (CTI), there was universally severe RCA spasm, albeit subclinical. However, these studies were performed with a pentaspline PFA catheter designed to create a broad electrical field, not with a focal spot ablation catheter. To evaluate the potential for PFA to cause coronary spasm during CTI ablation, but using a focal PFA catheter. As part of a clinical trial of persistent AF ablation (PersAFOne 3, NCT05272852), after PVI and posterior wall ablation using a 12F commercial pentaspline PFA catheter (Farawave, BSC Inc.), CTI ablation was performed using an investigational 8F deflectable focal catheter (Farapoint, BSC Inc.). PFA was performed at 2kV (2 x 2.5 sec applications per site) with fluoroscopy and ICE guidance. Coronary angiography of the RCA with FFR measurement (Abbott PressureWire X) was performed before, during and after PFA at each application site. Spasm was categorized as mild (<50%), moderate (50-90%) or severe (>90%). At a single center, PFA of the CTI was performed in 8 patients. Bidirectional CTI conduction block was achieved in all patients after a mean of 13.3 lesions/pt (range 8-18). One patient had a left dominant coronary arterial system, and a de minimis RCA; of the remaining, 6 of 7 patients developed moderate (n=5) to severe (n=1) spasm as determined by both angiography and FFR (mean pressure differential 0.60, range 0.31-0.78 among patients developing spasm). There were no EKG changes and no symptoms (albeit sedated patients). The mean time for spasm resolution was 13.8 min. In an additional patient, intracoronary NTG pretreatment (1 mg) was administered before PFA lesions were delivered to the CTI: no coronary spasm was provoked. Focal PFA to the CTI provokes subclinical coronary vasospasm when delivered adjacent to the RCA. Additional investigation is necessary to determine the optimal NTG dosing strategy to prevent this phenomenon.