Authors: Melanie A Gunawardene, Jens Hartmann, Eike Tigges, Johanna Jezuit, Stephan Willems
Categories: Case Report, Atrial fibrillation, Case report, Cavotricuspid isthmus, Coronary spasm, Pulsed field ablation, AcademicSubjects/MED00200, Eurheartj/1, Eurheartj/2, Eurheartj/3
Source: European Heart Journal: Case Reports
Pulsed field ablation (PFA) is a novel ablation technology. A rare side-effect is the occurrence of mostly subclinical coronary spasms when PF energy is applied in proximity to coronary arteries. However, it has been described that prior application of nitroglycerin attenuates these effects.
A 75-year-old female underwent catheter ablation with a penta-spline PFA catheter. After pulmonary vein isolation, the PFA catheter was positioned on the cavotricuspid isthmus (CTI). Before ablation, 2 mg of nitroglycerin was administered intravenously. After 10 PFA applications, the CTI was successfully blocked. After a timely delay of 95 s, a clinically apparent vasospasm with ST elevations in leads II, III, and aVF on the electrocardiogram was noticed. Shortly thereafter, the clinical course was aggravated by haemodynamically relevant non-sustained ventricular tachycardias (nsVTs) followed by asystole, requiring pacing and additional 4 mg of nitroglycerin. Twelve minutes later, a stable sinus rhythm with normalized ST segments was restored. The spasm resolved without any sequelae. Post-procedural coronary angiogram showed right dominant coronary circulation.
This is the first report of a timely delayed, clinically apparent coronary spasm with a presentation of haemodynamically relevant nsVT and asystole despite the prophylactic application of high-dose intravenous nitroglycerin prior to PFA along the CTI. Subclinical vasospasm during PFA at the CTI has been described before. Severe spasms could be prevented by nitroglycerin. A word of caution needs to be raised as prophylactic nitroglycerin did not prevent the haemodynamically relevant coronary spasm in the here reported patient. Until now, it remains unclear how much later such effects may occur; therefore, patients should be monitored closely.
Keywords: Pulsed field ablation, Coronary spasm, Atrial fibrillation, Cavotricuspid isthmus, Case report
Pulsed field ablation (PFA) is a novel ablation technology for treatment of atrial fibrillation (AF).^1^ Pulsed field ablation-related complications such as coronary spasms are rare, especially when the devices are used for pulmonary vein isolation (PVI) only.^2^ However, it has been shown that PFA routinely provokes subclinical coronary artery spasm when the energy is applied on structures close to coronary arteries, such as the cavotricuspid isthmus (CTI) or mitral isthmus.^3,4^ It has been reported that a prior dose of 1–2 mg nitroglycerin intravenously prevented severe coronary spasms during PFA along the CTI.^3^
Timeline of the ablation procedure. CTI, cavotricuspid isthmus; iv, intravenous; min, minutes; nsVT, non-sustained ventricular tachycardia; PFA, pulsed field ablation; PVI, pulmonary vein isolation; RV, right ventricular; sec, seconds; SR, sinus rhythm.
A 75-year-old female [CHA2DS2-VA 3 (2 points age and 1 point periphery artery disease)] with a history of symptomatic paroxysmal AF and typical atrial flutter underwent catheter ablation with a penta-spline PFA catheter (Farapulse™, Boston Scientific) in our institution. Prior to the procedure, she complained of palpitations and shortness of breath during her arrhythmia episodes. She reports one-time chest discomfort during an episode of atrial flutter. Other than that, she had never experienced angina pectoris-like symptoms. The patient did not undergo prior invasive or non-invasive diagnostics to rule out ischaemia or coronary artery disease. Her prior medical history included paroxysmal AF, atrial flutter, and a 70% stenosis of the left internal carotid artery. Physical examination prior to ablation was unremarkable, except for a carotid bruit detected during auscultation. A neurological consultation was obtained, and the patient was cleared to undergo analgosedation. Pre-procedural laboratory testing was normal [haemoglobin 13.8 g/dL (reference 12.0–16.0 g/dL); international normalized ratio 1.4 (no reference value); thyroid-stimulating hormone 1.94 mU/L (reference 0.27–4.20 mU/L); creatinine 0.7 mg/dL (reference 0.6–1.1 mg/dL)]. We performed pre-procedural transoesophageal echocardiography to rule out left atrial thrombus.
During the procedure, the patient presented in sinus rhythm (Summary figure), and PVI with 12 PFA applications at each PV (48 applications in total) was performed with a single left atrial access. After successful completion of PVI, the steerable sheath was retracted to the right atrium and the PFA catheter was positioned on the CTI in flower configuration (Summary figure). Then, 2 mg of nitroglycerin was administered intravenously 1 min prior to the start of ablation. In total, 10 PFA applications were delivered over a duration of 2 min, and successful block of the CTI line was confirmed (Summary figure). The PFA catheter and diagnostic catheter were then retracted, and the large sheath was pulled back into the vena cava inferior to prepare for sheath removal. Ultimately, while the figure-of-eight suture was performed, a clinically apparent vasospasm with ST elevations in leads II, III, and aVF on the surface electrocardiogram (ECG) was noticed (Summary figure). The occurrence of ST elevations was detected 95 s after the last PFA application. This was shortly followed by haemodynamically relevant non-sustained ventricular tachycardias (nsVTs) and asystole (Summary figure). Echocardiography was performed to rule out pericardial effusion, and immediate re-introduction of the diagnostic catheter for right ventricular pacing was carried out. To treat the underlying vasospasm, an additional 4 mg of nitroglycerin, accompanied by doses of the vasopressor noradrenaline, was administered intravenously through the sheaths. Twelve minutes after the first appearance of ST elevations and a cumulative dose of 6 mg of intravenous nitroglycerin (2 mg prior and 4 mg after the manifestation of spasm), a stable sinus rhythm with normalized ST segments was restored. Due to complete normalization of the ST segments after additional nitroglycerin doses and shared decision-making within the team, no immediate coronary angiography was performed.
The spasm resolved without any sequelae.
After gaining patient informed consent, a coronary angiogram the next day showed right dominant coronary—circulation with minor sclerosis of both left and right coronary arteries (Figure 1).
Figure 1 Anatomy of the coronary system. (Left) Fluoroscopic image of the pulsed field ablation catheter positioned on the cavotricuspid isthmus in an left anterior oblique 30° view. (Middle) Coronary angiogram of the right coronary artery on the next day following the ablation procedure. The angiogram shows a right dominant coronary—circulation with minor sclerosis. (Right) Coronary angiogram of the left coronary arteries with minor sclerosis in a right anterior oblique 25° and cranial 20° view. CTI, cavotricuspid isthmus; CFX, circumflex artery; CRA, cranial; LAD, left anterior descending artery; LAO, left anterior oblique; PFA, pulsed field ablation; PVI, pulmonary vein isolation; RAO, right anterior oblique; RCA, right coronary artery.
We here report a case with a timely delayed, clinically apparent coronary spasm and a presentation of haemodynamic relevant nsVT and asystole despite the prophylactic application of high-dose intravenous nitroglycerin prior to PFA along the CTI.
Coronary spasms are a rare complication of catheter ablation and appear to be more frequent with PFA applied in close proximity to coronary arteries than thermal radiofrequency ablation.^5^
These vasospasms provoked by PFA are frequently described as subclinical phenomena.^3,5,6^ However, reports on clinically apparent spasms with ST elevations and/or ventricular arrhythmias have been reported.^4,7^
Therefore, treatment strategies to prevent such spasms have been Reddy et al.^3^ investigated the vasospastic potential of PFA, both remote from and adjacent to coronary arteries in 25 consecutive patients of whom 20 underwent ablation of the CTI, which is adjacent to the right coronary artery (RCA). Without nitroglycerin treatment, coronary spasm of the RCA was seen in all patients during simultaneous coronary angiography, but none of them were clinically apparent. No ECG changes were detected. The study showed that pre-ablation nitroglycerin administration (intracoronary as well as intravenously) eliminated severe vasospasm successfully. However, 20% of patients with intravenous nitroglycerin pre-treatment revealed mild to moderate spasms. Yet, none of them were accompanied with ECG changes—as compared to our patient. Of note, this patient showed a right dominant coronary circulation. A severe spasm of the dominant RCA may therefore be more susceptible to become clinically relevant.
Even though coronary spasm was observed in 100% of patients undergoing PFA of the CTI without prior treatment,^3^ we did not perform an immediate coronary angiography in our patient to confirm the diagnosis. Therefore, although unlikely, differential diagnosis such as thrombus formation following left atrial ablation or air embolism could be potential alternatives of our finding. Ablation in the LA was, however, already completed, and no sheath was in the LA during the occurrence of ST elevations. Air embolism may also present over a shorter period. Furthermore, the ST elevations in our patient resolved with the administration of additional nitroglycerin, and PFA was applied in close proximity to the RCA with the ST elevations being detected in the inferior leads, making a vasospasm the most likely diagnosis.
Of note, the coronary spasm in our patient transpired 95 s after the last PFA application.
This timely delay needs to be considered. Reddy et al.^3^ reported that in all instances of mild to moderate spasm, the spasm occurred during the last or next to the last PF application with a mean of 6 applications. This finding could be explained by pharmacodynamics and vanishing of the nitroglycerin effect due to its short (1–3 min) half-life.^3^ In our patient, nitroglycerin was administered 1 min before ablation and ablation time of the CTI was 2 min. The ECG changes revealing the coronary spasm in our patient occurred 4.5 min after the initial nitroglycerin bolus.
In a study, investigating focal PFA, it has been shown that a less intensive nitroglycerin regimen may not be as effective in spasm prevention.^6^ Of note, all spasms in this study were subclinical with no ECG changes present. Nitroglycerin was less effective when used in smaller doses or if several minutes had passed between nitroglycerin administration and start of PFA.^6^
Therefore, the authors proposed a pre-treatment strategy that included not only a pre-ablation bolus of nitroglycerin but also maintenance boluses every 2 min.^6^ In our patient, the total administration of nitroglycerin until the end of procedure time was only 3 min. Even if the recommended strategy would have been used, ablation was finished before the next anticipated nitroglycerin bolus (every 2 min). Yet, the initial dose of 2 mg nitroglycerin might have not been enough in our patient, although this is already on the higher margin of recommended doses.^3,6^
Interestingly, the occurrence of vasospasm during CTI ablation with PFA has been described not only with different catheter designs (large footprint,^7^ focal,^6^ and penta-spline design^3^) but also with different PFA waveforms, such as mono- and bipolar PFA.^3,7^ For now, this side-effect may be anticipated with any PFA device until proven otherwise.
Larger studies are needed to evaluate the timing, dose, and route of administration and the efficacy and safety of prophylactic nitroglycerin administration in the context of PFA-induced coronary spasms.
It remains unclear how the distance of the PFA catheter to the coronary artery relates to the severity of a spasm. Additionally, PFA dosing effects and ablation- to spasm-time warrant further investigation.
Limitations of this case presentation are the coronary angiography was not performed immediately. Due to the restoration of sinus rhythm with normalized ST segments after additional nitroglycerin doses, we decided to first gain patient informed consent and performed coronary angiography the following day to rule out severe arteriosclerosis. Furthermore, no biomarkers on myocardial tissue damage have been collected after the procedure.
To conclude, clinically manifest vasospasms shortly after PFA adjacent to coronary arteries can occur despite the prophylactic use of 2 mg intravenous nitroglycerin.
Until now, it remains unclear how much later in time such coronary spasms may occur and close post-PFA ECG monitoring of patients appears to be crucial.
Melanie A Gunawardene, Department of Cardiology and Intensive Care Medicine, Asklepios Hospital St. Georg, Lohmühlenstr. 5, Hamburg 20099, Germany; Department of Cardiology, University Hospital Giessen, Klinikstrasse 33, Giessen 35392, Germany; Semmelweis University, Üllői út 26, Budapest 1085, Hungary; DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, IEPT, N30, Martinistraße 52, Hamburg 20246, Germany.
Jens Hartmann, Department of Cardiology and Intensive Care Medicine, Asklepios Hospital St. Georg, Lohmühlenstr. 5, Hamburg 20099, Germany; Semmelweis University, Üllői út 26, Budapest 1085, Hungary.
Eike Tigges, Department of Cardiology and Intensive Care Medicine, Asklepios Hospital St. Georg, Lohmühlenstr. 5, Hamburg 20099, Germany; Semmelweis University, Üllői út 26, Budapest 1085, Hungary; DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, IEPT, N30, Martinistraße 52, Hamburg 20246, Germany.
Johanna Jezuit, Department of Cardiology and Intensive Care Medicine, Asklepios Hospital St. Georg, Lohmühlenstr. 5, Hamburg 20099, Germany; Semmelweis University, Üllői út 26, Budapest 1085, Hungary.
Stephan Willems, Department of Cardiology and Intensive Care Medicine, Asklepios Hospital St. Georg, Lohmühlenstr. 5, Hamburg 20099, Germany; Semmelweis University, Üllői út 26, Budapest 1085, Hungary; DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, IEPT, N30, Martinistraße 52, Hamburg 20246, Germany.
Dr Melanie Gunawardene is a German senior cardiac electrophysiologist, certified in catheter ablation of arrhythmias. Her research focuses on clinical studies regarding catheter ablation of atrial fibrillation and the implementation of new ablation technologies. She is based in Hamburg, Germany working for the Asklepios Hospital St. Georg. Currently, Dr Gunawardene serves as editor and reviewer of peer-reviewed journals and is a co-author of the German national AWMF guidelines on atrial fibrillation and faculty of the German Cardiac Society (EP nucleus) and a co-chair of the EHRA patient committee 2024–26.
Consent: The patient gave written informed consent to this publication. The original filled-out form from the EHJ Case report is stored at our institution. Additionally, the patient is participating of the ablation registry of the institution which has been approved by the local ethics committee. We confirm compliance with COPE guidelines. This case has not been published elsewhere.
Funding: None declared.
All relevant data are within the manuscript. No data have been shared.
All relevant data are within the manuscript. No data have been shared.