Cardiac arrest due to late-onset coronary artery spasm after radiofrequency catheter ablation in a patient with an implantable cardioverter-defibrillator

Abstract

Coronary artery spasm (CAS) associated with catheter ablation is an important perioperative complication. Here we describe a case of late-onset CAS with cardiogenic shock that occurred five hours after ablation.

A 55-year-old man diagnosed with CAS previously underwent implantable cardioverter-defibrillator (ICD) implantation due to ventricular fibrillation. Inappropriate defibrillation was repeatedly conducted for frequent episodes of paroxysmal atrial fibrillation. Therefore, pulmonary vein isolation and linear ablation, including cava-tricuspid isthmus line, were performed. Five hours after the procedure, the patient experienced chest discomfort and lost his consciousness. Electrocardiogram monitoring of lead II revealed atrioventricular sequential pacing and ST-elevation. Cardiopulmonary resuscitation and inotropic support were immediately started. Meanwhile, coronary angiography revealed diffuse narrowing in the right coronary artery. Intracoronary infusion of nitroglycerin immediately dilated the narrowed lesion; however, the patient required intensive care with percutaneous cardiac pulmonary support and a left ventricular assist device. Pacing thresholds obtained immediately after cardiogenic shock were stable and almost similar to previous results. This showed that the myocardium was electrically responsive to ICD pacing but was unable to contract effectively due to ischemia.

Learning objective

Coronary artery spasm (CAS) associated with catheter ablation commonly occurs during ablation, but rarely as a late-onset complication. CAS may cause cardiogenic shock despite proper pacing of the dual chamber. Continuous monitoring of the electrocardiogram and arterial blood pressure is crucial for the early detection of late-onset CAS. Continuous infusion of nitroglycerin and admission into the intensive care unit after ablation may prevent fatal outcomes.

Introduction

Coronary artery spasm (CAS) associated with catheter ablation is an important perioperative complication [1], [2]. CAS may be caused by radiofrequency or cryothermal energy. However, it has also been reported that pulsed field ablation also causes CAS [3], [4]. Moreover, previous reports have demonstrated that intravenous infusion of isoproterenol or dexmedetomidine used during ablation can trigger CAS [5], [6].

CAS generally manifests with noticeable symptoms or ST-elevation during ablation [7]. However, cases of CAS leading to cardiogenic shock a few hours after ablation are rare. Herein, we report a case of late-onset CAS with cardiogenic shock in a patient with an implantable cardioverter-defibrillator.

Case report

A 55-year-old man was presented to the emergency room due to out-of-hospital cardiac arrest. Immediate electrical defibrillation against ventricular fibrillation (VF) that was judged by an automated external defibrillator successfully achieved restoration of sinus rhythm. The electrocardiogram during sinus rhythm did not show an ST-segment elevation in any leads; however, coronary angiography revealed an obstruction in the left anterior descending artery (LAD) (Fig. 1A). Percutaneous coronary intervention was performed, and a drug-eluting stent was placed at the proximal LAD. Following the procedure, the patient required intensive care, including hypothermia therapy.

Fig. 1.

A: Coronary angiography performed in the first hospitalization reveals LAD obstruction. B: Right coronary angiography shows well-developed collateral branches (white arrows) connected with the LAD. C & D: Coronary angiography before and after ergonovine loading test. Ergonovine loading induces coronary artery spasm and obstruction at the proximal site of the drug eluting stent (white dotted arrows) placed in the LAD.

The patients actually had few episodes of chest discomfort or pain before the hospitalization. Furthermore, he had only one risk factor of cardiovascular disease that was >45 years of age. Blood pressure, cholesterol level, glucose level, and body mass index were well controlled without treatment. He had no smoking history and family history associated with cardiovascular disease.

The peak of the serum creatine kinase-MB level was 15 ng/mL during the hospitalization. Moreover, the right coronary angiography revealed well-developed collateral branches connected with the LAD (Fig. 1B). The existence of the collateral branches and the laboratory test results indicated that VF was not caused by acute myocardial infarction. Therefore, the patient underwent implantable cardioverter-defibrillator (ICD) implantation based on the diagnosis of idiopathic VF.

One month after ICD implantation, the patient noted chest discomfort and lost his consciousness. The ICD recorded neither ventricular arrhythmia nor ICD malfunction. We diagnosed his condition as coronary artery spasm (CSA) after performing an ergonovine loading test (Fig. 1C & D). Benidipine hydrochloride and nifedipine were administered, and the patient responded well to drug therapy.

Oral anticoagulants and anti-arrhythmia drugs were added because frequent episodes of paroxysmal atrial fibrillation (AF) with palpitations were recorded by the ICD. However, repeated inappropriate defibrillation was conducted by the ICD despite maximum drug therapy, including amiodaron. Therefore, the patient underwent catheter ablation for AF.

The transthoracic echocardiogram obtained at the hospitalization showed a normal left ventricular ejection fraction of 65 % and the left atrial diameter of 40 mm. The left ventricle chamber dimensions were 47 in end-diastolic and 31 in end-systolic phase, respectively.

The strategy for catheter ablation was pulmonary vein (PV) isolation using an irrigated tip ablation catheter under general anesthesia. Radiofrequency pulses (30 W for 40 s or a lesion size index of 5.0) were delivered point by point and supported by a steerable introducer to gain adequate contact force and stability. Propofol and dexmedetomidine were used for general anesthesia. Despite achieving complete PV isolation, recurrent AF was recorded by the ICD three months after the first ablation, and rapid AF again caused inappropriate defibrillation. Therefore, a second ablation was performed six months after the first. This time, the strategy was re-isolation of the PV followed by linear ablations of the roof, floor, mitral isthmus, and cava-tricuspid isthmus line. Radiofrequency pulses delivered to each line was set at 30 W for 40 s or a lesion size index of 5.0, which was same to PV isolation. Chemical ablation infusing anhydrous ethanol into the vein of Marshall was also performed during this session. All procedures were successfully performed without any complications. Coronary angiography performed at the end of the session revealed slight narrowing lesion at the distal left circumflex artery (Fig. 2A). The electrocardiogram obtained just after ablation showed atrial paced and ventricular sensed rhythm without ST-segment elevation in any leads (Fig. 3A).

Fig. 2.

A: Coronary angiography performed at the end of ablation showing slight narrowing (white arrows) at the distal left circumflex artery near the area of coronary sinus ablation. B: Coronary angiography performed just after cardiac arrest showing diffuse narrowing (black arrows) of the right coronary artery. The previous narrowing in the left circumflex artery already improved.

Fig. 3.

A: A 12‑lead electrocardiogram recorded after ablation showed atrial paced and ventricular sensed rhythm without ST-segment elevation. B: Electrocardiogram monitoring five hours after ablation showing ST-segment elevation with a prolonged atrioventricular interval after the patient complained of chest discomfort. Cardiopulmonary resuscitation was started immediately after the patient lost consciousness despite atrioventricular sequential pacing. C: A 12‑lead electrocardiogram recorded in the catheter laboratory. The ST segments in the leads II, III, and aVF were slightly elevated, meanwhile reciprocal ST segment depressions were observed in leads V2–6.

Five hours after the procedure, the patient lost his consciousness after complaining of chest discomfort. He presented with pulseless electrical activity despite atrioventricular sequential pacing on the electrocardiogram monitoring (Fig. 3B), and lead II showed an ST-segment elevation. Cardiopulmonary resuscitation using a percutaneous cardiopulmonary support and a left ventricular assist device was immediately started. Coronary angiography was then performed, which revealed diffuse narrowing in the right coronary artery (Fig. 2B) that was dilated by intracoronary infusion of nitroglycerin. The pacing threshold of the right ventricle was 2.5 V at 0.4 ms, which was similar to the previous results. The patient was admitted into the intensive care with the abovementioned mechanical supports to recover the left ventricular wall motion. After withdrawing nitroglycerin infusion, isosorbide dinitrate patches were added to the patient's regular medications. Ultimately, the patient was discharged without any lasting effects. AF and CAS did not recur during the one-year follow up.

Discussion

A retrospective multicenter study reviewed the incidence of CAS related to AF ablation [7]. In that study, CAS occurred in 42 patients (0.19 %) of 22,232 AF ablation cases; of the 42 CAS cases, 40 (95 %) occurred during ablation, and late on-set CAS was observed in only 1/42 (2.5 %) patient. Tsushima et al. recently summarized five cases of late-onset CAS that occurred within three hours after ablation, and four out of them underwent cava-tricuspid isthmus ablation [8]; in two cases, electrical defibrillation was required to restore sinus rhythm due to ventricular fibrillation. In our case, CAS occurred five hours after ablation, which was later compared to previous cases of late-onset CAS. Furthermore, the ICD in our patient failed to prevent cardiac arrest. Although electrocardiogram monitoring showed atrioventricular sequential pacing against an atrioventricular block, the patient presented with pulseless electrical activity and cardiogenic shock. This suggests that the ICD pacing evoked an electrical response from myocardium, but myocardial contractility was weak due to severe ischemia.

CAS associated with ablation procedure can also be caused by anesthetic drugs such as dexmedetomidine, thiopental, and propofol. Some papers have recently reported that CAS occurred immediately after intravenous infusion of these anesthetic drugs and prior to radiofrequency or cryothermal energy delivery [5], [6]. In our case, dexmedetomidine and propofol were intravenously infused during the procedure. However, the relationship between anesthetic drugs and late-onset CAS remains unclear.

Late-onset CAS can be a fatal even in the hospital because cardiac arrest occurs outside the catheter laboratory. Hence, preventing this predictable cardiac arrest must be a priority. In our case, we did not administer regular medicines, including benidipine hydrochloride and nifedipine, just before the procedure because ablation was performed under general anesthesia. In contrast, nitroglycerin should continuously be infused to prevent CAS during the perioperative period. Additionally, dexmedetomidine and propofol should be avoided during the procedure. Moreover, intensive monitoring, including arterial blood pressure monitoring, in the intensive care unit should be considered. Although it would be ideal to immediately notice cardiac arrest in these patients, we were fortunate to notice the event as the patient initially complained of chest discomfort despite the electrocardiogram monitor showing a normal atrioventricular sequential pacing. Finally, we should temporarily set a maximum output amplitude of the ICD pacing during the perioperative period. It is possible to extensively capture the myocardial status and its effective ventricular contraction. This case highlights several clinical implications to prevent fatal outcomes.

Conclusions

We experienced a case of late-onset CAS five hours after AF ablation, which caused cardiac arrest despite ICD pacing. Countermeasures during the perioperative period are crucial to prevent fatal outcomes.

Patient permission/consent statement

Informed consent was obtained from the patient and patient's family for publication of the case and accompanying images.

Declaration of competing interest

Yoshio Kobayashi has received remuneration for lectures from Amgen Astellas BioPharma Co., Ltd., Bristol-Myers Squibb Co., and Boehringer Ingelheim and scholarships from Medtronic Japan Co. Ltd., Daiichi Sankyo, Inc., Abbott Vascular Japan Co., Ltd., Boston Scientific Corp., Otsuka Pharmaceutical Co., Ltd., Pfizer Inc., Astellas Pharma Inc., Takeda Pharmaceutical Co., Ltd., and Japan Lifeline Co., Ltd. The rest of the authors have no conflicts of interest.