CVJA Volume 25, Issue 2

Page 55

AFRICA

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 2, March/April 2014

e1

Case Report Unusual perforation of the left ventricle during radiofrequency catheter ablation for ventricular tachycardia Jin-Tao Wu, Jian-Zeng Dong Case report

Abstract Cardiac perforation during catheter-based radiofrequency ablation procedures is relatively uncommon but potentially fatal if tamponade ensues. This complication should be promptly recognised. We present a case of incomplete perforation of the left ventricle with transient ST-segment elevation in leads V1 to V3 during catheter ablation of ventricular tachycardia. Complete perforation was avoided because of rapid diagnosis by the detection of subtle changes in electrode potentials and by performing angiography via an externally irrigated ablation catheter lumen. Keywords: cardiac perforation, tamponade, left ventricle, catheter ablation, ventricular tachycardia Submitted 27/3/13, accepted 9/12/13 Cardiovasc J Afr 2014; 25: e1–e4

www.cvja.co.za

DOI: 10.5830/CVJA-2013-087

Catheter-based radiofrequency ablation procedures are currently being performed in invasive laboratories with increasing frequency. An increased incidence of catheter-related complications may be encountered.1 One potentially fatal complication is acute haemorrhagic tamponade secondary to inadvertent cardiac perforation. Cardiac perforation should be promptly recognised to avoid subsequent tamponade. We present a case of incomplete perforation of the left ventricle with transient ST-segment elevation in leads V1 to V3 during catheter ablation of ventricular tachycardia (VT). Complete perforation was avoided because of rapid diagnosis by the detection of subtle changes in electrode potentials and by performing angiography via an externally irrigated ablation catheter lumen. This case study shows that physicians should be aware of the need to promptly recognise cardiac perforation.

Department of Cardiology, Henan Provincial People’s Hospital, Zhengzhou University, Zhengzhou, China Jin-Tao Wu, MD

Department of Cardiology, Centre for Atrial Fibrillation, Beijing Anzhen Hospital, Capital Medical University, Beijing, China Jian-Zeng Dong, MD, jz_d2007@aliyun.com

A 60-year-old woman with a history of drug-refractory paroxysmal VT underwent two unsuccessful catheter ablations at two different institutions nine years and one year previously. She was then referred to our centre for VT ablation. Her physical examination and chest X-ray were normal. Transthoracic echocardiography showed normal anatomical structure of the heart and left ventricular ejection fraction (60%). Arrhythmogenic right ventricular cardiomyopathy (ARVC) was excluded by myocardial magnetic resonance imaging. Percutaneous coronary artery angiography was performed before the ablation procedure and coronary artery disease was excluded. An electrophysiological study was then performed. Left subclavian vein access was obtained and a steerable 10-pole catheter (Inquiry™, IBI, St. Jude Medical, St Paul, MN, USA) was positioned in the coronary sinus. One quadripolar catheter (Cordis, Biosense Webster, Diamond Bar, CA, USA) was positioned in the right ventricle via left femoral vein access and another quadripolar catheter was positioned across the tricuspid valve to record the His bundle electrogram via right femoral vein access. Paroxysmal supraventricular tachycardia was excluded. The geometry of the right and left ventricle was reconstructed using the CARTO system with a 3.5-mm tip saline-irrigated ablation catheter (ThermoCool NaviStar, Biosense Webster). VT was induced by stimulation of the ablation catheter in the right ventricle (Fig. 1A, B). However, the tachycardia persisted for less than one minute before termination, and it was not induced again after termination. Pace mapping was then used first in the right ventricle, and then in the left. During mapping in the left ventricular apex, the heart at first failed to follow the impulse, and then the stimulation signal suddenly disappeared and the potential in the distal ablation catheter was significantly reduced (Fig. 2). Immediately after these findings were recognised, the catheter was slightly withdrawn. Subsequently, a stimulus signal occurred again. However, the ventricle still failed to respond to the stimulus signal (Fig. 2). Almost simultaneously, the patient complained of mild chest pain. A small amount of diluted contrast agent was then injected via the ablation catheter lumen to identify the location of the catheter tip. Angiography showed that the catheter had perforated the left ventricular apex, with the tip lying immediately under the epicardium (Fig. 3A, B). Subsequently, the ST segment in leads V1 to V3 was elevated (Fig. 4A), similar to what occurs in patients presenting with anteroseptal myocardial infarction. However, there was no significant change in blood pressure and heart rate in the patient and she did not complain of discomfort or mild chest pain.


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