(Circulation. 2008;117:e471.)
© 2008 American Heart Association, Inc.
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From the Hôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France.
Correspondence to Seiichiro Matsuo, MD, Service de Rythmologie, Hôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Adress: Avenue de Magellan, 33604 Bordeaux-Pessac, France. E-mail mattsuu{at}tc4.so-net.ne.jp
A 38-year-old man with a history of arrhythmogenic right ventricular cardiomyopathy and right ventricular hypokinesia was referred for catheter ablation of an incessant symptomatic ventricular tachycardia resistant to antiarrhythmic drugs. Twelve-lead electrogram during tachycardia revealed wide QRS complexes negative in V1 and positive in inferior leads, suggesting a right ventricular outflow tract origin. An electrophysiological study was performed, and surprisingly, endocardial activation of the tachycardia was earliest in the left ventricle, on the lateral wall. The earliest recorded endocardial potential was 20 ms before the QRS, but 5 radiofrequency applications using an externally irrigated ablation catheter (Thermocool, Biosense Webster, Diamond Bar, Calif) failed to terminate the tachycardia.
A subxiphisternal pericardial puncture was performed to gain access to the pericardial space and the epicardium. With this approach, the origin of the arrhythmia was confirmed as the high lateral left ventricular wall, with earlier epicardial activation compared with endocardial activation. A perfect pace map was obtained; however, it was accompanied by phrenic nerve capture. One hundred milliliters of air were then injected via the hemostatic sheath into the pericardium to create a space between the phrenic nerve and the ablation catheter (Figure and Movie). The patient remained hemodynamically stable throughout the procedure. After air injection, we could not capture the phrenic nerve with high-output pacing. Radiofrequency energy was delivered with fluoroscopic monitoring to continually assess diaphragmatic movement, and the tachycardia was terminated within a few seconds without complication. After successful ablation, the air was aspirated, and the patient has had no recurrence of ventricular tachycardia.
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The present case describes an original technique to prevent phrenic nerve injury during epicardial ablation, without which we would have been unable to proceed. Although epicardial catheter ablation can cure arrhythmia resistant to endocardial ablation,1 the risk of collateral damage to adjacent structures is increased with the epicardial approach, including the left phrenic nerve injury given its close contact to the left lateral ventricular wall.2 Careful monitoring of both blood pressure and diaphragmatic movement is necessary with this maneuver to prevent iatrogenic tamponade and phrenic nerve injury, respectively. There may be more applications of this novel technique, including atrial fibrillation ablation, given that phrenic nerve damage can occur in this procedure.3
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2. Rumbak MJ, Chokshi SK, Abel N, Abel W, Kittusamy PK, McCormack J, Patel MM, Fontanet H. Left phrenic nerve paresis complicating catheter radiofrequency ablation for Wolff-Parkinson-White syndrome. Am Heart J. 1996; 132: 1281–1285.[CrossRef][Medline] [Order article via Infotrieve]
3. Sacher F, Monahan KH, Thomas SP, Davidson N, Adragao P, Sanders P, Hocini M, Takahashi Y, Rotter M, Rostock T, Hsu LF, Clémenty J, Haïssaguerre M, Ross DL, Packer DL, Jaïs P. Phrenic nerve injury after atrial fibrillation catheter ablation: characterization and outcome in a multicenter study. J Am Coll Cardiol. 2006; 47: 2498–2503.
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