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Utility of Compound Motor Action Potentials as a Superior Predictor of Phrenic Nerve Injury in Cryoballoon Ablation of Atrial Fibrillation
1535-2226
Introduction
Pulmonary vein isolation (PVI) is an effective therapy for symptomatic, drug-refractory paroxysmal atrial fibrillation (AF). Radiofrequency ablation (RFA) has long been the standard of care, while cryoballoon technology has emerged as a novel approach with promising results in paroxysmal AF.1 Phrenic nerve palsy (PNP) remains the most dreaded complication associated with cryoballoon-based PVI.2 We sought to characterize our experience with different monitoring techniques for phrenic nerve injury in a patient who developed a transient PNP during cryoablation of paroxysmal AF.
Case Description
A 61-year-old male with paroxysmal AF (CHA2DS2-VASc score of 1, HAS-BLED score of 0) since July 2014 was referred for cryoballoon ablation for pulmonary vein isolation. No structural heart disease or thrombus was noted on preprocedural echocardiogram.
An ablation procedure was performed under general anesthesia with intermittent positive pressure ventilation (endotracheal tube). Maintenance of anesthesia was done with oxygen, air, and isoflurane. A 6 French (Fr) deflectable decapolar catheter was inserted in the coronary sinus via left femoral venous access. Left atrial access was obtained via single transseptal puncture under transesophageal echocardiography (TEE) and fluoroscopic guidance. After transseptal access, intravenous heparin was administered as a bolus (100 IU/kg) to maintain an activated clotting time >300 seconds. Thereafter, the standard transseptal sheath was exchanged with a 15 Fr steerable sheath, through which a second-generation 28 mm cryoballoon and 20 mm 8-pole circular recording catheter were advanced into the left atrium. The cryoballoon was inflated within the left atrium under fluoroscopic and TEE guidance, and advanced to the PV ostium. A mapping catheter was then repositioned as proximally to the PV ostium as possible, without compromising the degree of pulmonary venous occlusion. Occlusion was assessed by distal contrast injection. Left-sided pulmonary veins were electrically isolated for a maximum of 180 seconds.
Prior to ablation of the right-sided pulmonary veins, the right phrenic nerve was paced at 75 beats/min at an amplitude of 20 V with a 3.0 ms pulse width using a 6 Fr quadripolar catheter in the superior vena cava. Right hemidiaphragmatic excursion was monitored by continuous abdominal palpation. In addition, a stable surface compound motor action potential (CMAP) was continuously recorded. (A surface CMAP was recorded on modified lead I by placing a standard surface right arm EKG electrode 5 cm above the xiphoid, and a left arm EKG electrode 16 cm along the right costal margin.2 Studies have shown that a decrease in CMAP amplitude by 35% from baseline predicted phrenic nerve injury).3,4
In this procedure, we used diaphragmatic excursion during pacing as the predictor for phrenic nerve injury, as per company recommendation. CMAP was also monitored but not used as the primary tool, due to a perception that there may be confounding impact of variation in amplitude due to respiration.
During this ablation, at 95 seconds after initiating the freeze in the right superior PV (temperature -41º C), there was a loss of diaphragmatic motion. Therefore, ablation was terminated with forced balloon deflation by ‘double-tap’ technique. The phrenic nerve function returned 15 minutes after stopping the ablation. Subsequently, the right inferior PV isolation was completed.
We later analyzed the CMAP tracing and found there was an initial change in amplitude of CMAP signal when we started the freeze (Figure 1). This was due to respiratory variation. At 12 seconds of freeze (temperature -1º C), the amplitude started progressively decreasing from the baseline value (Figures 2 and 3), followed by complete absence of CMAP signals at 72 seconds when the temperature was -39 ºC (Figure 4). This decrease in amplitude was obvious even after taking into account the intermittent respiratory variation. It is important to note that during this period, the diaphragmatic excursion remained intact as monitored by pacing-palpation technique. Therefore, CMAP amplitude variation significantly preceded the diaphragmatic motion loss. If we had used the former as a monitoring tool, this complication might have been avoided. In published studies, the average time interval from CMAP amplitude decrease of 35% to palpable phrenic nerve injury was 59 seconds (range 30-110 seconds).4 In the present case, it was 83 seconds.
Conclusion
This case illustrates that electromyographic phrenic nerve monitoring using the surface CMAP seems to be more reliable, easy to perform, and offers an “early warning” for impending phrenic nerve injury. It may be considered as a primary monitoring tool to avoid phrenic nerve injury during cryoballoon-based PVI procedures.
Disclosures: The authors have no conflicts of interest to report regarding the content herein.
References
- Packer DL, Kowal RC, Wheelan KR, et al; STOP AF Cryoablation Investigators. Cryoballoon ablation of pulmonary veins for paroxysmal atrial fibrillation: first results of the North American Arctic Front (STOP AF) pivotal trial. J Am Coll Cardiol. 2013;61:1713-1723.
- Mondésert B, Andrade JG, Khairy P, et al. Clinical experience with a novel electromyographic approach to preventing phrenic nerve injury during cryoballoon ablation in atrial fibrillation. Circ Arrhythm Electrophysiol. 2014;7:605-611.
- Franceschi F, Dubuc M, Guerra PG, et al. Diaphragmatic electromyography during cryoballoon ablation: a novel concept in the prevention of phrenic nerve palsy. Heart Rhythm. 2011;8:885-891.
- Lakhani M, Saiful F, Parikh V, Goyal N, Bekheit S, Kowalski M. Recordings of diaphragmatic electromyograms during cryoballoon ablation for atrial fibrillation accurately predict phrenic nerve injury. Heart Rhythm. 2014;11:369-374.
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