Editorial CommentElectrode catheter ablation (ECA) is a well-established treatment modality for patients with cardiac arrhythmias. 1 Depending on the characteristics of each arrhythmia, the technique of ECA can be relatively simple or rather complex. In general, the risk of ECA complications is determined by the ECA tool and energy source used, the anatomic location of the tissue targeted and the learning curve (experience) of the electrophysiology team involved. Potential serious complications include excessive bleeding, cardiac perforation (cardiac tamponade), atrioventricular conduction block, valvular disruption, coronary artery spasms/injury (myocardial infarction), cerebrovascular embolism (stroke), phrenic nerve injury (PNI), left atrio-esophageal fistula, and ventricular tachycardia/fibrillation (circulatory collapse/cardiac arrest). Although the incidence of these complications is generally low (1-3%), they may cause significant morbidities and even mortality. 2 In this issue of Journal of Cardiovascular Electrophysiology, Bai et al. 3 described 17 cases of PNI (16 right sided and 1 left sided) after ECA of cardiac arrhythmias. This series was gathered from three centers over a period of 6 years (December 1999 to December 2005). Since various ECA tools and energy sources had been applied for different arrhythmias, the true incidence of PNI could not be accurately addressed. However, it was noted that 13 of 1,300 cases (0.1%), 1 of 160 cases (0.6%), 2 of 35 cases (6%), and 1 of 20 cases (5%) were associated with the use of radiofrequency, cryothermal, ultrasound, and laser energies, respectively. Of the 16 cases with right-sided PNI, 13 had ECA for atrial fibrillation (AF) and 3 for sinus node modification. In the remaining case with left-sided PNI, epicardial mapping followed by ablation was performed for idiopathic left ventricular tachycardia.All patients were followed up for 30.1 ± 16.7 (3-52) months. Two patients had transient PNI that resolved immediately following the procedure, and the other 15 had persisted PNI that recovered within a mean time of 7.7 ± 6.3 (3-28) months. Although most of these patients were asymptomatic, subsequently one developed pneumonia apparently related to PNI, and another one had pulmonary insufficiency requiring temporary mechanical ventilator support at night. As all patients eventually had full recovery of phrenic nerve function,