Phrenic nerve injury: An underrecognized and potentially preventable complication of pulmonary vein isolation using a wide-area circumferential ablation approach.

INTRODUCTION: Phrenic nerve injury (PNI) is a well-known, although uncommon, complication of pulmonary vein isolation (PVI) using radiofrequency energy. Currently, there is no consensus about how to avoid or minimize this injury. The purpose of this study was to determine how often the phrenic nerve, as identified using a high-output pacing, lies along the ablation trajectory of a wide-area circumferential lesion set. We also sought to determine if PVI can be achieved without phrenic nerve injury by modifying the ablation lesion set so as to avoid those areas where phrenic nerve capture (PNC) is observed. METHODS AND RESULTS: We prospectively enrolled 100 consecutive patients (age 61.7 ± 9.2 years old, 75 men) who underwent RF PVI using a wide-area circumferential ablation approach. A high-output (20 mA at 2 milliseconds) endocardial pacing protocol was performed around the right pulmonary veins and the carina where a usual ablation lesion set would be made. A total of 30% of patients had PNC and required modification of ablation lines. In the group of patients with PNC, the carina was the most common site of capture (85%) followed by anterior right superior pulmonary vein (RSPV) (70%) and anterior right inferior pulmonary vein (RIPV) (30%). A total of 25% of PNC group had capture in all 3 (RSPV, RIPV, and carina) regions. There was no difference in the clinical characteristics between the groups with and without PNC. RF PVI caused no PNI in either group. CONCLUSION: High output pacing around the right pulmonary veins and the carina reveals that the phrenic nerve lies along a wide-area circumferential ablation trajectory in 30% of patients. Modification of ablation lines to avoid these sites may prevent phrenic nerve injury during RF PVI.

Electrophysiologic study: its predictive value for ventricular arrhythmias.

Studies have shown the predictive value of inducible ventricular tachycardia and clinical arrhythmia in patients who have structural heart disease. We examined the possible predictive value of electrophysiologic study before the placement of an implantable cardioverter-defibrillator. Our retrospective study group comprised 315 patients who had ventricular tachycardia that was inducible during electrophysiologic study and who had undergone at least 1 month of follow-up (247 men; mean age, 66.9 +/- 13.5 yr; mean follow-up, 24.9 +/- 14.8 mo). Recorded characteristics included induced ventricular tachycardia cycle length, atrio-His and His-ventricular electrograms, PR and QT intervals, QRS duration, and drug therapy. Of the 315 patients, 97 experienced ventricular arrhythmia during the follow-up period, as registered by 184 of more than 400 interrogations. There were 187 episodes of ventricular arrhythmia (tachycardia, 178; fibrillation, 9) during 652.5 person-years of follow-up. Subjects with a cycle length > or =240 msec were more likely to have an earlier 1st arrhythmia than those with a cycle length <240 msec (P=0.032). A quarter of the subjects with a cycle length > or =240 msec had their 1st arrhythmia by 19.14 months, compared with 23.8 months for a quarter of the subjects with a cycle length <240 msec (P <0.032). Among the electrophysiologic characteristics examined, inducible ventricular tachycardia with a cycle length > or =240 msec is predictive of appropriate implantable cardioverter-defibrillator therapy at an earlier time. This may have prognostic implications that warrant implantable cardioverter-defibrillator programming to enable appropriate antitachycardia pacing in this group of patients.

Dual atrioventricular-nodal physiology, elicited by pacing and leading to a reversible cardiomyopathy.

Atrioventricular nodal re-entry tachycardia is the most common form of regular paroxysmal tachycardia in the adult population. This tachycardia is a re-entrant rhythm that uses the anatomic location of the atrioventricular node and its surrounding perinodal atrial tissue. The simplest concept regarding the atrioventricular nodal physiology that allows re-entry is founded upon the postulated existence of 2 atrioventricular nodal pathways with different conduction velocities and refractory periods. Herein, we present the case of a 64-year-old man who had a history of paroxysmal atrial fibrillation; he had a permanent pacemaker for sick-sinus syndrome. He developed a tachycardia-induced cardiomyopathy with a perpetual dual response to the pacemaker stimulus. The tachycardia displayed characteristic dual atrioventricular-nodal physiology that was suppressed by amiodarone therapy, leading to a reversal of the cardiomyopathy. We discuss the mechanisms that surround such phenomena.

Clinical investigation: Utility of left ventricular end diastolic diameter in the prediction of susceptibility to ventricular tachyarrhythmias.

BACKGROUND: Prior studies have shown the utility of using both QRS duration and QT dispersion (QTd) as predictors of risk for ventricular tachyarrhythmias (VA). Lengthening of the QRS duration represents dyssynchrony of regional myocardial wall contraction, and increased QTd similarly represents variations in myocardial repolarization. We sought to examine the left ventricular end diastolic diameter (LVEDD) as a predictor of VA susceptibility. METHODS: Eighty-eight patients referred for electrophysiologic (EP) studies were evaluated. EP testing was performed using a standard protocol of up to three extrastimuli. QTd and QRS duration analyses were performed in a blinded manner. Values were defined as abnormal if QRS duration>120 ms, QTd>60 ms, and LVEDD>6 cm. RESULTS: Of 88 patients (65 males; 23 females; mean age 67+/-15 years), 33 were inducible by EP testing. Patients with either increased QRS duration or QTd are shown to be at greater risk for VA inducibility. LVEDD is a strong predictor of inducibility for VA (p<0.02 between inducible and non-inducible patients). LVEDD in combination with QRS duration and QTd, further strengthens predictability for VA (p<0.03 for QRS duration and p<0.02 for QTd) with a trend towards inducibility as each value increases. Combination of the three parameters of QRS duration, QTd, and LVEDD was 91% sensitive for the identification of those patients inducible for VA. CONCLUSION: The LVEDD is an echocardiographic value that strongly predicts VA inducibility, and when combined with QRS duration and QTd, identifies patients at higher risk for these tachyarrhythmias.