From September 2006 to May 2010, a total of 318 patients without structural heart disease were presented for catheter ablation for PVCs in our hospital. Only patients with idopthic PVCs from the left ventricular septum were enrolled in the present study. All patients were verified as having no structural heart disease, including coronary artery disease, valvular heart disease, congenital heart disease, left ventricle hypertrophy, and right ventricle abnormalities by routine biochemistry tests, X-ray, color echocardiography examination, exercise electrocardiogram testing, and/or cardiac catheterization with coronary angiography. Before RFCA, a 12-lead ECG was obtained, and 24 hours ambulatory ECG monitoring (Holter) was carried out at least once. The ECG was monitored for 24 hours just before catheter ablation.

The selection criteria of patients were the following reasons: (1) frequent PVCs occurrence, the average PVC count ≥ 10000 times/24 h; (2) inability of the patient to tolerate PVCs or unsuccessful treatment with at least two antiarrhythmic drugs; (3) no structural heart disease; and (4) consent for the catheter ablation procedure.

Twelve-lead electrocardiograms of the clinical arrhythmia were available for all patients with PVCs originating from the left ventricular septum. The analysis of ECG pattern was focusing on the following characteristics: (1) The QRS morphology of the PVC in all 12 leads, (2) the duration of QRS complex, (3) the axis deviation.

Electrophysiologic study was performed after withdrawal of all anti-arrhythmic drugs for at least five half-lives. Under fluoroscopic guidance, two quadripolar electrode catheter (Cordis, USA) were advanced from the right femoral vein and positioned in the right ventricular apex and near the His bundle. One additional catheter was inserted via the internal jugular vein and positioned in the coronary sinus. A 12-lead surface electrocardiogram was monitored and recorded on a multichannel oscilloscopic recorder. Programmed electrical stimulation was performed from right ventricular apex at basic drive cycle lengths of 600, 500, and 430 msec, delivering a maximum of three extrastimuli. A 7F quadripolar deflectable catheter was advanced into the left ventricle using retrograde aortic approach via the right femoral artery for mapping and ablation (Cordis, USA). The mapping/ablation catheter has a 4 mm distal electrode, with interelectrode spacing of 2-5-2 mm. Pace mapping and endocardial activation mapping were performed. If the clinical arrhythmia did not occur spontaneously and was not induced in the baseline, intravenous isoproterenol (2-4 μg/min) was administered to induce arrhythmia.

The target site of RFCA was determined by two steps:1) a careful search was firstly performed for Purkinje potentials preceding the onset of QRS during sinus rhythm along the left ventricular septum in all patients, and radiofrequency energy was delivered at sites demonstrating local endocardial recording with earliest presystolic Purkinje potentials during PVCs, or in sinus rhythm if there was insufficient ectopy to permit activation mapping; 2) next step is to obtain the complete or near complete pace mapping with the earliest local activation time if RFCA is not successful, and when the PVC occurred rarely during the electrophysiologic study, only pace mapping was performed, aiming to identify the site where pacing reproduced QRS morphology that is similar to the clinical PVC (≧ 11/12-lead concordance of major and minor deflections). After the target site was located, the energy of RFCA was delivered using maximum power of 40 W, maximum temperature of 60°C and impedance of 80-140 Ωin the temperature-controlled mode. If the PVC was terminated within 10 seconds or frequently PVCs and/or nonsustained ventricular tachycardia occurred during ablation at the target site, additional current was applied for another 60 to 180 seconds. Successful ablation was defined as complete elimination of spontaneous or inducible ventricular arrhythmias. Programmed electrical stimulation was repeated at 30 minutes after the last application of radiofrequency energy to confirm the absence of inducible ventricular arrhythmias before removing all catheters and sheaths. If PVC did not terminate within 10 s, the radiofrequency energy application was terminated and another target site was sought.

Successful ablation was defined as the absence of spontaneous or induced clinical PVC and ventricular tachycardia, both with or without isoproterenol at the end of the procedure. Absence of PVC or ventricular tachycardia in ECG monitoring over 48 hours without anti-arrhythmia drugs. No recurrence of arrhythmia in the absence of anti-arrhythmic drug therapy during follow-up.

After RFCA, all patients underwent 72-hour ECG monitoring. Holter was carried out one week after RFCA. Patients were not given any antiarrhythmic drugs after RFCA, and underwent color echocardiography and Holter examination three month after RFCA. ECG echocardiography and 24-hour ECG monitoring were performed whenever the patient had symptoms suggestive of recurrence of ventricular arrhythmias..

PVC was considered to originate from the left ventricular septum, not from the left anterior and posterior fascicles, based on (1) the local endocardial recordings; (2) the characteristic of left ventricular septum location and motion (when viewed in the right and left anterior oblique fluoroscopic views after successful RFCA); (3) programmed electrical stimulation could not induce sustained ventricular tachycardia; (4) unsuccessful ablation at Purkinje potential site, and (5) purkinje potentials were not identified at successful sites during point mapping.

Ethical approval was obtained from the Ethics Committee of the Second Affiliated Hospital of Wenzhou Medical College, and all patients gave informed consent before participation in the study.

A total of 20 patients (10 males and 10 females) were enrolled in the present study. Among patients with idiopathic ventricular ectopy, the incidence of left septal ventricular arrhythmias was 6.29% (Table 1). PVCs in 8 of 318 patients originated from fascicles (Table 1). The mean PVC burden during the preoperative 24 hours ambulatory Holter monitoring was 17774.05 ± 5861.66.

First, the mechanism of the PVCs arising from the left ventricular septum is thought to be due to enhanced antomaticity, but not reentry, but this remains speculative in the limited clinical study. Second, although the PVCs may occur from the myocardium of the septum, instead of the Purkinje network, it is unknown that how distributed were these septal sites. To increase the accuracy of our study, our results need to be confirmed in a larger prospective randomized patient population.