The glucagon-like peptide-1 receptor agonist liraglutide improves hypoxia-induced pulmonary hypertension in mice partly via normalization of reduced ET(B) receptor expression.

The glucagon-like peptide-1 receptor (GLP-1R) agonist liraglutide is an incretin hormone mimetic used in the treatment of diabetes. However, the effects of liraglutide on pulmonary hypertension (PH) and pulmonary endothelin (ET) system are unknown. Eight-week-old C57BL6/J mice were injected liraglutide or vehicle for 5 weeks. One week after injection, the mice were exposed to either room air (normoxia) or chronic hypoxia (10 % O(2)) for 4 weeks. The right ventricular systolic pressure (RVSP) was significantly higher in hypoxia + vehicle group than in normoxia + vehicle group. ET-1 mRNA expression in the lungs was comparable among all the groups. ET(B) mRNA and protein expression in the lungs was significantly lower in hypoxia + vehicle group than in normoxia + vehicle group. The above changes were normalized by liraglutide treatment. The expression of phospho-eNOS and phospho-AMPK proteins in the lungs was significantly higher in hypoxia + liraglutide group than in normoxia + vehicle group. We demonstrated for the first time that liraglutide effectively improved RVSP and RV hypertrophy in hypoxia-induced PH mice by activating eNOS through normalization of impaired ET(B) pathway and augmentation of AMPK pathway. Therefore, GLP-1R agonists can be promising therapeutic agents for PH.

Which are the most reliable predictors of recurrence of atrial fibrillation after transcatheter ablation?: a meta-analysis.

CONTEXT: Transcatheter ablation of atrial fibrillation (AF) has undergone important development, with acceptable midterm results in terms of the safety and recurrence. A meta-analysis was performed to identify the periprocedural complications, midterm success rates and predictors of recurrence after AF ablation. METHODS AND RESULTS: 4357 patients with paroxysmal AF, 1083 with persistent AF and 1777 with long standing AF were included. The pooled analysis showed that there was an in-hospital complication rate of tamponade requiring drainage of 0.99% (0.44-1.54; CI 99%), stroke with neurological persistent impairment of 0.22% (0.04-0.47; CI 99%), and stroke without of 0.36% (0.03-0.70; CI 99%) After a follow up of 22 (13-28) months and 1.23 (1.19-1.5; CI 99%) procedures per patient, the AF recurrence rate was 31.20% (24.87-34.81; CI 99%). The persistent AF patients exhibited a greater risk of recurrence after the first ablation (OR 1.78 [1.14, 2.77] CI 99%), but a trend towards non significance was present in the patients with more than one procedure (OR 1.69 [0.95, 3.00] CI 99%). The most powerful predictors of an AF ablation failure in the overall population were a recurrence within 30-days (OR 4.30; 2.00-10.80), valvular AF (OR 5.20; 2.22-9.50) and a left atrium diameter of more than 50mm (OR 5.10 2.00-12.90; all CI 95%). CONCLUSIONS: Persistent AF remains burdened from higher recurrence rates, however not so following redo-procedures. Three predictors, valvular AF, a left atrium diameter longer than 50mm and recurrence within 30 days, could be appraised to drive selection of patients and therapeutic strategy.

Impact of serum flecainide level on control of atrial fibrillation in a case treated with cardiac resynchronization therapy.

A 72-year-old male patient with dilated cardiomyopathy was treated with oral flecainide (100 mg/day) for persistent atrial fibrillation (AF) that could not be converted to sinus rhythm by electrical cardioversion. Initiation of flecainide treatment provided sinus rhythm without prolongation of QRS and QTc, bradycardia and first-degree atrioventricular block at a serum flecainide level of 438 ng/mL. Then, he received cardiac resynchronization therapy (CRT). Dose reduction to 50 mg/day because of stabilization of heart rate after CRT produced AF at a serum flecainide level of 270 ng/mL. Electrical cardioversion did not restore the AF to a sinus or pacing rhythm. Dose escalation of flecainide (to 100 mg/day) restored the pacing rhythm at a serum flecainide level of 401 ng/mL. This case suggests that in the Japanese population, serum flecainide level should be maintained at >300 ng/mL to control AF even after effective CRT.

Tissue factor expression as a possible determinant of thromboembolism in ovarian cancer.

Ovarian cancer, and clear cell carcinoma in particular, reportedly increases the risk of venous thromboembolism (VTE). However, the mechanisms remain unclear. Tissue factor (TF) supposedly represents a major factor in the procoagulant activities of cancer cells. The present study examined the involvement of TF expression in VTE for patients with ovarian cancer. Subjects comprised 32 consecutive patients (mean age 49.8 years) with histologically confirmed ovarian cancer. Presence of VTE was examined using a combination of clinical features, D-dimer levels and venous ultrasonography. Immunohistochemical analysis was used to evaluate TF expression into 4 degrees. Venous thromboembolism was identified in 10 of the 32 patients (31%), including five of the 11 patients with clear cell carcinoma. Tissue factor expression was detected in cancer tissues from 24 patients and displayed significant correlations with VTE development (P=0.0003), D-dimer concentration (P=0.003) and clear cell carcinoma (P<0.05). Multivariate analysis identified TF expression as an independent predictive factor of VTE development (P<0.05). Tissue factor (TF) expression is a possible determinant of VTE development in ovarian cancer. In particular, clear cell carcinoma may produce excessive levels of TF and is more likely to develop VTE.

Clinical characteristics of rapid atrial fibrillation preceding ventricular tachycardia.

Spontaneous degeneration of rapid atrial fibrillation (AF) to ventricular fibrillation has been documented in patients with hypertrophic cardiomyopathy (HCM) and Wolff-Parkinson-White (WPW) syndrome. However, the importance of rap

Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia.

OBJECTIVES: The purpose of this study was to determine the relation of diastolic and presystolic potentials recorded during verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) to reentry circuit. BACKGROUND: Successful ablation of verapamil-sensitive ILVT at the zone of slow conduction from which the diastolic potential is recorded has been reported. However, the relationship between the diastolic potential and the reentrant circuit remains a matter of debate. METHODS: Radiofrequency (RF) ablation was performed in 20 patients with verapamil-sensitive ILVT. After identifying the ventricular tachycardia (VT) exit site, we searched for the mid-diastolic potential (P1) during VT. Entrainment followed by RF current application was performed. If the mid-diastolic potential could not be detected, RF current was applied at the VT exit site showing the earliest ventricular activation with a single fused presystolic Purkinje potential (P2). RESULTS: In 15 of 20 patients, both P1 and P2 were recorded during VT from midseptal region. Entrainment pacing captured P1 orthodromically and reset the VT. The interval from stimulus to P1 was prolonged as the pacing rate was increased. Radiofrequency ablation was successfully performed at this site in all 15 patients. After successful ablation, P1 appeared after the QRS complex during sinus rhythm with the identical sequence to that during VT. In the remaining five patients, the diastolic potential could not be detected, and a single fused P2 was recorded only at the VT exit site. Successful ablation was performed at this site in all five patients. CONCLUSIONS: This study demonstrates that P1 and P2 are critical potentials in a circuit of verapamil-sensitive ILVT and suggests the presence of a macroreentry circuit involving the normal Purkinje system and the abnormal Purkinje tissue with decremental property and verapamil-sensitivity.

Pilsicainide for conversion and maintenance of sinus rhythm in chronic atrial fibrillation: a placebo-controlled, multicenter study.

BACKGROUND: Pilsicainide is a newly synthesized antiarrhythmic agent with class Ic properties. Various antiarrhythmic agents have been used to convert atrial fibrillation (AF) to sinus rhythm or decrease the rate of relapse of AF. METHODS: We randomly assigned 62 patients with chronic AF to oral treatment of either a placebo (10 patients) or 150 mg/day of pilsicainide (52 patients) for 4 weeks before electrical cardioversion. Before oral administration of pilsicainide, 41 patients underwent transesophageal echocardiography to investigate whether there was thrombus formation in the heart chambers. Patients without pharmacologic defibrillation underwent direct current cardioversion to restore sinus rhythm. After successful cardioversion, all patients continued to receive pilsicainide and were monitored for up to 2 years. RESULTS: Before cardioversion, 11 patients in the pilsicainide group (21%) reverted to sinus rhythm. No patients in the placebo group reverted to sinus rhythm. Direct current cardioversion was performed in 51 patients; however, 8 patients were not converted to sinus rhythm (5 patients receiving pilsicainide, 3 patients receiving placebo), and 3 patients needed intracardiac cardioversion to convert to sinus rhythm. Asymptomatic bradyarrhythmias were observed in 5 patients in the pilsicainide group. During the follow-up period, 33 patients (71%) in the pilsicainide group remained in sinus rhythm at 1 month; this number decreased to 23 patients (49%) at 3 months, 20 (43%) at 6 months, 16 (34%) at 12 months, 16 (34%) at 18 months, and 16 (34%) at 24 months. All patients receiving placebo continued to receive placebo after the cardioversion, and AF recurred a few days after cardioversion in all cases. No independent discriminant variables were identified in the groups between maintenance and nonmaintenance of sinus rhythm. Although no serious side effects regarding pilsicainide have been documented, one patient died of acute myocardial infarction, most likely not related to pilsicainide administration. CONCLUSIONS: Pilsicainide is effective in restoring or maintaining sinus rhythm in patients with chronic AF lasting longer than an average duration of 22 months. No major adverse effects were observed.

Successful radiofrequency catheter ablation from the supravalvular region of the aortic valve in a patient with outflow tract ventricular tachycardia.

Outflow tract ventricular tachycardia (OT-VT) was successfully ablated from the right coronary cusp of the aortic valve. The 12-lead ECG was totally different from the typical right ventricular OT-VT because the R/S ratio in precordial lead V1 was equal to 1 and tall R waves in precordial leads V2-6 were seen. Radiofrequency energy application from the right coronary cusp of the aortic valve successfully ablated this VT without complications. Radiofrequency catheter ablation from the right coronary cusp of the aortic valve can be done safely and effectively.

Nonlinear ablation targeting an isthmus of critically slow conduction detected by high-density electroanatomical mapping for atypical atrial flutter.

Focused high-density atrial endocardial mapping was performed with a three-dimensional electroanatomical mapping system or a multielectrode basket catheter in six men and two women (mean age = 54 years) with atypical atrial flutter (AFL) to characterize its reentry circuit and identify its isthmus of critically slow conduction (ICSC). Activation mapping revealed figure-8 reentry with ICSC between a surgical atrial scars in three atypical AFLs following atriotomy, and between the crista terminalis (CT) and the inferior (IVC) or superior (SVC) vena cavae in atypical right atrial (RA) AFL in absence of prior atriotomy. Figure-8 double loop reentry was documented in one RA atypical AFL. ICSC was characterized by concealed entrainment with a post-pacing interval identical to the AFL cycle length, and a mid-diastolic fractionated electrogram, 129 +/- 23 ms in duration, spanning the isoelectric line between double potentials on adjacent area of conduction block. All AFLs were successfully ablated with 4.9 +/- 4.3 RF pulses applied at ICSC. A possible mechanism of atypical AFL consists of figure-8 reentry with ICSC between surgical scars in postoperative AFL, and between the CT and the IVC/SVC in RA AFL not preceded by cardiac surgery. Late and partial regeneration of conduction across the atriotomy scar can create an ICSC. Nonlinear ablation targeting ICSC can cure atypical AFL, whether it follows surgery or not.

Electrocardiographic characteristics of left ventricular outflow tract tachycardia.

Catheter ablation of idiopathic left ventricular outflow tract tachycardia (LVOT-VT) is rare because a safe ablation technique at this site has not been described, and serious complications may occur. This study compared the QRS morphology of LVOT-VT with that of idiopathic right ventricular outflow tract tachycardia. A comparison was made between the electrocardiographic characteristics of LVOT-VT originating from the supravalvular region of a coronary cusp (Supra-Ao group) with those of LVOT-VT originating from the infravalvular endocardial region of a coronary cusp of the aortic valve within the LV (Infra-Ao group). After precise mapping of the right ventricle, left ventricle, pulmonary artery, coronary cusps, and proximal portion of the anterior interventricular vein, there were 17 patients in whom VT was thought to be located at the LVOT by both activation and pace mapping. They were divided between a Supra-Ao group (n = 8), and an Infra-Ao group (n = 9). Analysis of the 12-lead electrocardiogram (ECG) revealed an S wave in lead I in all 17 patients. A precordial R wave transition was also observed at V1 or V2 in 16 patients (94%). In 7 of 8 patients (88%) with Supra-Ao LVOT-VT, no S wave was observed in either V5 or V6. In contrast, an Rs pattern was observed in both V5 and V6, or in V6 only, in 100% of the patients with Infra-Ao LVOT-VT. A LVOT-VT should be suspected when the ECG shows an S wave in lead I and an R/S ratio greater than 1 in lead V1 or V2, versus a coronary cusp location if there is no S wave in either lead V5 or V6.

A jump in cycle length of orthodromic common atrial flutter during catheter ablation at the isthmus between the inferior vena cava and tricuspid annulus; evidence of dual isthmus conduction directed to dual septal exits.

INTRODUCTION: In orthodromic common atrial flutter (AFL), details of intraseptal propagation of the flutter (FL) wave exiting from the isthmus between the inferior vena cava and tricuspid annulus (IVC-TA isthmus) remain unknown. We hypothesized the existence of dual septal exits of the FL wave from the IVC-TA isthmus to both the anterior, coronary sinus ostium (CSO-TA) isthmus, and the posterior septal (IVC-CSO) isthmus, and that the IVC-TA isthmus might consist of dual muscle bundles directed to both septal isthmuses over the eustachian ridge; therefore, segmental ablation of the IVC-TA isthmus could change intraseptal FL wave propagation. METHODS AND RESULTS: To test the hypothesis, we investigated the influence of segmental ablation of the IVC-TA isthmus on intraseptal FL wave propagation. In seven of 40 (18%) consecutive patients, segmental ablation of the ventricular side of the IVC-TA isthmus during orthodromic common AFL led to sudden prolongation of the flutter cycle length (FCL) (from 266 +/- 33 ms to 291 +/- 45 ms) associated with changes in intraseptal activation sequences. They consisted of prolongation of the interval between the IVC-TA isthmus and the CSO (from 38 +/- 13 ms to 86 +/- 25 ms), shortening of the interval between the CSO and His (from 31 +/- 15 ms to 9 +/- 15 ms), and atrial electrogram polarity change at the His-bundle recording site. Morphological change in the FL wave was also seen on the 12-lead ECG. CONCLUSIONS: In some patients, segmental ablation of the IVC-TA isthmus can lead to a jump in FCL and changes in intraseptal activation sequences of FL waves due to anterior-to-posterior shifting of the septal exit. This indicates that the IVC-TA isthmus may contain dual circumferential muscle bundles as conduction pathways directed to dual septal exits both anterior and posterior to the CSO.

Thrombolytic therapy can reduce the arrhythmogenic substrate after acute myocardial infarction: a study using the signal-averaged electrocardiogram, endocardial catheter mapping and programmed ventricular stimulation.

Thrombolytic therapy improves survival after acute myocardial infarction (AMI) primarily by preserving left ventricular function. Its influence on the arrhythmogenic substrate remains uncertain. To investigate the electrophysiologic effects of thrombolytic therapy, signal-averaged electrocardiography, endocardial catheter mapping and programmed stimulation were performed in 93 consecutive patients with their first AMI who underwent thrombolytic therapy. Early reperfusion was achieved in 75 patients (group 1), but not in 18 patients (group 2). The incidence of the signal-averaged electrocardiogram abnormality was 11% in group 1 (8 of 75 patients) and 33% in group 2 (6 of 18 patients) (p<0.02). Catheter mapping detected delayed endocardial electrograms in 30 group 1 patients and 10 group 2 patients (p=NS). The spatial distribution of these electrograms was smaller, and the longest duration of endocardial electrograms was shorter in group 1 than in group 2 (p<0.01). Sustained monomorphic ventricular tachycardia was induced less commonly in group 1 (20%) than in group 2 (44%) (p<0.05). In conclusion, thrombolytic therapy can reduce the arrhythmogenic substrate and improve electrical stability after AMI. This antiarrhythmic effect may contribute, in part, to the improved survival of patients treated with thrombolytic drugs.

Radiofrequency catheter ablation for sinoatrial node reentrant tachycardia: electrophysiologic features of ablation sites.

The aim of this study was to investigate catheter ablation of sino-atrial reentrant tachycardia (SART) and the electrophysiologic characteristics of the ablation sites. From January 1990 to October 1997, 651 patients with supraventricular tachycardia were referred and 11 patients were found to have SART. Ablation was successful in all cases with a mean number of 3.3 radiofrequency (RF) current pulses. SART terminated during 22 of 36 RF pulses. In spite of prompt termination, tachycardia could be re-induced in 3 of 11 patients with its earliest activation site shifted. At effective ablation sites, the electrograms during tachycardia were characterized as fractionated (75+/-17 ms), and 38+/-16 ms prior to surface P wave, and 42+/-18 ms prior to the high right atrium. Unipolar electrograms revealed a sharp negative unipolar deflection, so called QS pattern, in 15 of 20 sites during SART and 15 of 15 sites during sinus rhythm. During effective applications, atrial premature beats (APB) with activation sequences identical to sinus rhythm appeared in 14 of 22 cases. Effective ablation sites of SART showed fractionated electrograms during tachycardia and sinus rhythm. Unipolar electrogram with a QS pattern and APB during energy application could be an indicator of the optimal ablation sites.

Retrograde Purkinje potential activation during sinus rhythm following catheter ablation of idiopathic left ventricular tachycardia.

We describe two patients with idiopathic left ventricular tachycardia that were cured by radiofrequency catheter ablation. Tachycardia was inducible by ventricular stimulation and was verapamil sensitive. Two distinct presystolic potentials (P1 and P2) were recorded during tachycardia in the mid-septal or inferoapical area, but only one potential (P2) was recorded during sinus rhythm. After catheter ablation at this site, the P1 potential was noted after the QRS complex during sinus rhythm, while the P2 was still observed before the QRS complex. The P1 potential showed a decremental property during atrial or ventricular pacing. These data suggest that Purkinje tissue with decremental properties was responsible for the tachycardia mechanism, and that the reentry circuit involving this tissue is likely to be of considerable size.

Verapamil-sensitive left anterior fascicular ventricular tachycardia: results of radiofrequency ablation in six patients.

INTRODUCTION: Verapamil-sensitive left ventricular tachycardia (VT) with a right bundle branch block (RBBB) configuration and left-axis deviation has been demonstrated to arise from the left posterior fascicle, and can be cured by catheter ablation guided by Purkinje potentials. Verapamil-sensitive VT with an RBBB configuration and right-axis deviation is rare, and may originate in the left anterior fascicle. METHODS AND RESULTS: Six patients (five men and one woman, mean age 54+/-15 years) with a history of sustained VT with an RBBB configuration and right-axis deviation underwent electrophysiologic study and radiofrequency (RF) ablation. VT was slowed and terminated by intravenous administration of verapamil in all six patients. Left ventricular endocardial mapping during VT identified the earliest ventricular activation in the anterolateral wall of the left ventricle in all patients. RF current delivered to this site suppressed the VT in three patients (ablation at the VT exit). The fused Purkinje potential was recorded at that site, and preceded the QRS complex by 35, 30, and 20 msec, with pace mapping showing an optimal match between the paced rhythm and the clinical VT. In the remaining three patients, RF catheter ablation at the site of the earliest ventricular activation was unsuccessful. In these three patients, Purkinje potential was recorded in the diastolic phase during VT at the mid-anterior left ventricular septum. The Purkinje potential preceded the QRS during VT by 66, 56, and 63 msec, and catheter ablation at these sites was successful (ablation at the zone of slow conduction). During 19 to 46 months of follow-up (mean 32+/-9 months), one patient in the group of ablation at the VT exit had sustained VT with a left bundle branch block configuration and an inferior axis, and one patient in the group of ablation at the zone of slow conduction experienced typical idiopathic VT with an RBBB configuration and left-axis deviation. CONCLUSION: Verapamil-sensitive VT with an RBBB configuration and right-axis deviation originates close to the anterior fascicle. RF catheter ablation can be performed successfully from the VT exit site or the zone of slow conduction where the Purkinje potential was recorded in the diastolic phase.

Catheter ablation of ventricular tachycardia in patients with right ventricular dysplasia: Identification of target sites by entrainment mapping techniques.

OBJECTIVE: To identify target sites for radiofrequency ablation of ventricular tachycardia (VT) by entrainment mapping techniques in patients with arrhythmogenic right ventricular dysplasia. METHODS: Entrainment mapping and radiofrequency ablation of eight VTs was performed in seven patients. Radiofrequency ablation was applied at 31 reentry circuits sites that were classified based on findings during entrainment. RESULTS: By entrainment criteria the 31 sites were classified as: exit sites (n = 12), proximal sites (n = 6), and outer loop sites (n = 13). Radiofrequency current application terminated VT at 7 of 31 sites: 2 of 12 exit sites (17%), 4 of 6 proximal sites (67%), and 1 of 13 outer loop sites (8%). CONCLUSION: Radiofrequency ablation terminated VTs most often at sites proximal to the exit as opposed to outer loop sites and exit sites (P = 0.05). The critical isthmus for ablation of VT in right ventricular dysplasia often may be distant to the exit.

Catheter ablation for ventricular tachycardia from a diverticulum at the right ventricular outflow tract.

A case is presented of a 73-year-old man with drug resistant ventricular tachycardia that originated from the right ventricular outflow tract. A right ventriculogram showed a diverticulum in the interventricular septum at the right ventricular outflow tract. Low energy radiofrequency catheter ablation within the diverticulum was performed successfully and safely.

Retrograde multiple and multifiber accessory pathway conduction in the Wolff-Parkinson-White syndrome: potential precipitating factor of atrial fibrillation.

INTRODUCTION: The determinants of susceptibility to atrial fibrillation (AF) and the existence of accessory pathway conduction have remained unidentified in the Wolff-Parkinson-White (WPW) syndrome. We tested the hypothesis that excitation inputs into the atrium over a retrograde multiple or multifiber accessory pathway during AV reentrant tachycardia (AVRT) could precipitate initiation of AF. METHODS AND RESULTS: Two hundred fifty consecutive patients with WPW syndrome underwent electrophysiologic study and radiofrequency catheter ablation. The patients were classified into two groups according to the study results: 29 with retrograde multiple or multifiber accessory pathway (MP) and 221 with retrograde single accessory pathway (SP). Compared with the SP patients, the MP patients showed a significantly higher incidence of clinical AF (MP vs SP: 19/29 vs 51/221, P < 0.01), induced AF (12/29 vs 32/221, P < 0.01), and initiated AF during ventricular pacing and AVRT (10/12 vs 17/32, P < 0.05). There were no differences between the two groups in incidence of clinical and induced AVRT (24/29 vs 200/221 and 25/29 vs 206/221, respectively), mean cycle length of induced AVRT, or electrophysiologic parameters of the accessory pathway. AF inducibility during AVRT or ventricular pacing was eliminated by partial ablation in 7 of 10 patients with MP. After total ablation, the incidence of induced AF was similar between the two groups (MP vs SP: 1/29 vs 11/221). CONCLUSION: The existence of a retrograde multiple or multifiber accessory pathway in patients with WPW syndrome is associated with a higher incidence of clinical and induced AF. Successful ablation of the retrograde multiple or multifiber accessory pathway can eliminate the induction of both AVRT and AF.

High energy radiofrequency catheter ablation for common atrial flutter targeting the isthmus between the inferior vena cava and tricuspid valve annulus using a super long tip electrode.

There have been controversies concerning the optimal target sites and approaches in radiofrequency catheter ablation of common atrial flutter. We attempted high energy radiofrequency catheter ablation targeting the isthmus between the inferior vena cava and tricuspid valve annulus (IVC-TV isthmus) with a super long (8 mm) tip electrode, and compared the efficacy of this anatomical approach with the electrophysiological approach targeting the posteroseptal right atrium posterior to the coronary sinus using a standard 4-mm tip electrode. Atrial flutter was successfully ablated in 12 of 12 patients (100%) without recurrence with the anatomical approach, while, in 7 of 9 patients (64%) with 2 recurrences with the electrophysiological approach. In comparison of ablation data between the anatomical and electrophysiological approaches, there were significant differences in the mean number of application pulses (anatomical vs electrophysiological: 2.3 +/- 0.8 vs 9.9 +/- 6.4, P < 0.01), applied wattage (39 +/- 12 W vs 24 +/- 6 W, P < 0.01), applied energy per application (1,986 +/- 426 J vs 659 +/- 323 J, P < 0.01), fluoroscopic time (26 +/- 11 min vs 74 +/- 30 minutes, P < 0.01), and procedure time (59 +/- 8 min vs 181 +/- 53 min, P < 0.01). In conclusion, the anatomical approach is superior to the electrophysiological one with respect to procedure and radiation time, and linear ablation at the IVC-TV isthmus with an 8-mm tip electrode and high energy application is highly effective and safe.