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Background: Pulmonary vein isolation (PVI) is an established ablation procedure for atrial fibrillation (AF), however, PVI alone is insufficient to suppress AF recurrence. Non-pulmonary vein (non-PV) trigger ablation is one of the promising strategies beyond PVI and has been shown to be effective in refractory/persistent AF cases. To make non-PV trigger ablation more standardized, it is essential to develop a simple method to localize the origin of non-PV triggers., Methods: We retrospectively analyzed 37 non-PV triggers in 751 ablation sessions for symptomatic AF from January 2017 to December 2020. Regarding non-PV triggers, intra-atrial activation interval from the earliest in right atrium (RA) to proximal coronary sinus (CS) (RA-CSp) and that from the earliest in RA to distal CS (RA-CSd) obtained by a basically-positioned duodecapolar RA-CS catheter were compared among 3 originating non-PV areas [RA, atrial septum (SEP) and left atrium (LA)]., Results: RA-CSp of RA non-PV trigger (56.4 ± 23.4 ms) was significantly longer than that of SEP non-PV (14.8 ± 25.6 ms, p = 0.019) and LA non-PV (-24.9 ± 27.9 ms, p = 0.0004). RA-CSd of RA non-PV (75.9 ± 32.1 ms) was significantly longer than that of SEP non-PV (34.2 ± 32.6 ms, p = 0.040) and LA non-PV (-13.3 ± 41.2 ms, p = 0.0008). RA-CSp and RA-CSd of SEP non-PV were significantly longer than those of LA non-PV (p = 0.022 and p = 0.016, respectively). Sensitivity and specificity of an algorithm to differentiate the area of non-PV trigger using RA-CSp (cut-off value: 50 ms) and RA-CSd (cut-off value: 0 ms) were 88% and 97% for RA non-PV, 81% and 73% for SEP non-PV, 65% and 95% for LA non-PV, respectively., Conclusions: The analysis of intra-atrial activation sequences was useful to differentiate non-PV trigger areas. A simple algorithm to localize the area of non-PV trigger would be helpful to identify non-PV trigger sites in AF ablation., Competing Interests: The authors have declared that no competing interests exist.

Introduction: Ectopic beats originating from the pulmonary vein (PV) trigger atrial fibrillation (AF). The purpose of this study was to clarify the electrophysiological determinant of AF initiation from the PVs., Methods: Pacing studies were performed with a single extra stimulus mimicking an ectopic beat in the left superior PVs (LSPVs) in 62 patients undergoing AF ablation. Inducibility of AF, effective refractory period (ERP), and conduction properties within the PVs were analyzed., Results: A single extra stimulus in LSPV induced AF in 20 patients (32% of all patients) at the mean coupling interval (CI) of 172 ms. A CI-dependent anisotropic conduction at the AF onset was visualized in a three-dimensional mapping. Onset of AF was site-specific with reproducibility in each individual. Mean ERP in LSPV in the AF-inducible group was shorter than that in the AF-noninducible group (182 ± 55 vs. 254 ± 51 ms, p < .0001). LSPV ERP dispersion was greater in the AF-inducible group than in the AF-noninducible group (45 ± 28 vs. 27 ± 19 ms, p < .01). Circumferential intra-PV conduction time (IPVCT) exhibited decremental properties in response to shortening of CI and the prolongation of IPVCT in the AF-inducible site was greater than that in the AF-noninducible site (p < .05) in each individual., Conclusions: Location and CI of an ectopic excitation ultimately determine the initiation of AF from the PVs. ERP dispersion and circumferential conduction delay may lead to anisotropic conduction and reentry within the PVs that initiate AF., (© 2022 The Authors. Journal of Cardiovascular Electrophysiology published by Wiley Periodicals LLC.)

Serial changes of electrocardiograms (ECG) could be used to assess their clinical features in atrial septal defects (ASD) after transcatheter closure together with other clinical parameters. We retrospectively studied 100 ASD patients who underwent transcatheter closure. Complications of persistent atrial fibrillation occurred in five ASD patients, and they were excluded. We divided the other 95 patients according to PQ intervals before closure (normal: < 200 ms, n = 51; prolonged: ≥ 200 ms, n = 44) to evaluate their clinical characteristics and parameters such as echocardiography, chest X-rays, and brain natriuretic protein (BNP) levels. Individuals in the prolonged PQ group were significantly older, had higher incidences of paroxysmal atrial fibrillation (PAF) and heart failure (HF) treated with more β-blockers and diuretics, and with a higher tendency of NYHA functional classification and BNP levels than the normal PQ group. The prolonged PQ group also had a significantly higher incidence of complete right bundle branch block, wider QRS intervals, and larger cardiothoracic ratios in chest X-rays accompanied by larger right atrial-areas and larger left atrial dimensions in echocardiograms. Furthermore, the prolonged PQ intervals with less PQ interval shortening after transcatheter closure revealed that the patients were the oldest at the time of closures and showed less structural normalization of the right heart and left atrium after ASD closure. PAF and HF also occurred more frequently in this subgroup. These results suggested that the ASD patients with prolonged PQ intervals with less PQ shortening were accompanied by more advanced clinical conditions. Together with other clinical parameters, detailed analyses of ECG and their changes after closure could elucidate the clinical characteristics and status of ASD patients with transcatheter closure and were useful for predicting structural normalization after transcatheter closure.

The pathophysiology of non-pulmonary vein (PV) triggers of atrial fibrillation (AF) is unclear. We hypothesized that left atrial non-PV (LANPV) triggers are associated with atrial tissue degeneration. This study analyzed 431 patients that underwent catheter ablation (mean age 62 yrs, 303 men, 255 paroxysmal AF [pAF] patients). Clinical and electrophysiological characteristics of non-PV trigger were analyzed. Fifty non-PV triggers in 40 patients (9.3%) were documented; LANPV triggers were the most prevalent (n = 19, 38%). LANPV triggers were correlated with non-paroxysmal AF (non-pAF) (OR 3.31, p = 0.04) whereas right atrial non-PV (RANPV) triggers (n = 14) and SVC triggers (n = 17) were not. The voltage at the LANPV sites during SR was 0.3 ± 0.16 mV (p < 0.001 vs. control site). Low-voltage areas (LVAs) in the LA were significantly greater in non-pAF compared to pAF (14.2% vs. 5.8%, p < 0.01). RANPV trigger sites had preserved voltage (0.74 ± 0.48 mV). Long-term outcomes of patients with non-PV triggers treated with tailored targeting strategies were not significantly inferior to those without non-PV triggers. In conclusion, non-PV triggers arise from the LA with degeneration, which may have an important role in AF persistence. A trigger-oriented, patient-tailored ablation strategy considering LA voltage map may be feasible and effective in persistent/recurrent AF.

Background: The proportion of patients with atrial fibrillation (AF) treated with anticoagulation varies from country to country. In Japan, little is known about regional differences in frequency of warfarin use or prognosis among patients with non-valvular AF (NVAF)., Methods and results: In J-RHYTHM Registry, the number of patients recruited from each of 10 geographic regions of Japan was based on region population density. A total of 7,406 NVAF patients were followed up prospectively for 2 years. At baseline, significant differences in various clinical characteristics including age, sex, type of AF, comorbidity, and CHADS2score, were detected among the regions. The highest mean CHADS2score was recorded in Shikoku. Frequency of warfarin use differed between the regions (P<0.001), with lower frequencies observed in Hokkaido and Shikoku. Baseline prothrombin time international normalized ratio differed slightly but significantly between the regions (P<0.05). On univariate analysis, frequency of thromboembolic events differed among the regions (P<0.001), with the highest rate seen in Shikoku. An inverse correlation was detected between frequency of thromboembolic and of major hemorrhagic events (P=0.062). On multivariate analysis, region emerged as an independent risk for thromboembolism., Conclusions: Thromboembolic risk, frequency of warfarin use, and intensity and quality of warfarin treatment differed significantly between geographic regions of Japan. Region was found to be an independent predictor of thromboembolic events. (Circ J 2016; 80: 1548-1555).

Background: Concomitant use of vitamin K antagonist (VKA) and aspirin (ASA) is becoming increasingly prevalent among atrial fibrillation (AF) patients. We quantified the net clinical benefit of adding ASA to a VKA using nationwide prospective AF registry data., Methods: We studied 6074 patients (VKA monotherapy: 83% and VKA+ASA: 17%) between January 2009 and July 2009, and followed them for a mean follow-up period of 2years. The risk of strokes and bleeding was calculated by the CHA2DS2-VASc and HAS-BLED scores. The net clinical benefit was defined as the annual rate of ischemic strokes and systemic emboli prevented by VKAs minus intracranial hemorrhages attributable to the VKA+ASA, multiplied by an impact weight of 1.5., Results: Patients on a VKA+ASA were older with more medical comorbidities than those on VKA alone. Using VKA monotherapy as a reference, higher major bleeding rates and all-cause death were evident in those on VKA+ASA. The net clinical benefit of VKA+ASA for the overall cohort was -0.1%/year (95% confidence interval, -0.74% to 0.46%). There was a trend toward a negative net clinical benefit from VKA+ASA in patients with a CHA2DS2-VASc≥2 and HAS-BLED≤2 (-1.17%/year). The VKA+ASA yielded a positive net clinical benefit in patients with a CHA2DS2-VASc≥2 and HAS-BLED≥3 (1.16%/year). The result patterns were relatively constant using impact weight of 1.0 and 2.0., Conclusions: Our estimates of the net clinical benefit can provide a useful anchoring point for adding ASA to VKA in patients with AF., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Introduction: Recently, direct-acting oral anticoagulants (DOACs) have been introduced, with increasing use in patients with non-valvular atrial fibrillation (NVAF). However, warfarin continues to be widely used and the benefits and risks of warfarin in NVAF patients warrant closer inspection., Materials and Methods: Thromboembolism, major hemorrhage, and total and cardiovascular mortalities were analyzed in 7,406 NVAF patients in the J-RHYTHM Registry from January to July 2009, prior to DOAC introduction. Propensity score matching analysis was performed to reduce the differences in clinical characteristics between non-anticoagulant (n=1002) and warfarin (n=6404) cohorts to reassess warfarin outcomes over 2years., Results: The incidence of thromboembolism was significantly greater in the non-anticoagulant cohort (3.0%) than in the warfarin cohort (1.5%, P<0.001) with less frequent major hemorrhage in the non-anticoagulant cohort (0.8%) than in the warfarin cohort (2.1%, P=0.009). Using propensity score matching, new subsets (n=896 each) were obtained, with matching of the clinical characteristics between warfarin and non-anticoagulant subsets. The warfarin subset had lower risk factors compared with the total warfarin cohort. The incidence of thromboembolism was higher in the non-anticoagulant subset (2.9%) than in the warfarin subset (0.7%, P<0.001). However, major hemorrhage was not significantly different between the two subsets., Conclusions: Although warfarin was associated with a significantly higher incidence of hemorrhage in the unmatched cohorts, propensity score matching revealed that warfarin reduced thromboembolism without a significant increase in hemorrhage in the matched subsets with lower risks. Propensity score matching reduced selection bias and provided rational comparisons although it had indwelling limitations., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background: Hypertension is a powerful risk factor of atrial fibrillation (AF). The pathophysiology of AF with hypertension is associated with sympathoexcitation or the renin-angiotensin system; however, current therapies cannot sufficiently prevent its development. We previously revealed that brain angiotensin II type 1 receptor (AT1R) blockade causes a depressor response via sympathoinhibition. Herein, we evaluated whether brain AT1R contributes to AF development in hypertensive rats., Methods: We divided the stroke-prone spontaneously hypertensive rats (SHRSP) treated with intracerebroventricular (ICV) infusion of vehicle, ICV infusion of losartan (S-LOS), or oral administration of hydralazine (S-HYD); and Wistar Kyoto rats treated with ICV S-VEH., Results: Two weeks later, systolic blood pressure was significantly lower in the S-LOS group than in the S-VEH group and was even lower in the S-HYD group. Urinary norepinephrine excretion for 24h, an indirect marker of sympathoexcitation, significantly reduced in the S-LOS group but increased in the S-HYD group despite depressor response. AF was induced by transesophageal burst pacing. AF duration was significantly shorter in the S-LOS group than in the S-VEH group (5.0±0.4 vs. 15.2±3.7 s; n = 8 each; P < 0.05). However, it was significantly longer in the S-HYD group than in the S-VEH group. Interstitial atrial fibrosis and echocardiographic parameters did not differ between the SHRSP groups., Conclusions: Brain AT1R blockade suppresses AF inducibility and maintenance independent of depressor response in hypertensive rats., (© American Journal of Hypertension, Ltd 2014. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Treatment guidelines for atrial fibrillation (AF) used in Western countries describe female gender as a risk factor for thromboembolic events in patients with nonvalvular AF (NVAF). The present study aimed to determine the impact of gender on prognosis of Japanese patients with NVAF. A subanalysis of 7,406 patients with NVAF (mean age 70 years) who were followed-up prospectively for 2 years was performed using data from the J-RHYTHM registry. The primary end points were thromboembolic events, major hemorrhaging, total mortality, and cardiovascular mortality. Compared with male subjects (n = 5,241), female subjects (n = 2,165) were older and displayed greater prevalences of paroxysmal AF, heart failure, and hypertension but less prevalences of diabetes, previous cerebral infarction, and coronary artery disease. Male and female patients had mean CHADS2 (Congestive heart failure, Hypertension, Age of 75 years or more, Diabetes mellitus and prior Stroke or transient ischemic attack) scores of 1.6 and 1.8, respectively (p <0.001). Warfarin was given to 87% of male patients and 86% of female patients (p = 0.760), and the 2 genders displayed similar mean international normalized ratio of prothrombin time values at baseline (1.91 vs 1.90, respectively, p = 0.756). Multivariate logistic regression analysis indicated that male gender was an independent risk factor for major hemorrhaging (odds ratio 1.59, 95% confidence interval 1.05 to 2.40, p = 0.027) and all-cause mortality (odds ratio 1.78, 95% confidence interval 1.25 to 2.55, p <0.002) but not for thromboembolic events (odds ratio 1.24, 95% confidence interval 0.83 to 1.86, p = 0.297) or cardiovascular mortality (odds ratio 0.96, 95% confidence interval 0.56 to 1.66, p = 0.893). In conclusion, female gender is not a risk factor for thromboembolic events among Japanese patients with NVAF who were treated mostly with warfarin. However, male gender is a risk factor for major hemorrhaging and all-cause mortality., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Target anticoagulation levels for warfarin in Japanese patients with non-valvular atrial fibrillation (NVAF) are unclear., Methods and Results: Of 7,527 patients with NVAF, 1,002 did not receive warfarin (non-warfarin group), and the remaining patients receiving warfarin were divided into 5 groups based on their baseline international normalized ratio (INR) of prothrombin time (≤1.59, 1.6-1.99, 2.0-2.59, 2.6-2.99, and ≥3.0). Patients were followed-up prospectively for 2 years. Primary endpoints were thromboembolic events (cerebral infarction, transient ischemic attack, and systemic embolism), and major hemorrhage requiring hospital admission. During the follow-up period, thromboembolic events occurred in 3.0% of non-warfarin group, but at lower frequencies in the warfarin groups (2.0, 1.3, 1.5, 0.6, and 1.8%/2 years for INR values of ≤1.59, 1.6-1.99, 2.0-2.59, 2.6-2.99, and ≥3.0, respectively; P=0.0059). Major hemorrhage occurred more frequently in warfarin groups (1.5, 1.8, 2.4, 3.3, and 4.1% for INR values ≤1.59, 1.6-1.99, 2.0-2.59, 2.6-2.99, and ≥3.0, respectively; P=0.0041) than in non-warfarin group (0.8%/2 years). These trends were maintained when the analyses were confined to patients aged ≥70 years., Conclusions: An INR of 1.6-2.6 is safe and effective at preventing thromboembolic events in patients with NVAF, particularly patients aged ≥70 years. An INR of 2.6-2.99 is also effective, but associated with a slightly increased risk in major hemorrhage. (UMIN Clinical Trials Registry UMIN000001569)

Objective: Efficacy and safety of long-term administration of bepridil as a rhythm and rate controller were comprehensively evaluated in patients with multidrug-resistant paroxysmal atrial fibrillation (PAF)., Methods: A retrospective survey from 1992 to 2006 was conducted on 62 multidrug-resistant PAF patients treated with bepridil from 480 consecutive PAF patients. In addition, a 5-year follow-up study was conducted on 28 of the 62 patients, being continued from 2006 to 2011. The efficacy of bepridil, improvement in symptoms including patients' quality of life (QOL), ECGs, hemodynamics, and its adverse effects were examined., Results: In the retrospective survey, 127 ± 44 mg of bepridil was given for 21 ± 18 months and 40.3% maintained sinus rhythm. Reductions in the frequency and the duration of each episode of PAF and improvement in symptoms were seen in 48.4, 50.0 and 93.5% of the 62 patients, respectively. Reversible torsades de pointes (TdP) occurred in two aged women. Bradycardia and hepatic dysfunction developed in one patient each. In the follow-up study, 100 ± 20 mg of bepridil was given. Sinus rhythm was maintained in 13 patients. Although the occurrences of PAF continued in 14 patients, their symptoms and QOL were improved. No adverse effects were noted in all 28 patients of the follow-up study., Conclusions: Bepridil was effective in rhythm control in 40% of PAF patients resistant to other antiarrhythmics. Even in those who had failed to maintain sinus rhythm, continued administration of low-dose bepridil improved their symptoms and QOL with few adverse effects. Bepridil is worth returning to use.

Background: The mortality and morbidity rates of various cardiovascular diseases differ between Western countries and Japan. The age- and gender-specific prevalence rate of atrial fibrillation (AF) in the general population of Japan was determined using the data from periodic health examinations in 2003., Methods: Data of 630,138 subjects aged 40 years or more (47% were men and 34% were employees of companies and local governments) were collected from northern to southern Japan. The prevalence of diagnosed AF in each 10-year age group of both men and women was determined. Based on these prevalence rates and the Registry of Residents, the number of people having AF in Japan was estimated., Results: The prevalence rate of AF increased as both male and female subjects aged, and it was 4.4% for men but only 2.2% for women aged 80 years or more (p<0.0001). As a whole, the AF prevalence of men was three times that of women (1.35 versus 0.43%, p<0.0001). There may be approximately 716,000 people (95% confidence interval (CI), 711,000-720,000) with AF in Japan, an overall prevalence of 0.56%. The number of people having AF was projected to be 1.034 (95% CI, 1.029-1.039) million, an overall prevalence of 1.09%, in 2050., Conclusions: The prevalence of AF increased in Japan as the population aged, as in Western countries. The overall prevalence of AF in Japan is approximately two-thirds of that in the USA. The projected increase in the number of people having AF is modest in Japan in 2050.

A 64-year-old man had demonstrated palpitations caused by paroxysmal atrial fibrillation (AF) documented by ambulatory electrocardiographic monitoring. Effectiveness of antiarrhythmic agent (disopyramide: 300 mg/day) was limited. Based on the gastrointestinal endoscopic findings, proton pump inhibitor (PPI: rabeprazole, 10 mg/day) was administered to eliminate heart burn due to reflux esophagitis. Symptoms of paroxysmal AF and reflux esophagitis were confusing due to the anatomical proximity of the diseased organs and concomitant occurrence in the evening and when in a supine position. After the additional PPI therapy, not only was reflux esophagitis improved subjectively and endoscopically but also paroxysms of AF markedly reduced. Because esophagus is attached to left atrial posterior wall and the role of inflammatory process on the development of AF is highlighted, amelioration of reflux esophagitis by PPI may have been followed by the remarkable reduction of paroxysms of AF.

We continuously observed successive pairs of R-R intervals during atrial fibrillation and hypothesized that the shortest R-R interval for a given preceding R-R interval in a pair represents the functional refractory period of the atrioventricular node at that preceding interval. To test this hypothesis we simulated atrial fibrillation in 28 isolated cross-perfused canine hearts and obtained an R-R interval scatterplot by plotting the R-R intervals as a function of the immediately preceding R-R interval. This scatterplot enabled us to detect a series of the shortest R-R intervals for a wide range of preceding R-R intervals, and this allowed us to estimate the rate-dependent functional refractory period of the atrioventricular node in simulated atrial fibrillation. The estimated functional refractory periods correlated well with those measured by the conventional method (r = 0.93). We conclude that the proposed method makes it possible to estimate the rate-dependent functional refractory periods of the atrioventricular node in atrial fibrillation.

Abstract Background The pulmonary veins (PVs) have unique electrophysiological properties triggering and maintaining atrial fibrillation (AF). Bigeminal PV electrical activity (PV bigeminy) during sinus rhythm has been reported; however, its mechanisms and clinical implication remain unclear. We hypothesized that PV bigeminy indicates arrhythmogenic activities and influences clinical outcome. Methods and Results We retrospectively analyzed electrophysiological studies in 465 patients with AF who underwent first session PV isolation (PVI). PV bigeminy was observed in 30 PVs of 23 patients (4.9% of patients). PV bigeminy was observed in left inferior PV (LIPV) in 15 patients, which was the most prevalent, followed by left superior in seven and right superior in seven and right inferior in one. In response to atrial extra stimulus, the second PV potentials (PV2) showed decremental conduction properties, suggesting reentrant mechanisms involved (n = 5). Interestingly, AF was initiated from the 23 PVs with bigeminy in 21 patients (76.7% of 30 PVs with bigeminy), spontaneously or in response to drugs, which was significantly more prevalent from the AF initiation rate from each PV in the control 442 patients (182 firings in 1290 PVs, 14.1%, P

Abstract Background Induction test of atrial fibrillation (AF) is one of endpoint measures in catheter ablation (CA). However, its predictive value in long‐term outcome remains controversial. Methods Ninety‐eight patients (61 years, 77 males) with persistent AF who underwent pulmonary vein antrum isolation‐based CA were retrospectively analyzed. We determined whether inducibility of AF/atrial tachyarrhythmias (AT) by atrial burst pacing at the end of CA and other characteristics were associated with the recurrence of AF/AT. Atrial burst pacing was performed with 30‐beat from the coronary sinus; increasing from 240 to 320 ppm. Inducibility was defined as AF/AT lasting ≥5 minutes following atrial burst pacing. Results AF/AT was induced in 50 patients (51%). During 1 year of follow‐up, 71 patients (72.4%) had no recurrence of AF/AT. A logistic regression analysis showed that female gender (OR 3.8; P = 0.02), multiple sessions (OR 3.5; P = 0.02), and early recurrence of AF/AT (OR 5.3; P = 0.004) were associated with clinical recurrence. AF/AT Inducibility was not associated with clinical recurrence (P = 0.65). A subanalysis in patients with enlarged LA (LA diameter ≥45 mm, n = 40) showed that AF/AT inducibility was associated with recurrence (OR 8.1; P = 0.04). The positive and negative predictive values of AF/AT inducibility for AF/AT recurrence were 41 and 89%, respectively. Negative predictive value was increased to 92.3% when the inducibility was defined as AF/AT of ≥30 seconds following atrial burst pacing. Conclusions AF/AT inducibility cannot predict long‐term clinical recurrence in patients with persistent AF. However, it may have a prognostic value especially in patients with enlarged LA.

We report the case of an otherwise healthy 64-year-old female who developed cardiopulmonary arrest after the administration of pilsicainide for treatment of paroxysmal atrial fibrillation. She had had an episode of paroxysmal atrial fibrillation, but no liver dysfunction, renal dysfunction, or echocardiographic abnormality before her admission. On the day of admission and the following day, 50 mg of pilsicainide was administered intravenously over 10 min (total 100 mg). Shortly after the second injection, she developed marked bradycardia and hypotension and eventually fell into a state of pulseless electrical activity. Immediate cardiopulmonary resuscitation was started. Although application of a temporary pacemaker restored her heart rate, echocardiography revealed no left ventricular contraction. We started percutaneous cardiopulmonary support (PCPS) and intra-aortic balloon pumping (IABP). Her cardiac contraction gradually recovered and returned to completely normality 3 days after the onset. The patient was discharged in an ambulatory condition.

Background: The pulmonary veins (PVs) have unique electrophysiological properties triggering and maintaining atrial fibrillation (AF). Bigeminal PV electrical activity (PV bigeminy) during sinus rhythm has been reported; however, its mechanisms and clinical implication remain unclear. We hypothesized that PV bigeminy indicates arrhythmogenic activities and influences clinical outcome. Methods and Results: We retrospectively analyzed electrophysiological studies in 465 patients with AF who underwent first session PV isolation (PVI). PV bigeminy was observed in 30 PVs of 23 patients (4.9% of patients). PV bigeminy was observed in left inferior PV (LIPV) in 15 patients, which was the most prevalent, followed by left superior in seven and right superior in seven and right inferior in one. In response to atrial extra stimulus, the second PV potentials (PV2) showed decremental conduction properties, suggesting reentrant mechanisms involved (n = 5). Interestingly, AF was initiated from the 23 PVs with bigeminy in 21 patients (76.7% of 30 PVs with bigeminy), spontaneously or in response to drugs, which was significantly more prevalent from the AF initiation rate from each PV in the control 442 patients (182 firings in 1290 PVs, 14.1%, P <.0001). PVI‐based ablation was completed in the 23 patients with PV bigeminy and no recurrence was observed during 1‐year follow‐up, whereas four patients needed second sessions. Conclusions: PV bigeminy is relatively rare but a unique electrophysiological finding in AF patients, suggesting reentrant substrate within the PV and/or surrounding tissue. PV bigeminy is a strong indicator of arrhythmogenic vein triggering AF, and ensures an excellent clinical outcome after PVI. [ABSTRACT FROM AUTHOR]

Background: Induction test of atrial fibrillation (AF) is one of endpoint measures in catheter ablation (CA). However, its predictive value in long‐term outcome remains controversial. Methods: Ninety‐eight patients (61 years, 77 males) with persistent AF who underwent pulmonary vein antrum isolation‐based CA were retrospectively analyzed. We determined whether inducibility of AF/atrial tachyarrhythmias (AT) by atrial burst pacing at the end of CA and other characteristics were associated with the recurrence of AF/AT. Atrial burst pacing was performed with 30‐beat from the coronary sinus; increasing from 240 to 320 ppm. Inducibility was defined as AF/AT lasting ≥5 minutes following atrial burst pacing. Results: AF/AT was induced in 50 patients (51%). During 1 year of follow‐up, 71 patients (72.4%) had no recurrence of AF/AT. A logistic regression analysis showed that female gender (OR 3.8; P = 0.02), multiple sessions (OR 3.5; P = 0.02), and early recurrence of AF/AT (OR 5.3; P = 0.004) were associated with clinical recurrence. AF/AT Inducibility was not associated with clinical recurrence (P = 0.65). A subanalysis in patients with enlarged LA (LA diameter ≥45 mm, n = 40) showed that AF/AT inducibility was associated with recurrence (OR 8.1; P = 0.04). The positive and negative predictive values of AF/AT inducibility for AF/AT recurrence were 41 and 89%, respectively. Negative predictive value was increased to 92.3% when the inducibility was defined as AF/AT of ≥30 seconds following atrial burst pacing. Conclusions: AF/AT inducibility cannot predict long‐term clinical recurrence in patients with persistent AF. However, it may have a prognostic value especially in patients with enlarged LA. [ABSTRACT FROM AUTHOR]

BACKGROUND Hypertension is a powerful risk factor of atrial fibrillation (AF). The pathophysiology of AF with hypertension is associated with sympatho-excitation or the renin-angiotensin system; however, current therapies cannot sufficiently prevent its development. We previously revealed that brain angiotensin II type 1 receptor (AT1R) blockade causes a depressor response via sympathoinhibition. Herein, we evaluated whether brain AT1R contributes to AF development in hypertensive rats. METHODS We divided the stroke-prone spontaneously hypertensive rats (SHRSP) treated with intracerebroventricular (ICV) infusion of vehicle (S-VEH), ICV infusion of losartan (S-LOS), or oral administration of hydralazine (S-HYD); and Wistar Kyoto rats treated with ICV infusion of vehicle. RESULTS Two weeks later, systolic blood pressure was significantly lower in the S-LOS group than in the S-VEH group and was even lower in the S-HYD group. Urinary norepinephrine excretion for 24h, an indirect marker of sympathoexcitation, significantly reduced in the S-LOS group but increased in the S-HYD group despite depressor response. AF was induced by transesophageal burst pacing. AF duration was significantly shorter in the S-LOS group than in the S-VEH group (5.0 ± 0.4 vs. 15.2 ± 3.7 s; n = 8 each; P < 0.05). However, it was significantly longer in the S-HYD group than in the S-VEH group. Interstitial atrial fibrosis and echocardiographic parameters did not differ between the SHRSP groups. CONCLUSIONS Brain AT1R blockade suppresses AF inducibility and maintenance independent of depressor response in hypertensive rats. [ABSTRACT FROM AUTHOR]

Many previous clinical studies have suggested that atrial fibrillation (AF) is closely associated with hypertension. However, the benefits of antihypertensive therapy on AF are still inconsistent, and it is necessary to explore the factors augmenting AF in hypertensive rats. The aim of the present study was to investigate the correlation between arterial pressure or voltage stimulus and to the duration of electrically induced AF in normotensive or hypertensive rats. Methods. AF was reproducibly induced by transesophageal atrial burst pacing in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We did the burst pacing at high (20 V) or low (5 V) voltage. Results. Duration of AF did not correlate with systolic blood pressure (SBP) and stimulus voltage in WKY. However, only in SHR, duration of AF with high stimulus voltage significantly correlated with SBP and was significantly longer in high than in low voltage stimulus. Discussion and Conclusion. Duration of AF is augmented by high voltage stimulus with higher blood pressure in SHR. [ABSTRACT FROM AUTHOR]

We report the case of an otherwise healthy 64‐year‐old female who developed cardiopulmonary arrest after the administration of pilsicainide for treatment of paroxysmal atrial fibrillation. She had had an episode of paroxysmal atrial fibrillation, but no liver dysfunction, renal dysfunction, or echocardiographic abnormality before her admission. On the day of admission and the following day, 50 mg of pilsicainide was administered intravenously over 10 min (total 100 mg). Shortly after the second injection, she developed marked bradycardia and hypotension and eventually fell into a state of pulseless electrical activity. Immediate cardiopulmonary resuscitation was started. Although application of a temporary pacemaker restored her heart rate, echocardiography revealed no left ventricular contraction. We started percutaneous cardiopulmonary support (PCPS) and intra‐aortic balloon pumping (IABP). Her cardiac contraction gradually recovered and returned to completely normality 3 days after the onset. The patient was discharged in an ambulatory condition. [ABSTRACT FROM AUTHOR]