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Cavotricuspid isthmus (CTI) ablation is an important treatment strategy for CTI-dependent atrial flutter (AFL). The location of the catheter contact area is confirmed by the contact vector direction (CVD) through three-dimensional mapping during the procedure. However, the relationship between CVD during radiofrequency ablation and its efficacy in achieving CTI block has not been clarified. This study aimed to investigate the relationship between CVD and efficacy in achieving CTI block. CVDs during radiofrequency ablation were divided into proximal vectors against the distal tip (P-vector) and other vectors (normal-vector). In 39 patients who underwent CTI linear ablation, the CTIs were divided into two segments: the tricuspid valve area (anterior) and inferior vena cava area (posterior). The frequency of the residual conduction gap was compared between segments in which the P- and normal-vectors were observed. P-vectors were observed in 13 of the 78 segments. The median ablation index was not significantly different between segments in which the P-vector and normal-vector were observed (398.2 [384.2-402.2] vs. 393.3 [378.3-400.1], p = 0.15). However, residual conduction gaps were significantly more frequently observed in the segment in which the P-vector was observed than those in which only the normal-vector was observed (6/13, 46.2% vs. 3/65, 4.6%; p < 0.01). During a 6-month follow-up, two patients required a second session of ablation due to AFL recurrence. A residual conduction gap was observed in one patient at the site where the P-vector was observed in the first session. Avoiding the P-vector might be an important factor in improving CTI block and reducing AFL recurrence., (© 2023. The Author(s).)

Background: Mitral regurgitation is frequently complicated with atrial fibrillation without apparent organic changes in the leaflet, which occasionally improves after successful radiofrequency catheter ablation. We aimed to evaluate a possible geometric effect of radiofrequency catheter ablation on the mitral valve apparatus., Methods: Forty-three consecutive patients who underwent successful catheter ablation for persistent atrial fibrillation (maintaining sinus rhythm for 6 months after their procedure) were examined by serial real-time 3-dimensional transesophageal echocardiography before and 6 months after catheter ablation. Mitral valve complex geometry was measured using dedicated software for 3-dimensional transesophageal echocardiography., Results: Mitral valve apparatus showed significant reverse remodeling along with left atrial reverse remodeling 6 months after successful catheter ablation (50.5 [39.2-61.0] versus 36.4 [28.9-43.1] mL/m 2 ; P <0.001). The degree of mitral regurgitation decreased in a majority of patients (mitral regurgitation jet area; 1.83 [0.78-3.09] versus 0.77 [0.36-1.47] cm 2 ; P <0.001). Annular area significantly decreased (5.32±0.91 versus 4.73±0.76 cm 2 /m 2 ; P <0.001) in both anterior-posterior and medial-lateral directions. Mitral annular contraction significantly recovered after maintaining sinus rhythm for 6 months (7.51 [4.82-9.62]% versus 9.71 [6.27-13.85]%; P =0.008). There were no significant changes in tenting volume or tenting height (0.46 [0.27-0.89] versus 0.51 [0.32-0.72] mL/m 2 , P =0.744; 2.34 [1.75-3.48] versus 2.76 [1.99-3.08] mm/m 2 , P =0.717). The leaflet surface area also significantly decreased after catheter ablation (5.74 [5.01-6.33] versus 5.19 [4.63-5.64] cm 2 /m 2 ; P <0.001)., Conclusions: Maintaining sinus rhythm after successful catheter ablation promotes reverse remodeling in the mitral valve apparatus and improves so-called atrial functional mitral regurgitation. The positive geometric effect of catheter ablation would be expected to be a possible contributor to better outcomes in patients with atrial fibrillation, in addition to the postprocedural freedom from rhythm disturbance.

Background: After previous earthquakes, a high prevalence of deep vein thrombosis (DVT) has been reported. We examined DVT prevalence and risk factors in evacuees of the Kumamoto earthquakes by performing mobile DVT screening at various evacuation centers around the epicenter., Methods and results: For 1 month after the Kumamoto earthquake on 14 April 2016, mobile DVT screening using portable ultrasonography (US) was performed at 80 evacuation centers. Questionnaires, physical examination, and US of the lower limb were carried out, and simple D-dimer measurements were undertaken for DVT-positive examinees. The total number of examinees was 1,673, of whom 178 (10.6%) had DVT. The prevalence of DVT seemed to be gradually decreasing in the screening period, but age, use of sleep medication, prevalence of hypertension, dyslipidemia, leg edema, and lower leg varix were significantly higher in the DVT positive group than in the negative group. On multivariable logistic regression analysis, high age (≥70 years old), use of sleep medication, lower leg edema, and lower leg varix were significant predictors of DVT. In examinees with these 4 predictors, the DVT positive rate was 71.4%., Conclusions: In the first month after the Kumamoto earthquakes, DVT prevalence and severity, evaluated on D-dimer level, decreased with the passage of time. Mobile DVT screening indicated significant factors stratifying DVT risk in the evacuees.

Background: Experimental studies suggest that angiotensin II-receptor blockers can influence atrial remodeling and may prevent atrial fibrillation (AF). Therefore, we hypothesized that irbesartan may prevent the recurrence of AF following either catheter ablation or electrical cardioversion of AF., Methods: Study on the Effect of Irbesartan on Atrial Fibrillation Recurrence in Kumamoto (SILK study) is a prospective, multicenter, randomized, and open-label comparative evaluation of the effects of irbesartan and amlodipine on AF recurrence in hypertensive patients with AF who are scheduled to undergo catheter ablation or electrical cardioversion of AF. The primary end point was either AF or atrial tachycardia (AT) recurrence. AF/AT recurrence was evaluated for 6 months using 24-h Holter electrocardiogram and portable electrocardiogram. The secondary endpoints included the change in blood pressure, the interval from the procedure to the first AF/AT recurrence, cardiovascular events, left atrial diameter (LAD), left ventricular ejection fraction (LVEF), and changes in the biomarkers [brain natriuretic polypeptide (BNP), high-sensitivity C-reactive protein (hs-CRP), urinary albumin/creatinine]., Results: The study enrolled 98 patients (irbesartan; n=47, amlodipine; n=51). The recurrence of AF/AT was observed in 8 patients (17.0%) in the irbesartan group and in 10 patients (19.6%) in the amlodipine group. There was no significant difference in the AF/AT recurrence between the irbesartan and amlodipine groups. Blood pressure decreased similarly in both groups. There were no significant differences between the two groups as regards to the interval from the procedure to the first AF/AT recurrence, occurrence of cardiovascular events, changes in LAD and LVEF. BNP and urinary albumin/creatinine significantly decreased similarly in both groups, but no significant difference was found in hs-CRP between the two groups., Conclusions: In hypertensive patients with AF, treatment with irbesartan did not have any advantage over amlodipine in the reduction of AF/AT recurrence after catheter ablation or electrical cardioversion., (Copyright © 2017 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

A 79-year-old woman was admitted with a left femoral neck fracture and she immediately developed circulatory shock. Echocardiography showed a markedly enlarged right ventricle (RV) with systolic ballooning of the mid-ventricular wall and preserved contractility of the apex. The left ventricular (LV) motion was normal. Multi-detector-row computed tomography showed severe congestion of the contrast media in the right atrium with no forward flow to RV, but no pulmonary embolism. She was successfully treated with percutaneous veno-arterial extracorporeal membrane oxygenation. This case presented with acute, profound, but reversible RV dysfunction triggered by acute stress in a manner similar to that seen in LV stress cardiomyopathy.

Background/objectives: Pericardial fat (PF) and complex fractionated atrial electrogram (CFAE) are both associated with atrial fibrillation (AF). Therefore, we examined the relation between PF and CFAE area in AF., Methods: The study population included 120 control patients without AF and 120 patients with AF (80 paroxysmal AF and 40 persistent AF) who underwent catheter ablation. Total cardiac PF volume, representing all adipose tissue within the pericardial sac, was measured by contrast-enhanced computed tomography. The location and distribution of CFAE region were identified by left atrial endocardial mapping using a three-dimensional mapping system. We analyzed the significance of total cardiac PF volume and total area of CFAE region on AF, persistence of AF from paroxysmal to persistent form, and the relation between total cardiac PF volume and total CFAE area. We also evaluated the regional distribution of PF volume and CFAE area in five areas of the left atrium (LA)., Results: Total cardiac PF volume correlated with AF (odds ratio [OR]: 1.024, p<0.001). Total cardiac PF volume and total CFAE area were both independently associated with persistence of AF (OR: 1.018, p=0.018, OR: 1.144, p=0.002, respectively). Multivariate linear regression analysis identified total cardiac PF volume as a significant and independent determinant of total CFAE area (r=0.488, p<0.001). Furthermore, regional PF volume correlated with local CFAE area in an each LA area., Conclusions: PF volume correlated significantly with CFAE area in patients with AF. This finding suggests that PF is directly related to the progression of CFAE area and promotes the pathogenic process of AF., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Background: Oxidative stress is considered to contribute to the pathological consequences of atrial fibrillation (AF). We examined the level of oxidative stress in AF patients and changes in its level following sinus rhythm restoration., Methods: Oxidative stress level was evaluated by urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of oxidative DNA damage, and urinary biopyrrin, an oxidative metabolite of bilirubin. In Study 1, we compared 8-OHdG/creatinine levels between patients with permanent AF (AF-group, n=40) and sinus rhythm (SR-group, n=133). In Study 2, we examined the changes in 8-OHdG and biopyrrin levels in 36 patients with persistent AF following sinus rhythm restoration by electrical or pharmacological cardioversion (n=15) and radiofrequency catheter ablation (n=21)., Results: In Study 1, 8-OHdG/creatinine levels were significantly higher in AF-group than in SR-group (19.1 ± 8.6 vs. 12.3 ± 5.5 ng/mg, p<0.001). Multivariate analysis showed that the presence of AF was an independent factor that significantly correlated with 8-OHdG/creatinine level after adjustment for other covariates to oxidative stress (β=0.36, p<0.001). Sinus rhythm was maintained at the chronic phase in patients of all Study 2 (7.2 ± 5.8 months after cardioversion or catheter ablation). 8-OHdG/creatinine and biopyrrin/creatinine levels at the chronic phase were significantly lower than those before cardioversion or catheter ablation (8.7 ± 3.2 vs. 21.7 ± 15.1 ng/mg, p<0.0001 and 1.7 ± 1.1 vs. 3.0 ± 1.9 mU/mg, p<0.0001)., Conclusions: Oxidative stress level is significantly increased in AF patients, but can be improved by restoration of sinus rhythm. The results suggest that the pathogenic process of AF is promoted by AF itself through the production of oxidative stress., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: Little is known about the effect of nifekalant, a pure I(Kr) -selective blocker, on typical atrial flutter (AFL) and its termination mechanism., Methods: The effects of nifekalant on AFL were elucidated in 17 patients. During AFL, the conduction time from the lateral to septal cavotricuspid isthmus (IS) and that through the reminder of the right atrium (nIS); AFL-cycle length (CL) variability, which was quantified by the standard deviation; and the maximum difference in AFL-CL were measured before and after administration of nifekalant (0.2-0.3 mg/kg). A single extrastimulus was delivered from the lateral cavotricuspid isthmus to elucidate the resetting response curves and atrial effective refractory period (AERP) before and after administration of nifekalant., Results: There was no significant difference in AFL-CL, IS, and nIS before and after nifekalant; however, AERP was increased after nifekalant (155 ± 22 ms vs 184 ± 32 ms, P < 0.001). The standard deviation and the maximum difference in AFL-CL were both increased after nifekalant (1.7 ± 0.7 ms vs 3.6 ± 2.3 ms, P < 0.001 and 4.1 ± 1.9 ms vs 8.5 ± 5.2 ms, P < 0.001). The total excitable gap decreased (94 ± 17 ms vs 66 ± 21 ms, P < 0.001) with rightward shift of the resetting response curves and loss of full excitability after nifekalant. In 11 patients (65%), AFL was terminated spontaneously (n = 7) or by a single extrastimulus (n = 4), which was not observed before nifekalant. Termination was associated with orthodromic block in the cavotricuspid isthmus in all patients., Conclusions: Nifekalant increases AERP and AFL-CL variability by abolishing a fully excitable gap, without prolongation of AFL-CL. These unique effects facilitate the termination of AFL., (©2013, The Authors. Journal compilation ©2013 Wiley Periodicals, Inc.)

Background: Angina without significant stenosis, or nonobstructive coronary artery disease, attracts clinical attention. Microvascular coronary artery spasm (microvascular CAS) can cause nonobstructive coronary artery disease. We investigated the clinical features of microvascular CAS and the therapeutic efficacy of calcium channel blockers., Methods and Results: Three hundred seventy consecutive, stable patients with suspected angina presenting nonobstructive coronary arteries (<50% diameter) in coronary angiography were investigated with the intracoronary acetylcholine provocation test, with simultaneous measurements of transcardiac lactate production and of changes in the quantitative coronary blood flow. We diagnosed microvascular CAS according to lactate production and a decrease in coronary blood flow without epicardial vasospasm during the acetylcholine provocation test. We prospectively followed up the patients with calcium channel blockers for microvascular coronary artery disease. We identified 50 patients with microvascular CAS who demonstrated significant impairment of the endothelium-dependent vascular response, which was assessed by coronary blood flow during the acetylcholine provocation test. Administration of isosorbide dinitrate normalized the abnormal coronary flow pattern in the patients with microvascular CAS. Multivariate logistic regression analysis indicated that female sex, a lower body mass index, minor-borderline ischemic electrocardiogram findings at rest, limited-baseline diastolic-to-systolic velocity ratio, and attenuated adenosine triphosphate-induced coronary flow reserve were independently correlated with the presence of microvascular CAS. Receiver-operating characteristics curve analysis revealed that the aforementioned 5-variable model showed good correlation with the presence of microvascular CAS (area under the curve: 0.820). No patients with microvascular CAS treated with calcium channel blockers developed cardiovascular events over 47.8±27.5 months., Conclusions: Microvascular CAS causes distinctive clinical features and endothelial dysfunction that are important to recognize as nonobstructive coronary artery disease so that optimal care with calcium channel blockers can be provided., Clinical Trial Registration: URL: www.umin.ac.jp/ctr. Unique identifier: UMIN000003839.

Background: The anatomical location of the reentry circuit in verapamil-sensitive atrial tachycardia originating from the vicinity of atrioventricular node (V-AT) is not well clarified., Objective: To define the reentry circuit of V-AT., Methods: In 17 patients with V-AT, rapid atrial pacing at a rate 5 beats/min faster than the tachycardia rate was delivered from multiple sites of the right atrium (RA) during tachycardia to define the direction of the proximity of the slow conduction area of the reentry circuit. After identification of manifest entrainment and orthodromic capture of the earliest atrial activation site (EAAS), radiofrequency energy was delivered starting at a site 2 cm away from the EAAS in the direction of the pacing site. Radiofrequency energy application site was then gradually advanced toward EAAS until the termination of tachycardia to define the entrance of the slow conduction area., Results: The EAAS was orthodromically captured by pacing delivered from one of the high anterolateral RA (n = 6), high posteroseptal RA (n = 9), and RA appendage (n = 2). Radiofrequency energy delivery to the site, 10.1 ± 2.8 mm away from the EAAS, terminated V-AT immediately after the onset of delivery (2.9 ± 1.0 seconds). The successful ablation site located outside the Koch's triangle, being more distant from the His bundle site than the EAAS (12.4 ± 2.9 vs 6.4 ± 1.9 mm; P <.0001)., Conclusion: The reentry circuit of V-AT located outside the Koch's triangle. V-AT was eliminated by the radiofrequency energy delivered to the entrance of the reentry circuit, which was more distant from the His bundle site than the EAAS, under the navigation of entrainment., (Copyright © 2012 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Shock patients with restrictive cardiomyopathy due to cardiac amyloidosis are refractory to medical treatment. Here, we report a case of early initiation of intra-aortic balloon pumping (IABP) in a patient with cardiac amyloidosis who developed postoperative shock. Continuous hemodiafiltration was also applied to control circulating fluid volume. The mechanical treatments allowed reduction of the doses of catecholamine and diuretics and resulted in full recovery. It is reasonable to initiate IABP and hemofiltration dialysis during the early stages for the appropriate control of hemodynamics and fluid in shock patients with cardiac amyloidosis.

Background: The complex fractionated atrial electrogram (CFAE) region has been suggested to contribute to the maintenance of atrial fibrillation (AF), but its role for the initiation of AF has not been clarified., Objective: We analyzed the mechanisms of the initiation of random reentrant wave propagation at AF onset, especially in relation to CFAE region., Methods: Endocardial mapping of the left atrium using a 3-dimensional noncontact mapping system was performed in 19 patients., Results: Thirty-two spontaneous AF onset episodes, which were initiated by the focal repetitive discharges (9 ± 9 beats), deriving from the pulmonary veins (PV) (n = 17) and from non-PV CFAE regions (n = 15) were observed. The coupling intervals of the focal discharges that initiated AF (AF-D) were significantly shorter than those that did not initiate AF (non-AF-D) (179 ± 33 ms vs. 217 ± 45 ms, P = .0005). After the AF-D, localized conduction blocks occurred in the CFAE region. Subsequently, the waves propagated to the remainder of the atrium, accompanying the anchored activation around the localized conduction block lines in the CFAE regions. Left atrial activation times of AF-D were significantly longer than those of non-AF-D (151 ± 35 ms vs. 83 ± 17 ms, P < .0001). These longer activation times after AF-D enabled the waves to reenter the previously blocked CFAE region from the opposite direction, and thus the meandering reentrant wave propagation was initiated., Conclusion: Unidirectional conduction block in the CFAE region and subsequent prolonged left atrial activation time following short coupled premature discharge were the underlying mechanisms of AF initiation, suggesting the importance of the CFAE region as the substrate for AF onset., (Copyright © 2011 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background and Purpose: Cardiac resynchronization therapy (CRT) is a beneficial strategy to improve severe cardiac dysfunction in patients with congestive heart failure (CHF). The improvement of endothelial function in CHF patients treated with CRT is reflected in the mortality risk reduction. However the precise mechanisms of the relationship between CRT and vascular endothelial function have not been well discussed., Methods and Subjects: Twenty-two severe consecutive CHF patients associated with dilated cardiomyopathy [New York Heart Association (NYHA) class 3.3 ± 0.5, left ventricular ejection fraction (LVEF) 24.4 ± 5.9%] were included in this study. We evaluated endothelial function, measured by reactive hyperemia peripheral arterial tonometry (RH-PAT), between optimal medical therapy alone group (medical therapy group: n = 10) and CRT group (n = 12) at the study enrolment and 12 weeks later. Furthermore we analyzed the association between the RH-PAT and cardiac function., Essential Results: Both therapies significantly and equally improved NYHA class, LVEF, end-diastolic left ventricular dimension and plasma levels of brain natriuretic peptide (BNP). CRT significantly increased RH-PAT index (medical therapy group: 1.5 ± 0.2 to 1.5 ± 0.3, p = 0.824; CRT group: 1.4 ± 0.2 to 1.7 ± 0.4, p = 0.003) and cardiac output (medical therapy group: 3.3 ± 1.1 to 3.5 ± 1.0, p = 0.600; CRT group: 2.7 ± 0.6 to 4.3 ± 1.5, p = 0.001), compared to the medical therapy group. There was significant positive correlation between the change in RH-PAT index and cardiac output (r = 0.600, p = 0.003)., Conclusions: CRT significantly improved endothelial function through the improvement of cardiac output in CHF patients, compared to optimal medical therapy., (Copyright © 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

We describe an 81-year-old man with multiple focal atrial tachycardias (ATs) originating from the tricuspid annulus. Non-contact mapping showed 3 incessant ATs, originating from the vicinity of His bundle region, inferior portion of coronary sinus ostium, and coronary sinus ostium, and 2 premature atrial contractions (PACs) originating from the tricuspid annulus in the 5 o'clock position and 6 o'clock position in the left anterior oblique view. Radiofrequency energy application to these 5 sites successfully eliminated the ATs and PACs. The patient has remained free from ATs or any symptoms without medication during the 16-month follow-up period. Non-contact mapping was useful in identifying the multiple AT origins, especially even if the tachycardia origin shifted occasionally or the tachycardia was non-sustained.

A 56-year-old man was admitted for the treatment of supraventricular tachycardia. After successful ablation of the left concealed accessory pathway, four fast-slow forms of atrioventricular nodal reentrant tachycardia associated with different right- and left-sided retrograde slow pathways were induced. The locations of retrograde slow pathway were observed at the left inferior paraseptum, left mid-septum, right inferior paraseptum, and coronary sinus ostium, respectively. These retrograde slow pathways formed the integral limb of each tachycardia because conduction block of each slow pathway by catheter ablation was associated with the termination of tachycardia or abrupt change in the atrial activation sequence.

Background: Calcium channel-dependent tissue has been suggested to be involved in the circuit of verapamil-sensitive atrial tachycardia originating from the atrioventricular (AV) node vicinity (V-AT), but little information exists., Methods and Results: To examine the tachycardia circuit of V-AT, a single extrastimulus was delivered during tachycardia to 10 sites of the intraatrial septum: the earliest atrial activation site; His bundle (HB) site; 3 arbitrarily divided sites on the AV junction extending from the HB site to the coronary sinus ostium (CSOS) (sites S, M, and I); the internal-CSOS, inferior-CSOS, superior-CSOS, posterior-CSOS, and posteroinferior-CSOS in 10 patients with V-AT. The longest coupling interval that reset V-AT and subsequent return cycle were measured. The longest coupling interval at earliest atrial activation site was significantly longer than the longest coupling interval at the HB site, site S, M, and I, internal-CSOS, inferior-CSOS, superior-CSOS, posterior-CSOS, and posteroinferior-CSOS, respectively (P<0.001 for HB site and P<0.0001 for the remaining 8 sites). The return cycle at earliest atrial activation site did not differ from the tachycardia cycle length, whereas those at the remaining 9 sites were significantly longer than tachycardia cycle length (P<0.001). Furthermore, a single extrastimulus delivered from sites inferior to the HB site advanced His potential without resetting V-AT in 7 patients in whom AV block was not observed during tachycardia., Conclusions: Atrial tissue within the Koch's triangle extending from the HB site to posteroinferior-CSOS is not involved in the tachycardia circuit. Verapamil-sensitive atrial tissue close to the AV node but not the AV nodal conducting system forms the tachycardia circuit of V-AT.

A 15-year-old boy without structural heart disease was admitted for the treatment of frequent episodes of premature ventricular contractions (PVCs). Left ventricular mapping revealed that the origin of PVC was at the posterior papillary muscle. Diastolic small potentials were observed during sinus rhythm with a constant interval following QRS beats. This potential eventually coupled with the ventricular myocardium, resulting in the generation of PVC, and thus preceded QRS by 31 msec. Catheter ablation to this site induced non-sustained ventricular tachycardia, followed by transient ventricular fibrillation. Repeated application of radiofrequency energy eliminated PVC accompanied by the split of the diastolic potential.

Background: The role of complex fractionated atrial electrograms (CFAEs) in the maintenance of atrial fibrillation (AF) has not been well clarified., Objective: The purpose of this study was to examine the mechanisms of AF maintenance, especially in relation to CFAE., Methods: Endocardial mapping of the left atrium was performed during AF using a three-dimensional noncontact mapping system in 16 patients with paroxysmal AF., Results: During AF, focal discharges were found at the pulmonary vein and sites within the CFAE region (3.0 +/- 1.9 vs. 2.8 +/- 1.5 times/s; P = NS) but not in the non-CFAE region. One to four meandering waves propagated over various pathways during AF. The frequency of the wave break and pivoting activation in the CFAE region were significantly higher than in the non-CFAE region (5.6 +/- 3.6 vs. 0 +/- 0 times/s, P <.0001 and 5.0 +/- 2.1 vs. 0.3 +/- 0.8 times/s; P <.0001). Wave fusion in the CFAE region was more frequently observed than in the non-CFAE region (6.5 +/- 5.8 vs. 3.6 +/- 3.1 times/s; P <.05). Conduction velocity in the CFAE region was slower than in the non-CFAE region (0.7 +/- 0.4 vs. 1.9 +/- 0.5 m/s; P <.0001). The generation of a new wave was associated with the wave break, fusion, and focal discharge. Furthermore, perpetuation of these waves accompanied by slow conduction and pivoting activation was mostly observed in the CFAE region., Conclusion: The CFAE region plays an important role in the perpetuation of AF. In addition to focal discharge, wave break and fusion associated with slow conduction and pivoting activation in the CFAE region sustained wave propagation, resulting in the maintenance of AF.

Introduction: Previous studies have shown raised plasma von Willebrand factor (VWF) levels in patients with atrial fibrillation (AF). However, little is known about changes of VWF associated with VWF-cleaving protease (ADAMTS13) in AF. The aim of this study was to examine the relationship between changes in plasma VWF and ADAMTS13 levels, and left atrial remodeling in AF patients., Materials and Methods: We measured plasma VWF and ADAMTS13 antigen levels in 70 paroxysmal AF (PAF) patients, 56 chronic AF (CAF) patients, and 55 control subjects., Results: Plasma VWF levels (mU/ml) were significantly higher in CAF and PAF patients compared with the controls (2103 +/- 743, 1930 +/- 676, 1532 +/- 555, respectively, P < 0.0001 in CAF vs. controls, P = 0.001 in PAF vs. control), while ADAMTS13 levels (mU/ml) were significantly lower in CAF and PAF patients compared with the controls (795 +/- 169, 860 +/- 221, 932 +/- 173, respectively, P = 0.0002 in CAF vs. controls, P = 0.04 in PAF vs. control). The VWF/ADAMTS13 ratio was significantly higher in patients with CAF than PAF or controls (2.81 +/- 1.30, 2.34 +/- 0.92, 1.73 +/- 0.83, respectively; P = 0.01 in CAF vs. PAF, P < 0.0001 in CAF vs. controls). There was a significant correlation between the VWF/ADAMTS13 ratio and left atrial diameter (positive correlation; r = 0.275, P = 0.0002) and left atrial appendage flow velocity (negative correlation; r = -0.345, P = 0.0018)., Conclusions: These findings suggest that the imbalance between plasma VWF and ADAMTS13 levels caused by left atrial remodeling might be closely associated with intra-atrial thrombus formation in AF patients.

Background: The precise nature of the upper turnaround part of atrioventricular nodal reentrant tachycardia (AVNRT) is not entirely understood., Methods: In nine patients with AVNRT accompanied by variable ventriculoatrial (VA) conduction block, we examined the electrophysiologic characteristics of its upper common pathway., Results: Tachycardia was induced by atrial burst and/or extrastimulus followed by atrial-His jump, and the earliest atrial electrogram was observed at the His bundle site in all patients. Twelve incidents of VA block: Wenckebach VA block (n = 7), 2:1 VA block (n = 4), and intermittent (n = 1) were observed. In two of seven Wenckebach VA block, the retrograde earliest atrial activation site shifted from the His bundle site to coronary sinus ostium just before VA block. Prolongation of His-His interval occurred during VA block in 11 of 12 incidents. After isoproterenol administration, 1:1 VA conduction resumed in all patients. Catheter ablation at the right inferoparaseptum eliminated antegrade slow pathway conduction and rendered AVNRT noninducible in all patients., Conclusion: Selective elimination of the slow pathway conduction at the inferoparaseptal right atrium may suggest that the subatrial tissue linking the retrograde fast and antegrade slow pathways forms the upper common pathway in AVNRT with VA block.

Ventricular tachycardia originating from the right ventricular outflow tract (RVOT) is considered benign, but sometimes it causes polymorphic ventricular tachycardia and ventricular fibrillation, resulting in sudden cardiac death. A 58-year-old woman without structural heart disease was admitted for evaluation of recurrent episodes of syncope. Surface ECG showed frequent repetitive premature ventricular contraction (PVC) of RVOT origin. Polymorphic ventricular tachycardia triggered by the same PVC was documented by Holter ECG during an episode of syncope. Radiofrequency catheter ablation was performed to eradicate this PVC. No polymorphic ventricular tachycardia has developed after the procedure, and the patient has had no recurrence of syncope.

Background: Little information exists regarding the precise distribution of verapamil-sensitive atrial tachycardia originating from the vicinity of the atrioventricular node (V-AT)., Methods: In 12 patients with V-AT, we examined the spatial and topologic distribution of tachycardia origin relative to the His bundle (HB) site. The V-AT origin was divided into six areas: anterior (A-HB), posterior (P-HB), superior (S-HB), inferior (I-HB), lateral (L-HB), and septal (SP-HB) portion of HB catheter. Three dimensional distance between the distal pair of the electrodes of HB catheter and that of V-AT origin (DIS) was obtained by calculating the distances on the right and left anterior fluoroscopic images. Topologic distribution was expressed as the interval between the onset of the atrial electrogram of V-AT origin and that of HB catheter (INT)., Results: The tachycardia origin was observed at the P-HB in four, S-HB in two, I-HB in two, SP-HB in three, and L-HB in one patient. The tachycardia cycle length, DIS, and INT were 369 +/- 67 ms, 12 +/- 3 mm, and -12 +/- 8 ms, respectively. After successful ablation of initial V-AT (1st V-AT), V-AT with a different origin (2nd V-AT) was induced in five patients. The tachycardia origin, tachycardia cycle length, DIS, and INT of the 2nd V-AT (P-HB in three, S-HB in one, and SP-HB in one patient; 333 +/- 66 ms, 8 +/- 3 mm, and -11 +/- 4 ms, respectively) were not different from those of 1st V-AT., Conclusions: V-AT often shows a shift in tachycardia origin to another site where the spatial and topologic distributions are similar to those of 1st V-AT.

Background: The incidence and mechanism of the dislocated antegrade fast pathway (A-FP) were examined in various forms of atrioventricular nodal reentrant tachycardia (AVNRT)., Methods and Results: To localize the A-FP, 5 atrial sites comprising the inferior coronary sinus ostium (CSOS), apex of the triangle of Koch (A-TOK), and 3 equidistant sites on the atrioventricular junction extending from A-TOK to CSOS (site S, M, and I) were pace mapped at 100 beats/min in 71 patients with slow-fast (n=49), fast-slow (n=7) and slow-intermediate (n=15) forms of AVNRT. The site with the shortest interval between the stimulus and His potential recorded at the A-TOK (shortest St-H) was defined as the A-FP site. The A-FP was located at A-TOK in 31 patients (nondislocated group), and inferior to A-TOK in 40 patients (site S in 26, M in 13, and I in one patient; dislocated group). There was no significant difference in the location of the A-FP among the 3 forms of AVNRT. Although the shortest St-H did not differ between groups, the St-H at A-TOK in the dislocated group was significantly longer than that in the nondislocated group. Additionally, the His potential preceding that of the A-TOK was observed more frequently inferior to the A-TOK in the dislocated group than in the nondislocated group, suggesting that the A-FP dislocation was accompanied by displacement of the His bundle., Conclusions: Dislocated A-FP was frequently and uniformly observed among various forms of AVNRT, and is probably caused by inferior displacement of the entire atrioventricular node - His bundle apparatus.

Background: Little is known about the exact boundaries of the reentrant circuit in the slow-slow form of atrioventricular nodal reentrant tachycardia (AVNRT)., Objective: The purpose of this study was to examine the tachycardia circuit in the slow-slow form of AVNRT., Methods: Single extrastimuli were delivered during the slow-slow form of AVNRT at 10 sites along the right interatrial septum: superior portion of the His-bundle (HB) site, the HB site, three equidistantly divided sites of the AV junction between HB site and coronary sinus ostium (CSOS; sites S, M, and I), and inferior, superior, posterior, posteroinferior, and internal portions of the CSOS in 13 patients. The longest coupling interval of a single extrastimulus that reset the tachycardia and the following return cycle were measured., Results: The tachycardia cycle length was 409 +/- 50 ms. The earliest atrial electrogram during tachycardia was observed at site I in all patients. The longest coupling intervals at superior-HB, HB site, sites S, M, and I, and inferior-CSOS, superior-CSOS, posterior-CSOS, posteroinferior-CSOS, and internal-CSOS were 340 +/- 52, 355 +/- 50, 367 +/- 50, 378 +/- 51, 398 +/- 49, 398 +/- 52, 355 +/- 60, 351 +/- 50, 371 +/- 48, and 363 +/- 54 ms, respectively. The following return cycles were 468 +/- 52, 453 +/- 52, 442 +/- 52, 431 +/- 50, 411 +/- 52, 410 +/- 49, 454 +/- 45, 457 +/- 57, 438 +/- 54, and 445 +/- 53 ms, respectively. The longest coupling intervals at site I and inferior-CSOS were significantly longer than those at the other sites (P <.0001). The return cycles at site I and inferior-CSOS did not differ from the tachycardia cycle length, whereas those at the other sites were significantly longer than the tachycardia cycle length (P <.0001)., Conclusion: Site I and inferior-CSOS are involved in the slow-slow form of AVNRT circuit, and the atrial tissue between those sites form an integral limb of the reentrant circuit.