Pulmonary Vein Intervention for Severe Pulmonary Vein Stenosis After Atrial Fibrillation Ablation　- A Retrospective Cohort Study.

BACKGROUND: Pulmonary vein (PV) stenosis (PVS) is a serious complication of atrial fibrillation (AF) ablation. The objective of this study was to describe interventional treatments for PVS after AF ablation and long-term outcomes in Japanese patients.Methods and Results: This multicenter retrospective observational study enrolled 30 patients (26 [87%] male; median age 55 years) with 56 severe PVS lesions from 43 PV interventional procedures. Twenty-seven (90%) patients had symptomatic PVS and 19 (63%) had a history of a single AF ablation. Of the 56 lesions, 41 (73%) were de novo lesions and 15 (27%) were retreated. Thirty-three (59%) lesions were treated with bare metal stents, 14 (25%) were treated with plain balloons, and 9 (16%) were treated with drug-coated balloons. All lesions were successfully treated without any systemic embolic event. Over a median follow-up of 584 days (interquartile range 265-1,165 days), restenosis rates at 1 and 2 years were 35% and 47%, respectively. Multivariate Cox regression analysis revealed devices <7 mm in diameter (hazard ratio [HR] 2.52; 95% confidence interval [CI] 1.04-6.0; P=0.040) and totally occluded lesions (HR 3.33; 95% CI 1.21-9.15; P=0.020) were independent risk factors for restenosis. CONCLUSIONS: All PVS lesions were successfully enlarged by the PV intervention; however, restenosis developed in approximately half the lesions within 2 years.

Histological validation of atrial structural remodelling in patients with atrial fibrillation.

BACKGROUND AND AIMS: This study aimed to histologically validate atrial structural remodelling associated with atrial fibrillation. METHODS AND RESULTS: Patients undergoing atrial fibrillation ablation and endomyocardial atrial biopsy were included (n = 230; 67 ± 12 years old; 69 women). Electroanatomic mapping was performed during right atrial pacing. Voltage at the biopsy site (Vbiopsy), global left atrial voltage (VGLA), and the proportion of points with fractionated electrograms defined as ≥5 deflections in each electrogram (%Fractionated EGM) were evaluated. SCZtotal was calculated as the total width of slow conduction zones, defined as regions with a conduction velocity of <30 cm/s. Histological factors potentially associated with electroanatomic characteristics were evaluated using multiple linear regression analyses. Ultrastructural features and immune cell infiltration were evaluated by electron microscopy and immunohistochemical staining in 33 and 60 patients, respectively. Fibrosis, intercellular space, myofibrillar loss, and myocardial nuclear density were significantly associated with Vbiopsy (P = .014, P < .001, P < .001, and P = .002, respectively) and VGLA (P = .010, P < .001, P = .001, and P < .001, respectively). The intercellular space was associated with the %Fractionated EGM (P = .001). Fibrosis, intercellular space, and myofibrillar loss were associated with SCZtotal (P = .028, P < .001, and P = .015, respectively). Electron microscopy confirmed plasma components and immature collagen fibrils in the increased intercellular space and myofilament lysis in cardiomyocytes, depending on myofibrillar loss. Among the histological factors, the severity of myofibrillar loss was associated with an increase in macrophage infiltration. CONCLUSION: Histological correlates of atrial structural remodelling were fibrosis, increased intercellular space, myofibrillar loss, and decreased nuclear density. Each histological component was defined using electron microscopy and immunohistochemistry studies.

Atrial Structural Remodeling in Patients With Atrial Fibrillation Is a Diffuse Fibrotic Process: Evidence From High-Density Voltage Mapping and Atrial Biopsy.

Background Low-voltage areas (LVAs) in the atria of patients with atrial fibrillation are considered local fibrosis. We hypothesized that voltage reduction in the atria is a diffuse process associated with fibrosis and that the presence of LVAs reflects a global voltage reduction. Methods and Results We examined 140 patients with atrial fibrillation and 13 patients with a left accessory pathway (controls). High-density bipolar voltage mapping was performed using a grid-mapping catheter during high right atrial pacing. Global left atrial (LA) voltage (VGLA) in the whole LA and regional LA voltage (VRLA) in 6 anatomic regions were evaluated with the mean of the highest voltage at a sampling density of 1 cm2. Patients with atrial fibrillation were categorized into quartiles by VGLA. LVAs were evaluated at voltage cutoffs of 0.1, 0.5, 1.0, and 1.5 mV. Twenty-eight patients with atrial fibrillation also underwent right atrial septum biopsy, and the fibrosis extent was quantified. Voltage at the biopsy site (Vbiopsy) was recorded. VGLA results by category were Q1 (<4.2 mV), Q2 (4.2-5.6 mV), Q3 (5.7-7.0 mV), and Q4 (≥7.1 mV). VRLA at any region was reduced as VGLA decreased. VGLA and VRLA did not differ between Q4 and controls. The presence of LVAs increased as VGLA decreased at any voltage cutoff. Biopsies revealed 11±6% fibrosis, which was inversely correlated with both Vbiopsy and VGLA (r=-0.71 and -0.72, respectively). Vbiopsy was correlated with VGLA (r=0.82). Conclusions Voltage reduction in the LA is a diffuse process associated with fibrosis. Presence of LVAs reflects diffuse voltage reduction of the LA.

Impact of Renal Dysfunction on Left Atrial Structural Remodeling and Recurrence After Catheter Ablation for Atrial Fibrillation　- A Propensity Score Matching Analysis.

BACKGROUND: Renal dysfunction coexists with other known risk factors of left atrial (LA) structural remodeling, expressed as low-voltage zones (LVZs), and the recurrence of atrial fibrillation (AF) after ablation. This study aimed to determine whether renal dysfunction had an independent effect on the presence of LVZs and recurrence after AF ablation, using propensity score (PS) matching analysis.Methods and Results:448 consecutive patients who underwent their initial AF ablation were enrolled. Chronic kidney disease (CKD) was defined as an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2, with 126 (28%) patients having CKD. Using PS matching analysis, new subsets (CKD and non-CKD group, n=103 each) were obtained, matched for age, sex, AF type, and LA volume. The presence of LVZs defined as bipolar voltage <0.5 mV was higher in the CKD group than in the non-CKD group (31% vs. 17%, P=0.034). Multivariate analysis showed eGFR was an independent predictor of the presence of LVZs (odds ratio 1.31 per 10-mL/min/1.73 m2decrease, P=0.029). AF-free survival rate was significantly lower in the CKD patients during 20±9 months of follow-up (63% vs. 82%, P=0.019), and eGFR was shown to be an independent predictor of recurrence (hazard ratio 1.29 per 10-mL/min/1.73 m2decrease, P=0.006), but the presence of LVZs did not predict recurrence. CONCLUSIONS: Renal dysfunction independently predicted not only the recurrence of AF after ablation but also the presence of LVZs.

Left atrial low-voltage zone ablation of persistent atrial fibrillation in a patient with myotonic dystrophy: A case report.

We here report a case of a 32-year-old man with genetically diagnosed myotonic dystrophy and persistent atrial fibrillation (AF) who underwent a low-voltage zone (LVZ) ablation. His cardiac function was normal except for a prophylactic pacemaker implantation for a high risk of complete atrioventricular block. An LVZ was found in the anteroseptal left atrium during sinus rhythm and was ablated during induced AF after a pulmonary vein antrum isolation, which terminated the AF and rendered it noninducible by rapid pacing and/or isoproterenol. During 20 months of follow-up, no atrial tachyarrhythmias were observed with pacemaker monitoring of antiarrhythmic drugs.

Impact of the extent of low-voltage zone on outcomes after voltage-based catheter ablation for persistent atrial fibrillation.

BACKGROUND: Low-voltage zones (LVZs), as measured by electroanatomic mapping, are thought to be associated with fibrosis. We reported the efficacy of atrial fibrillation (AF) ablation aiming to homogenize left atrial (LA) LVZ. The purpose of this study was to evaluate the impact of LVZ extension outcomes after LVZ homogenization in patients with nonparoxysmal AF. METHODS: This prospective observational cohort study included 172 patients with nonparoxysmal AF undergoing their initial ablation. LVZ was defined as an area with bipolar electrograms <0.5mV during sinus rhythm. LVZ extent was calculated as the percentage of LA surface area, and subsequently, LVZ was categorized into stages I (<5%), II (≥5% to <20%), III (≥20% to <30%), and IV (≥30%). Patients with LVZs underwent LVZ ablation aimed at homogenization of ≥80% of LVZs following pulmonary vein isolation. The primary endpoint was atrial tachyarrhythmia recurrence-free survival after a single procedure at 18 months off antiarrhythmic drugs. The association of %LVZ with recurrence-free survival was examined using Cox proportional hazard models. RESULTS: The survival rates were 76%, 74%, 57%, and 28% in patients with stages I, II, III, and IV LVZ, respectively. The difference was significant between stages I and IV (log-rank, p<0.001), while not significant between stages I vs. II and I vs. III (p=0.843, p=0.073, respectively). Cox proportional hazard model revealed that %LVZ was an independent predictor of recurrence-free survival (hazard ratio, 1.025 per 1% increase, p<0.001; unadjusted model). The results were similar after demographic and clinical covariate adjustments and after excluding 12 patients who did not achieve homogenization of ≥80% of LVZ. CONCLUSIONS: The extent of LVZ is an independent predictor for recurrence even after LVZ homogenization.

A case of Wolff-Parkinson-White syndrome presenting spontaneous mutual frequent transition between atrioventricular reciprocating tachycardia and atrioventricular nodal re-entrant tachycardia.

Atrioventricular reciprocating tachycardia (AVRT) and atrioventricular nodal re-entrant tachycardia (AVNRT) can coexist and present unidirectional transition (from AVRT to AVNRT, or from AVNRT to AVRT) in a single patient. Actually, such cases have already been reported previously. However, a case with spontaneous bidirectional transition of both tachycardias during supraventricular tachycardia has never been reported. This article describes a case with spontaneous, mutual, and frequent transition between AVRT and AVNRT.

Feasibility of total intravenous anesthesia by cardiologists with the support of anesthesiologists during catheter ablation of atrial fibrillation.

BACKGROUND: The optimal methodology for sedation and anesthesia during atrial fibrillation (AF) ablation has not been well established. We assessed the feasibility of total intravenous anesthesia (TIVA) by cardiologists with support from anesthesiologists during AF ablation and quality of pulmonary vein isolation (PVI) and single procedure success rate at 12 months. METHODS: TIVA was performed by cardiologists using IV propofol and fentanyl under controlled ventilation via i-gel™ without neuromuscular blocking drugs in 160 consecutive patients (80 nonparoxysmal) with no anticipated difficult airway or other severe diseases. Anesthesiologists were requested to be on standby during the procedure. The incidence of anesthesia-associated complications and ablation-associated complications were assessed. To evaluate the quality of PVI, the prevalence of acute adenosine triphosphate (ATP)-provoked PV reconnections and late PV reconnections among those requiring a redo procedure was analyzed. RESULTS: TIVA was successfully completed in 152 patients (95%). In five (3%), we requested help from anesthesiologists, and in three (2%), TIVA was abandoned. No major anesthesia-associated complications were observed. Ablation-associated complications were observed in seven patients (4%). ATP provocation test was performed in 141 patients, and no acute PV reconnections were observed in 134 (95%). Success rates at 12 months were 85% of patients off antiarrhythmic drugs. Twenty-one of 24 patients with recurrence underwent a redo session, and 18 (86%) had no PV reconnections. CONCLUSIONS: TIVA by cardiologists with support from anesthesiologists during AF ablation may be feasible. The success rate at 12 months was high, and prevalence of acute and late PV reconnection was very low.

A case of Type-C Wolff-Parkinson-White syndrome with severe left ventricular dysfunction: Efficacy of catheter ablation.

The present case report describes a 59-year-old female with manifest Wolff-Parkinson-White syndrome and severe left ventricular (LV) dysfunction, however, there was no indication of heart palpitations. The polarity of delta is consistent with the features of the right anteroseptal accessory pathways (APs). The echocardiography showed a remarkable dyssynchrony of the LV wall motion. To circumvent the cardiac dysfunctions, radiofrequency catheter ablation (RFCA) was successfully performed to disconnect the AP. Thereafter, the dyssynchrony disappeared, and the clinical reports observed 6 months following RFCA showed that the LV ejection fraction had been improved from 13% up to 48%, in addition to the improvement in other parameters. The RFCA prevented her from receiving a cardiac resynchronization therapy defibrillator as well as a heart transplantation. .

Exaggerated Reactivity of Parasympathetic Nerves Is Involved in Ventricular Fibrillation in J-Wave Syndrome.

INTRODUCTION: Brugada syndrome (BrS) and early repolarization syndrome (ERS) are termed the J-wave syndrome. In most cases of J-wave syndrome, ventricular fibrillation (VF) often occurs around midnight or in the early morning when parasympathetic tone is augmented. OBJECTIVE: The purpose of this study was to clarify the relationship between VF and autonomic nervous activity in patients with J-wave syndrome. METHODS AND RESULTS: We enrolled 28 consecutive patients with J-wave syndrome (20 BrS and 8 ERS) in whom implantable cardioverter defibrillators (ICDs) were implanted between January 2002 and December 2014. Eleven patients (39%) experienced ICD shock delivery due to VF recurrence after ICD implantation (recurrent-VF group). We investigated baroreflex sensitivity (BRS) using the phenylephrine method, heart rate variability (HRV) with Holter electrocardiography, plasma levels of norepinephrine, and cardiac 123 I-metaiodobenzylguanidine (MIBG) scintigraphy to estimate autonomic nervous function. Upon measurement of HRV, plasma levels of norepinephrine, and 123 I-MIBG testing, there was no significant difference between recurrent-VF and nonrecurrent-VF groups. However, BRS was significantly higher in the recurrent-VF group than in the nonrecurrent-VF group (P = 0.03). Kaplan-Meier curves suggested that high-BRS patients had higher VF recurrence than those with nonhigh-BRS (P = 0.04). Cox proportional hazards regression analyses showed that high BRS was associated independently with VF recurrence (P = 0.002). CONCLUSIONS: Our results suggest that exaggerated reactivity of parasympathetic nerves, as represented by increased BRS, may underlie VF in patients with J-wave syndrome.

Mast Cells Play an Important Role in the Pathogenesis of Hyperglycemia-Induced Atrial Fibrillation.

BACKGROUND AND OBJECTIVES: Recently, it was reported that mast cells (MCs) could underlie the mechanisms of several cardiovascular diseases. However, the role of MCs in diabetes-induced atrial fibrillation (AF) has not been notably investigated. We tested the hypothesis that MC deficiency attenuates hyperglycemia-induced AF in mice. METHODS AND RESULTS: Mast cell-deficient W/W(v)  mice, and congenic +/+ littermates (WT) were divided into either the vehicle (VEH)-injection group or the streptozotocin (STZ)-injection group (MCKO-VEH, MCKO-STZ, WT-VEH, and WT-STZ groups). On day 28 of our studies, we observed that (1) STZ-induced hyperglycemia increased MC infiltration in the left atrium (LA) in WT mice (P < 0.01), (2) atrium isolated from the WT-STZ group showed inhomogeneous interstitial fibrosis, abundant infiltration of macrophages, and enhanced apoptosis compared to the WT-VEH group (P < 0.01, P < 0.01, P < 0.05, respectively). However, the changes observed in the WT-STZ group were significantly attenuated in the MCKO-STZ mice. In addition, we observed that (3) messenger RNA levels of tumor necrosis factor-α, monocyte chemoattractant protein-1, interleukin-1ß, transforming growth factor-ß, and collagen-1 in the LA were increased in the WT-STZ group, but not in the MCKO-STZ group, (4) STZ-induced hyperglycemia increased AF induction and prolonged interatrial conduction time in the WT mice, which were not observed in the MCKO mice, and that (5) hyperglycemia-enhanced atrial production of reactive oxygen species (ROS) was equally observed in the WT and MCKO mice. CONCLUSIONS: Our results suggest that MCs contribute to the pathogenesis of hyperglycemia-induced AF via enhancement of inflammation and fibrosis.

A case of anomalous origin of the left coronary artery from the pulmonary artery presenting with sudden cardiac arrest due to coronary artery steal generated by excessive exercise.

This case report describes a 43-year-old man who temporarily survived cardiac arrest that was prospectively related to ventricular fibrillation due to the anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA). Prior to admission to our hospital, he was asymptomatic for ALCAPA syndrome. Emergent coronary angiography revealed that the dilated right coronary artery was connected with extensive collateral vessels to the left coronary artery. The origin of the latter was in the pulmonary artery. Moreover, coronary steal phenomenon was identified by examining the pulmonary arterial blood oxygen saturation. The patient later died of acute decompensated acidosis. .