Paradoxical delayed capture proved the dual-loop tachycardia mechanism of a cavotricuspid isthmus-dependent atrial flutter.

A 37-year-old man underwent catheter ablation for a cavotricuspid isthmus-dependent atrial flutter. Two 20-pole deflectable electrode catheters were placed in a parallel position on the tricuspid annulus and right atrial lateral wall. The dual-loop tachycardia mechanism of the atrial flutter was suggested by paradoxical delayed capture of the lateral wall of the right atrium during entrainment pacing from the lateral tricuspid annulus.

Cardiac vagus nerve denervation by pulmonary vein isolation was effective for swallowing-induced atrial tachycardia.

Swallowing-induced atrial tachycardia (SIAT) is a relatively rare arrhythmia. A 56-year-old woman was admitted to treat atrial tachycardia that occurs by not only eating and drinking but also yawning. Both the right and left upper pulmonary veins were suspected as the earliest activation site of the tachycardia and the abnormal activation of ectopies themselves were suppressed after pulmonary vein isolation (PVI). In a 24-hour Holter electrocardiogram, the HF component of the analysis of heart rate variability was suppressed both at 1 day and at 2 years after ablation. In this case, cardiac vagal nerve denervation by PVI was effective for SIAT.

Epicardial adipose tissue affects the efficacy of left atrial posterior wall isolation for persistent atrial fibrillation.

BACKGROUND: Epicardial adipose tissue (EAT) contributes to atrial fibrillation (AF). However, its impact on the efficacy of left atrial posterior wall isolation (LAPWI) is unclear. METHODS: Forty-four nonparoxysmal AF patients underwent LAPWI after pulmonary vein isolation. EAT overlap on LAPWI was assessed by fusing computed tomography images with electro-anatomical mapping. RESULTS: During the 21 ± 7 months of follow-up, AF recurred in 10 patients (23%). The total and left atrial EAT volumes were 113 ± 36 and 33 ± 12 cm3, respectively. No differences were found between the AF-free and AF-recurrent groups regarding EAT volume. The EAT overlaps on LAPWI lines and LAPWI area were 1.2 ± 1.0 and 0.5 ± 0.9 cm2 respectively. Although no difference was found between groups regarding the EAT overlap on LAPWI area, the AF-free group had a significantly larger EAT overlap on LAPWI lines (1.4 ± 1.0 vs 0.6 ± 0.6 cm2, P = .014). Multivariate analysis identified EAT overlap on LAPWI lines as an independent predictor of AF recurrence (hazard ratio: 0.399, 95% confidence interval: 0.178-0.891, P = .025). Kaplan-Meier analysis revealed that, during follow-up, 92% of the large EAT overlap group (≥1.0 cm2) and 58% of the small EAT overlap group (<1.0 cm2) remained AF-free (P = .008). CONCLUSIONS: EAT overlap on LAPWI lines is related to a high AF freedom rate. Direct radiofrequency application to EAT overlap may be necessary to suppress AF.

Ripple map guided catheter ablation targeting abnormal atrial potentials during sinus rhythm for non-paroxysmal atrial fibrillation.

BACKGROUND: Abnormal atrial potential (AAP) during sinus rhythm may be a critical ablation target for atrial fibrillation. However, the assessment of local electrograms throughout the left atrium is difficult. Thus, we sought to investigate the effectiveness of Ripple map guided AAP ablation. METHODS AND RESULTS: AAP areas were determined by Ripple mapping on the CARTO system in 35 patients (Ripple group) by marking the area where small deflections persisted after the first deflection wavefront had passed. Following pulmonary vein isolation, AAP areas were ablated. If AAP areas were located on the left atrial posterior wall, the posterior wall was isolated. The outcome of this approach was compared with that of 66 patients who underwent an empirical linear ablation approach (control group). There were no differences in patient characteristics between the groups. The total radiofrequency application time and procedure time were shorter in the Ripple group than in the control group (radiofrequency application time, 48 ± 14 minutes vs 61 ± 13 minutes, P < .001; procedure time, 205 ± 30 minutes vs 221 ± 27 minutes, P = .013). Gastroparesis occurred in one patient in each group (P = .645), but in both cases this was relieved with conservative therapy. Kaplan-Meier analysis revealed that rate of freedom from atrial arrhythmia was higher in the Ripple group than in the control group (91% vs 74% during the 12 months' follow up; P = .040). CONCLUSION: Ripple map guided AAP ablation effectively suppressed atrial arrhythmia in patients with non-paroxysmal AF.

P-wave vector magnitude predicts the left atrial low-voltage area in patients with paroxysmal atrial fibrillation.

BACKGROUND: P-wave amplitude (PWA) parameters can be the surrogate measures of the left atrial low-voltage areas (LVAs). METHODS: We measured PWAs using an automated system in 50 patients with paroxysmal atrial fibrillation (AF). We examined the relationships between left atrial LVAs and PWA parameters, including P-wave vector magnitude, calculated as the square root of the sum of lead II PWA squared, lead V6 PWA squared, and a one-half lead V2 PWA squared. RESULTS: Lead I PWA was most strongly correlated with LVAs in the anterior wall and appendage (anterior wall, R = -0.391, P = 0.006; appendage, R = -0.342, P = 0.016), whereas lead II PWA was most strongly correlated with LVAs in the septum, posterior wall, and bottom wall (septum, R = -0.413, P = 0.003; posterior wall, R = -0.297, P = 0.039; bottom wall; R = -0.288, P = 0.045). Although maximum, minimum, mean, and lead I PWAs were not correlated with total LVA, P-wave vector magnitude and lead II PWA were significantly correlated with total LVA (P-wave vector magnitude, R = -0.430, P = 0.002; lead II PWA, R = -0.323, P = 0.023). P-wave vector magnitude achieved the highest accuracy for predicting significant LVA (total LVA > 10%) with an area under the curve of 0.772; sensitivity, specificity, and positive and negative predictive values were 64%, 88%, 85%, and 69%, respectively, for the cutoff value of 0.130 mV. CONCLUSION: P-wave vector magnitude is a useful electrocardiographic predictor of left atrial LVAs.

Left atrial wall thickness is associated with the low-voltage area in patients with paroxysmal atrial fibrillation.

PURPOSE: To identify a potential morphological marker of remodeling and electrophysiological dysfunction, we investigated if low wall thickness is associated with low-voltage areas (LVAs) in the left atrium. METHODS: Wall thickness was measured by computed tomography and LVA (% area with bipolar voltage < 0.5 mV) by voltage mapping in 43 paroxysmal AF patients. The left atrium was divided into five segments: septal wall, anterior wall, roof wall, posterior wall, and bottom wall in regional analysis. RESULTS: Left atrial wall thickness and LVA were 3.2 ± 0.6 mm and 14% ± 9%, respectively. Multivariate analysis identified left atrial wall thickness and volume as independent determinants of left atrial LVA (thickness, standardized ß - 0.374, 95%CI - 23.289 to - 4.534, P = 0.005; volume, standardized ß 0.452, 95%CI 0.049-0.214, P = 0.002). In regional analysis, significant LVA (> 10% of segment surface area) was observed in 123 of 215 segments (57%). Segments in the low tertile of wall thickness (< 1.76 mm) had larger LVAs compared with segments in middle (1.76-2.14 mm) and high tertiles (≥ 2.14 mm) (low tertile, 20.3% ± 14.9%; middle tertile, 12.6% ± 11.2%; high tertile, 12.5% ± 12.1%; low vs. middle tertile, P = 0.001; low vs. high tertile, P = 0.001). Area under the receiver operating curve of wall thickness was 0.706 for prediction of significant LVA. A thickness cut-off of 1.90 mm yielded 62% sensitivity, 73% specificity, 75% positive predictive value, and 59% negative predictive value for significant LVA. CONCLUSION: A thin left atrial wall is an independent predictor of LVA in patients with paroxysmal AF.

Correlation between the left atrial low-voltage area and the cardiac function improvement after catheter ablation for paroxysmal atrial fibrillation.

BACKGROUND: The impact of the left atrial low-voltage area (LVA) on the cardiac function improvement following ablation for atrial fibrillation (AF) is unclear. METHODS: In 49 patients with paroxysmal AF who underwent ablation, the left ventricular stroke volume index (SVI) was repeatedly measured using an impedance cardiography until 6 months after ablation. We defined the cardiac function improvement as a 20% increase in the SVI. The LVA (the area with the voltage amplitude of <0.5 mV) was assessed before ablation. RESULTS: The reduced baseline SVI (<33 mL/m2) was observed in 18 (37%) patients. The SVI increased following ablation (from 36 ± 5 to 39 ± 6 mL/m2, P < .001). We observed the cardiac function improvement in 14 (29%) patients. The LVA was smaller in patients with the improved cardiac function than in those without (8.3% ± 5.2% vs 14.0% ± 8.5%, P = .026). The multivariate analysis revealed that only the LVA was independently associated with the cardiac function improvement (odds ratio, 0.878; 95% confidence interval: 0.778-0.991, P = .036). Furthermore, LVAs of the anterior (7.9% ± 7.6% vs 18.2% ± 15.5%, P = .022), septal (12.0 ± 7.3% vs 20.7% ± 13.8%, P = .031), and roof walls (6.9% ± 6.0% vs 16.9% ± 15.2%, P = .022) were smaller in patients with the improved cardiac function than in those without. CONCLUSIONS: The LVA was related to the cardiac function improvement following ablation in patients with paroxysmal AF.

Left atrial posterior wall isolation affects complex fractionated atrial electrograms in persistent atrial fibrillation.

BACKGROUND: The impact of left atrial posterior wall isolation (LAPWI) on the complex fractionated atrial electrogram (CFAE) is unknown. METHODS: CFAE mapping was performed before and after LAPWI in 46 patients with persistent atrial fibrillation (AF). RESULTS: LAPWI decreased both the variable (fractionated index ≤ 120 ms; from 60 ± 4 cm2 to 50 ± 4 cm2, P < 0.001) and continuous (fractionated index ≤ 50 ms; from 4.2 ± 1.0 cm2 to 3.5 ± 0.9 cm2, P = 0.036) CFAE areas. Especially, the CFAE areas on the bottom and roof walls of the left atrium and on the posterior and bottom walls of the right atrium significantly decreased after LAPWI. The distribution of variable CFAE areas was not different between the AF-recurrence (n = 9) and AF-free (n = 37) groups before LAPWI; however, it was larger in the anterior and septal walls of the right atrium in the AF-recurrence group than in the AF-free group after LAPWI (anterior wall, 8% ± 2% vs 5% ± 1%, P = 0.048; septal wall, 23% ± 4% vs 16% ± 1%, P = 0.043). The distribution of continuous CFAE areas on the bottom wall of the right atrium was larger in the AF-recurrence group than in the AF-free group both before LAPWI (30% ± 20% vs 4% ± 2%, P = 0.008) and after LAPWI (25% ± 25% vs 3% ± 1%, P = 0.027). CONCLUSIONS: LAPWI decreased the CFAE areas and affected their distribution, which contributed to AF recurrence.

P-wave vector magnitude predicts recurrence of atrial fibrillation after catheter ablation in patients with persistent atrial fibrillation.

BACKGROUND: The predictive efficacies of parameters related to P-wave amplitude (PWA) for atrial fibrillation (AF) recurrence after catheter ablation are unclear. METHODS: We measured multiple PWA parameters using an automated system in 126 consecutive patients with persistent and long-standing persistent AF who underwent catheter ablation. The relationships between AF recurrence and various PWA parameters were examined, including the association with P-wave vector magnitude (calculated as the square root of the sum of lead II PWA squared, lead V6 PWA squared, and a one-half lead V2 PWA squared). RESULTS: Atrial fibrillation did not recur in 87 patients (69%) during 32 ± 15 months of follow-up. The maximum PWA, mean PWA, and P-wave vector magnitude were lower in patients with AF recurrence than those without (maximum PWA, 0.14 ± 0.05 mV vs. 0.16 ± 0.05 mV, p = 0.017; mean PWA, 0.05 ± 0.02 mV vs. 0.06 ± 0.02 mV, p = 0.003; P-wave vector magnitude, 0.09 ± 0.03 mV vs. 0.13 ± 0.04 mV, p < 0.001). A multivariate Cox regression analysis revealed that the predictive ability of P-wave vector magnitude for AF recurrence was independent of other clinical properties (hazard ratio: 0.153, 95% confidence interval: 0.046-0.507, p = 0.002). Atrial fibrillation freedom rates of patients with P-wave vector magnitude higher and lower than 0.13 mV were 93% and 57%, respectively. P-wave vector magnitude weakly correlated with left atrial dimension (R = -0.280, p = 0.004). CONCLUSIONS: P-wave vector magnitude can predict AF recurrence after catheter ablation in patients with persistent AF.

Edoxaban suppresses the progression of atrial fibrosis and atrial fibrillation in a canine congestive heart failure model.

Coagulation factor Xa activates the protease-activated receptor 2 (PAR2) and causes tissue fibrosis; however, the effects of Xa inhibitor edoxaban on atrial fibrosis and atrial fibrillation (AF) have not been investigated. We examined the effect of edoxaban on the progression of atrial fibrosis in a canine congestive heart failure (CHF) model. Beagle dogs were assigned to sham, placebo, and edoxaban groups (n = 6/group). Dogs of the placebo or edoxaban groups received 19 days of medication with daily oral placebo or edoxaban, respectively, followed by 14 days of ventricular tachypacing. Dogs of the sham group had no medication or pacing. Ventricular tachypacing prolonged AF duration in dogs of the placebo group (159 ± 41 s, p < 0.01 vs. sham); however, this effect was suppressed by edoxaban treatment. Compared with the sham group, tachypacing alone also significantly increased the atrial fibrotic area (2.9 ± 0.1% vs. 7.8 ± 0.4%, p < 0.01), PAR2 expression (1.0 ± 0.1 vs. 1.8 ± 0.3, p < 0.05), and atrial fibronectin expression (1.0 ± 0.2 vs. 2.0 ± 0.2, p < 0.01). These responses were suppressed by edoxaban treatment (area 5.9 ± 0.4%, p < 0.01; PAR2 1.1 ± 0.1, p < 0.05; fibronectin 1.2 ± 0.2, p < 0.05 vs. placebo). Edoxaban showed suppressive effects on atrial remodeling, AF progression, and excessive expressions of PAR2 and fibronectin in a canine CHF model. The suppression of the Xa/PAR2 pathway might be a potential pharmacological target of edoxaban.

Coefficient of variation of P-wave duration measured using an automated measurement system predicts recurrence of atrial fibrillation.

BACKGROUND: P-wave parameters representing atrial conduction heterogeneity are associated with recurrence of atrial fibrillation (AF) after catheter ablation. However, intra- and inter-observer variabilities are unavoidable during manual measurement of P-wave parameters. METHODS: The study included 201 patients with paroxysmal AF who underwent catheter ablation. P-wave duration (PWD) was measured using a computerized automated measurement system with a surface 12-lead electrocardiogram. The coefficient of variation of PWD (CV-PWD) across the 12 electrocardiographic leads was determined as an index of atrial conduction heterogeneity. RESULTS: AF did not recur in 157 (78%) patients during a 12-month follow-up period. CV-PWD assessed before catheter ablation was not different between the AF-recurrent and AF-free groups (0.069 ±â€¯0.023 vs. 0.069 ±â€¯0.023, P = 0.090). However, CV-PWD measured after catheter ablation was significantly larger in the AF-recurrent group than in the AF-free group (0.090 ±â€¯0.037 vs. 0.073 ±â€¯0.024, P < 0.001). In receiver operating curve analysis, CV-PWD assessed after catheter ablation achieved an area under the curve of 0.702; the sensitivity, specificity, and positive and negative predictive values were 68%, 69%, 38%, and 88%, respectively, for the cut-off value of 0.080. During the follow-up period, AF freedom rates of high CV-PWD patients (CV-PWD ≥ 0.080) and low CV-PWD patients (CV-PWD < 0.080) were 65% and 88%, respectively. CONCLUSIONS: CV-PWD determined using an automated measurement system was associated with AF recurrence after catheter ablation in patients with paroxysmal AF.

Impacts of the body size on the left atrial wall thickness and atrial fibrillation recurrence after catheter ablation.

The increased body size correlates with the occurrence of atrial fibrillation (AF); however, the impact of the body size on the AF recurrence after ablation remains unclear. We enrolled 283 AF patients (179 paroxysmal, 51 persistent, and 53 long-standing persistent) who received ablation and assessed the correlation between the body surface area (BSA) and the AF recurrence. Furthermore, we measured the left atrial wall thickness using computed tomography. During the 12-month follow-up period, the AF freedom rates for patients with paroxysmal AF, persistent AF, and long-standing persistent AF were 83%, 76%, and 77%, respectively. The left atrial dimension, BSA, and body mass index (BMI) were higher in the AF-recurrent group compared with the AF-free group (left atrial dimension: 44.1 ± 7.5 mm vs. 41.7 ± 6.5 mm, P = 0.019; BSA: 1.81 ± 0.20 m2 vs. 1.72 ± 0.19 m2, P = 0.002; BMI 25.0 ± 3.2 kg/m2 vs. 24.0 ± 3.2 kg/m2, P = 0.035). The multivariate analysis revealed that only the BSA was an independent predictor of the AF recurrence after ablation (hazard ratio 6.843; 95% confidence interval 1.523-30.759, P = 0.012). The BSA significantly correlated with the left atrial wall thickness (R = 0.306, P < 0.001), and the left atrial wall thickness was higher in the AF-recurrent group compared with the AF-free group (2.00 ± 0.20 mm vs. 1.87 ± 0.17 mm, P < 0.001). The large body size correlates with the AF recurrence after ablation, which could be attributed to an increase in the left atrial wall thickness.

Improvement of Hemodynamic Parameters in Patients With Preserved Left Ventricular Systolic Function by Catheter Ablation of Atrial Fibrillation　- A Prospective Study Using Impedance Cardiography.

BACKGROUND: The effects of catheter ablation for atrial fibrillation (AF) on hemodynamic parameters in patients with preserved left ventricular (LV) systolic function are unclear. Methods and Results: We enrolled 178 patients with AF (paroxysmal, 108; persistent, 70) with preserved LV systolic function who underwent AF ablation. The stroke volume index (SVI) was repeatedly measured using impedance cardiography. Reduced SVI (SVI, <33 mL/m2) was observed in 55% of patients before ablation. In patients with paroxysmal AF, the SVI did not change immediately after ablation (from 35±6 mL/m2to 35±5 mL/m2; P=0.652); however, it increased 1 month after ablation and further increased 6 months after ablation (1 month, 37±6 mL/m2, P<0.001; 6 months, 38±6 mL/m2, P<0.001). In patients with persistent AF, the SVI increased immediately after ablation (from 30±5 mL/m2to 36±6 mL/m2; P<0.001) and further increased until 6 months after ablation (1 month, 37±6 mL, P<0.001; 6 months, 38±5 mL/m2, P<0.001). The baseline SVI was the strongest predictor of the cardiac function improvement with an area under the curve of 0.828. CONCLUSIONS: The restoration and maintenance of sinus rhythm using catheter ablation increased the SVI in patients with preserved LV systolic function.

Citrus fruits induced swallow syncope with atrioventricular block or sinus arrest.

Swallow syncope is a relatively rare syndrome and caused by various foods and drinks. A 76-year-old man was admitted with frequent syncope while eating. Holter electrocardiogram revealed frequent occurrence of atrioventricular block during meals. Both atrioventricular block and sinus arrest were induced by only eating citrus fruits, citrus jelly, and acidic foods but not by other drinks and foods. These arrhythmias were suppressed after administration of atropine. No further episodes of syncope recurred after the implantation of a DDD pacemaker. This case indicated that acidic stimulation of citrus induced a vasovagal reflex via esophageal nociceptors leading to syncope.

Heterogeneity in the left atrial wall thickness contributes to atrial fibrillation recurrence after catheter ablation.

Influence of left atrial wall thickness on outcome of catheter ablation for atrial fibrillation (AF) is unclear. Overall, 213 patients with AF (128 paroxysmal and 85 persistent) received ablation. We measured the wall thickness of 16 and 19 areas in the pulmonary vein antrum (PVWT) and left atrial body (LAWT), respectively. Coefficient of variation of wall thickness (CV-WT) was calculated to assess heterogeneity in the left atrial wall thickness. In patients with paroxysmal AF, maximum PVWT, mean PVWT, maximum LAWT, and CV-WT were higher in AF recurrent group than in AF-free group (maximum PVWT, 2.85 ± 0.52 vs. 2.50 ± 0.45 mm, P = 0.003; mean PVWT, 1.59 ± 0.13 vs. 1.50 ± 0.15 mm, P = 0.018; maximum LAWT, 3.85 ± 0.77 vs. 3.41 ± 0.61 mm, P = 0.005; CV-WT, 0.34 ± 0.06 vs. 0.32 ± 0.05, P = 0.039). In patients with persistent AF, maximum PVWT, mean PVWT, maximum LAWT, mean LAWT, and CV-WT were higher in the AF-recurrent group than in the AF-free group (maximum PVWT, 2.52 ± 0.36 vs. 2.31 ± 0.36 mm, P = 0.031; mean PVWT, 1.53 ± 0.12 vs. 1.45 ± 0.14 mm, P = 0.036; maximum LAWT, 3.68 ± 0.75 vs. 3.11 ± 0.50 mm, P < 0.001; mean LAWT, 2.34 ± 0.35 vs. 2.13 ± 0.21 mm, P = 0.002; CV-WT, 0.35 ± 0.06 vs. 0.31 ± 0.05, P = 0.005). Thick and heterogeneous left atrial wall contributes to AF recurrence after ablation.

Vasovagal syncope is associated with poor prognosis in patients with left ventricular dysfunction.

Vasovagal syncope (VVS) is known to have a benign prognosis and be associated with enhanced contraction and activation of the left ventricular (LV) mechanoreceptors. However, a little is known about VVS in patients with LV dysfunction. The present study aimed to investigate the prevalence and prognosis of VVS in patients with LV dysfunction. We enrolled 368 patients with unexplained syncope. In 7 of these patients, LV ejection fraction was lower than 40%. The results of a head-up tilt test (HUT) and the recurrence of syncope were compared between these 7 patients with LV dysfunction and the remaining patients. Positive HUT was obtained in the 6 patients (86%) with LV dysfunction; this rate tended to be higher as compared with normal cardiac function (192/361, 53%, P = 0.069). In patients with LV dysfunction, response in HUT was mostly vasodepressor type (62%); however, most of HUT responses were mixed type in patients with normal LV function (67%). Among patients with positive HUT, the recurrent rate of syncope after HUT was higher in those with LV dysfunction than in those with normal LV function (67 vs. 21%, P = 0.008). VVS in patients with LV dysfunction may be refractory to treatment and could be associated with poor prognosis.

Cryoballoon ablation with left lateral decubitus position in atrial fibrillation patient where the left atrium was compressed by the vertebra.

Catheter ablation of atrial fibrillation is difficult when the left atrium is compressed by the vertebra. The heart may shift forward, and compression of the left atrium may be relieved in the left lateral decubitus position. Therefore, catheter ablation could be performed in the left lateral decubitus position even in such cases.

Latent pathogenicity of the G38S polymorphism of KCNE1 K+ channel modulator.

KCNE1 encodes a modulator of KCNQ1 and KCNH2 channels. Although KCNE1(G38S), a single-nucleotide polymorphism (SNP) causing a G38S substitution in KCNE1, is found frequently, whether and how this SNP causes long QT syndrome (LQTS) remains unclear. We evaluated rate-dependent repolarization dynamics using Holter electrocardiogram (ECG) to assess the pathogenicity of KCNE1(G38S). Forty-five patients exhibiting long QT intervals, as assessed by their baseline ECGs, and 16 control subjects were enrolled. KCNE1(G38S) carriers were identified using genome sequencing. LQTS patients were classified into LQT1 or LQT2 using genetic analysis or epinephrine test. QT-RR relations were determined using 24-h Holter ECG recordings. Among the 15 patients (33.3 %) with KCNE1(G38S), four patients without any mutations or amino acid changes in other major cardiac ion channels were categorized as KCNE1(G38S) carriers. In the QT-RR regression lines, the QT-RR slope was greater in the KCNE1(G38S) carriers and the LQT2 patients (0.215 ± 0.021 and 0.207 ± 0.032, respectively) than in the LQT1 patients (0.163 ± 0.014, P < 0.05) and the control subjects (0.135 ± 0.025, P < 0.001). The calculated QT intervals at an RR interval of 1200 ms were longer in the KCNE1(G38S) carriers and LQT1 and LQT2 patients than in the control subjects. Patients with KCNE1(G38S) had a rate-dependent repolarization abnormality similar to patients with LQT2 and, therefore, may have a potential risk to develop lethal arrhythmias.