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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Coefficient of Variation of P-Wave Duration Is a Novel Atrial Heterogeneity Index to Predict Recurrence of Atrial Fibrillation After Catheter Ablation.

INTRODUCTION: Atrial conduction heterogeneity is associated with progression of atrial fibrillation (AF). However, the relationship between P-wave parameters representing atrial conduction heterogeneity and AF recurrence after catheter ablation (ABL) is still unclear. METHODS AND RESULTS: Subjects of the study were 126 consecutive patients with AF (78 paroxysmal and 48 persistent) who had received ABL. Coefficient of variation of P-wave duration (CV-PWD) was determined with all 12 surface electrocardiographic leads as an index of atrial conduction heterogeneity. Rates of freedom from AF recurrence were 78% and 77% in patients with paroxysmal and persistent AF, respectively, over a 12-month follow-up. CV-PWD measured before ABL was smaller in AF-free patients compared with AF-recurrent patients (0.089 ± 0.019 vs. 0.129 ± 0.042, P < 0.001). CV-PWD significantly decreased after ABL in AF-free patients, but did not change in AF-recurrent patients. CV-PWD after ABL was also smaller in AF-free patients compared with AF-recurrent patients (0.087 ± 0.025 vs. 0.133 ± 0.035, P < 0.001). In receiver operating curve analysis, CV-PWD before and after ABL achieved area under the curve of 0.829 and 0.854, respectively, for the ability to predict AF recurrence. CV-PWD correlated positively with left atrial (LA) diameter and negatively with LA appendage flow velocity. CONCLUSION: CV-PWD is a useful index to predict AF recurrence after ABL for both patients with paroxysmal and persistent AF. ABL may suppress AF by decreasing atrial conduction heterogeneity.

Differentiation of Slow-Slow Form of AVNRT from AVRT through a Posteroseptal Accessory Pathway by Retrograde P-Wave Amplitude.

BACKGROUND: This study aimed to clarify whether retrograde P-wave amplitude during tachycardia can be used to differentiate slow-slow form of atrioventricular nodal reentrant tachycardia (S/S-AVNRT) from atrioventricular reentrant tachycardia through a posteroseptal accessory pathway (PS-AVRT). METHODS: Sixteen patients with S/S-AVNRT and 14 patients with PS-AVRT constituted the study group. Electrocardiographic and electrophysiological parameters were compared between both the groups. HA(CS-His), which indicates the location of the earliest atrial activation site during tachycardia, was calculated as the difference of the shortest HA interval in the His bundle region and the coronary sinus region. RESULTS: Negative deflection of the retrograde P wave during tachycardia was significantly greater in S/S-AVNRT than in PS-AVRT in the inferior leads (lead aVF, -0.22 ± 0.04 mV vs -0.10 ± 0.07 mV; P < 0.001). Among the electrocardiographic parameters, retrograde P-wave amplitude in lead aVF had the highest diagnostic accuracy (area under the curve 0.975, sensitivity 93%, and specificity 88% for a cutoff value of -0.16 mV). HA(CS-His) was negatively greater in S/S-AVNRT than in PS-AVRT (-24 ± 13 ms vs -3 ± 18 ms; P = 0.001), and was significantly correlated with the retrograde P-wave amplitude in lead aVF (P = 0.004). CONCLUSION: Deeper negative deflection of the retrograde P wave in the inferior lead can help differentiate S/S-AVNRT from PS-AVRT.

Effect of irbesartan on development of atrial fibrosis and atrial fibrillation in a canine atrial tachycardia model with left ventricular dysfunction, association with p53.

Effects of an angiotensin II receptor blocker, irbesartan (IRB), on the development of atrial fibrosis and atrial fibrillation (AF) were assessed in a canine model of atrial tachycardia remodeling (ATR) with left ventricular dysfunction, together with its possible association with involvement of p53. Atrial tachypacing (400 bpm for 4 weeks) was used to induce ATR in beagles treated with placebo (ATR-dogs, n = 6) or irbesartan (IRB-dogs, n = 5). Non-paced sham dogs served as control (Control-dogs, n = 4). ATR- and IRB-dogs developed tachycardia-induced left ventricular dysfunction. Atrial effective refractory period (AERP) shortened (83 ± 5 ms, p < 0.05), inter-atrial conduction time prolonged (72 ± 2 ms, p < 0.05), and AF duration increased (29 ± 5 s, p < 0.05 vs. baseline) after 4 weeks in ATR-dogs. ATR-dogs also had a larger area of atrial fibrous tissue (5.2 ± 0.5 %, p < 0.05 vs. Control). All these changes, except for AERP, were attenuated in IRB-dogs (92 ± 3 ms, 56 ± 3 ms, 9 ± 5 s, and 2.5 ± 0.7 %, respectively; p < 0.05 vs. ATR for each). In ATR-dogs, p53 expression in the left atrium decreased by 42 % compared with Control-dogs (p < 0.05); however, it was highly expressed in IRB-dogs (+89 % vs. ATR). Transforming growth factor (TGF)-ß1 expression was enhanced in ATR-dogs (p < 0.05 vs. Control) but reduced in IRB-dogs (p < 0.05 vs. ATR). Irbesartan suppresses atrial fibrosis and AF development in a canine ATR model with left ventricular dysfunction in association with p53.

Time-Dependent Changes in QT Dynamics after Initiation and Termination of Paroxysmal Atrial Fibrillation.

BACKGROUND: Little is known about time-dependent changes in QT dynamics after initiation of atrial fibrillation (AF) and after restoration of sinus rhythm (SR) in patients with paroxysmal AF. METHODS: Beat-to-beat QT and RR intervals in CM5 lead were measured automatically in 13 patients with both AF and SR on the single 24-hour Holter electrocardiology recording. QT-RR relation was analyzed at six periods of time: 1 hour before AF onset (Pre(0-1h)), 0-1 hour and 4-5 hours after AF onset (AF(0-1h) and AF(4-5h)), and 0-1 hour, 2-3 hours, and 4-5 hours after the restoration of SR (SR(0-1h), SR(2-3h), and SR(4-5h)). RESULTS: QT-RR slope was gradually decreased after AF onset and gradually returned to the baseline level after restoration of SR. The slope became greater at SR(4-5h) than at AF(4-5h) and AF(0-1h). In patients receiving antiarrhythmic drugs (AADs; n = 5), QT-RR slope was greater at SR(4-5h) than in those not receiving AADs (n = 8). CONCLUSION: In patients with paroxysmal AF, bradycardia-dependent QT prolongation was attenuated during AF, and was corrected and gradually augmented along with continuation of SR, especially in patients receiving AADs. This could increase the risk of developing torsade de pointes.

Electrophysiological and anatomical differences of the slow pathway between the fast-slow form and slow-slow form of atrioventricular nodal reentrant tachycardia.

AIMS: This study aimed to clarify whether electrophysiological and anatomical properties of the slow pathway (SP) could be different between the fast-slow form (F/S) and the slow-slow form (S/S) atrioventricular nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: Nine patients with F/S and 15 patients with S/S of atypical AVNRT were studied. The patients with S/S were divided into two groups; those with the anterograde SP being eliminated (S/S aSP-E) or preserved (S/S aSP-P) during catheter ablation. HA (CS-His) was determined as the difference of the shortest HA interval between the His bundle region and the coronary sinus (CS) region. The ratio of the amplitudes of atrial and ventricular potential (A/V ratio) of the successful ablation site of the SP was also evaluated. Effective refractory period of the retrograde SP was shorter and HA intervals during both tachycardia and ventricular pacing were longer in F/S than in S/S. HA (CS-His) did not differ between F/S and S/S (-4.3 ± 20.2 vs.-4.4 ± 18.4 ms, NS). The A/V ratio was significantly greater in the S/S aSP-P group compared with the both groups of F/S and S/S aSP-E (0.83 ± 0.29 vs. 0.38 ± 0.09 and 0.26 ± 0.15 ms, P < 0.01). CONCLUSION: Properties of the retrograde SP differ between F/S and S/S of AVNRT. Fast-slow form may utilize the same pathway for the retrograde conduction as the anterograde SP in S/S.

Glycine/Serine polymorphism at position 38 influences KCNE1 subunit's modulatory actions on rapid and slow delayed rectifier K+ currents.

BACKGROUND: KCNE1 encodes a modulator of KCNH2 and KCNQ1 delayed rectifier K(+) current channels. KCNE1 mutations might cause long QT syndrome (LQTS) by impairing KCNE1 subunit's modulatory actions on these channels. There are major and minor polymorphismic KCNE1 variants whose 38(th) amino acids are glycine and serine [KCNE1(38G) and KCNE1(38S) subunits], respectively. Despite its frequent occurrence, the influence of this polymorphism on the K(+) channels' function is unclear. METHODS AND RESULTS: Patch-clamp recordings were obtained from human embryonic kidney -293T cells. KCNH2 channel current density in KCNE1(38S)-transfected cells was smaller than that in KCNE1(38G)-transfected cells by 34%. The voltage-sensitivity of the KCNQ1 channel current in KCNE1(38S)-transfected cells was lowered compared to that in KCNE1(38G)-transfected cells, with a +13mV shift in the half-maximal activation voltage. KCNH2 channel current density or KCNQ1 channel voltage-sensitivity was not different between KCNE1(38G)-transfected cells and cells transfected with both KCNE1(38G) and KCNE1(38S). Moreover, the KCNH2 channel current in KCNE1(38S)-transfected cells was more susceptible to E4031, a QT prolonging drug and a condition with hypokalemia, than that in KCNE1(38G)-transfected cells. CONCLUSIONS: Homozygous inheritance of KCNE1(38S) might cause a mild reduction of the delayed rectifier K(+) currents and might thereby increase an arrhythmogenic potential particularly in the presence of QT prolonging factors. By contrast, heterozygous inheritance of KCNE1(38G) and KCNE1(38S) might not affect the K(+) currents significantly. (Circ J 2014; 78: 610-618).

Combined dominant frequency and complex fractionated atrial electrogram ablation after circumferential pulmonary vein isolation of atrial fibrillation.

INTRODUCTION: Atrial substrates with high-dominant frequency (DF) and complex fractionated atrial electrogram (CFAE) sites have sources maintaining atrial fibrillation (AF) and are potential AF ablation targets. This study aimed to evaluate an approach of circumferential pulmonary vein isolation (PVI) followed by a DF and CFAE site ablation. METHODS AND RESULTS: Fifty consecutive AF patients (23 paroxysmal, 9 persistent, and 18 longstanding persistent) underwent ablation, using NavX. When AF continued after circumferential PVI, high-DF sites of ≥ 8 Hz and then continuous left atrial (LA) CFAE sites defined by fractionated intervals (FI) of ≤50 milliseconds including the coronary sinus and right atrium were targeted. A total of 45.1% of high-DF and 48.1% of continuous CFAE sites significantly decreased after PVI (P < 0.001). The mean LA DF and FI significantly decreased and prolonged, respectively, after PVI (P < 0.001). Only 14.1% of all high-DF sites after PVI overlapped with continuous CFAE sites. AF terminated at high-DF sites in 11 (22%) patients and continuous CFAE sites in 1 (2%). AF could be induced in only 8% of patients after the procedure. The mean LA DF value before ablation was significantly lower in those without recurrence (P = 0.003). AF freedom on antiarrhythmic drugs was 96% and 59%, respectively, in the paroxysmal and nonparoxysmal AF patients (89% persistent and 44% longstanding persistent) after 1 procedure over a 12-month follow-up. CONCLUSIONS: A combined high-DF and continuous CFAE site ablation in all chambers after circumferential PVI may be effective in the paroxysmal and persistent AF patients.