Kazuyoshi Ogura

Impact of postprocedural antiarrhythmic drug therapy with bepridil on maintaining sinus rhythm after catheter ablation for persistent atrial fibrillation.

BACKGROUND Although several studies have assessed the predictors of recurrent atrial fibrillation (AF) after catheter ablation for persistent AF, the impact of antiarrhythmic drug (AAD) therapy on maintaining sinus rhythm after catheter ablation for persistent AF has not been fully evaluated. This case-control study aimed to evaluate the effect of bepridil on maintaining sinus rhythm after catheter ablation for persistent AF. METHODS AND RESULTS We enrolled 122 consecutive patients (87 men; mean age: 62.3 years) who underwent catheter ablation for persistent AF and were administered AAD therapy after the initial procedure. Restoration of sinus rhythm was achieved in all of the patients by catheter ablation and cardioversion after the initial procedure. After a median 12-month follow up, 51 of 122 (41.8%) patients had recurrence of AF. In Cox proportional hazard regression analysis, postprocedural AAD therapy with bepridil was a significantly correlated factor with freedom from recurrent AF after the initial ablation procedure (hazard ratio 0.446, 95% confidence interval 0.236-0.842, p=0.012). In Kaplan-Meier analysis, AF-free survival was significantly better with bepridil compared with amiodarone (AMD) and sodium channel blocker (SCB) (log-rank test, bepridil vs AMD, p=0.012; bepridil vs SCB, p=0.018). CONCLUSIONS Bepridil reduced the recurrence of AF compared with AMD and SCB in patients who underwent catheter ablation for persistent AF.

Atrial defibrillation threshold as a novel predictor of clinical outcome of catheter ablation for persistent atrial fibrillation

AIMS Catheter ablation for persistent atrial fibrillation (AF) is currently performed with different procedural endpoints. When AF did not terminate during ablation procedure, electrical cardioversion was performed at different defibrillation threshold (DFT) according to AF characteristics and atrial electrophysiologic substrates. We sought to evaluate the impact of atrial DFT after catheter ablation for persistent AF on clinical outcome. METHODS AND RESULTS We studied 128 patients with persistent AF (age 63±9 years, 106 men). After completion of circumferential pulmonary vein isolation, the left atrial substrate ablation was performed until AF terminated or all identified complex fractionated electrograms were eliminated. If AF did not terminate during ablation, an internal cardioversion protocol was started at 5J and was increased incrementally in 5 J steps until successful cardioversion was accomplished. Procedural AF termination was achieved in 50 patients (Group A). Atrial fibrillation was terminated by cardioversion with DFT≤10 J in 47 patients (Group B) and with DFT>10 J in 31 patients (Group C). At 14±7 follow-up months after 1.3±0.5 sessions, 47 (94%) Group A patients, 42 (89%) Group B patients, and 14 (45%) Group C patients remained in sinus rhythm. In multivariate analysis of Group B and Group C, DFT (hazard ratio 5.54, P<0.001) and AF duration (hazard ratio 3.74, P=0.011) were independent predictors of recurrent arrhythmia. CONCLUSION When AF does not terminate after the completion of predetermined stepwise ablation, further extensive ablation to terminate AF might be unnecessary if the AF can be successfully terminated by electrical cardioversion at low DFT.

Long-term reliability of AAI mode pacing in patients with sinus node dysfunction and low Wenckebach block rate.

AIMS To compare the risk of atrioventricular (AV) conduction disturbance between patients with sinus node dysfunction on AAI pacing who had a low or high Wenckebach block rate (WBR). METHODS AND RESULTS Patients with sinus node dysfunction and normal AV conduction those underwent an electrophysiological study were studied. The patients were classified into two groups: Group L was with the patients with a WBR of 100 to 129 per minute and Group H was with the patients with a WBR > or = 130 per minute. All patients followed up every 3-6 months after an AAI pacemaker implantation. A total of 102 patients, including 35 Group L and 67 Group H, were followed for 90 +/- 44 months. Six patients died from non-cardiac cause and five patients required a new atrial lead implantation due to lead failure during follow-up. Symptomatic bradycardia requiring a new ventricular lead implantation developed in four patients (annual incidence 0.5%). In Group L, two patients developed AV block (annual incidence 0.7%). In Group H, two patients developed bradycardic atrial fibrillation (annual incidence 0.4%). Kaplan-Meier analysis revealed no significant difference between the two groups (P = 0.2983). CONCLUSION These results suggest that a long-term risk of developing AV conduction disturbance is low even in patients with a WBR of 100 to 129 per minute.

Left atrial branches of coronary arteries; clinical implications related to linear catheter ablation for atrial fibrillation.

BackgroundCoronary artery damage has been reported during catheter ablation procedures. Recently, linear ablation of thin left atrial tissue has been performed for atrial fibrillation.Objective and MethodsBecause we have little information about the arteries in the left atrium, this study was performed to evaluate the anatomy of these arteries, and to compare them with previously reported ablation lines. Coronary angiography was performed in 262 patients. Atrial coronary arteries between the left atrial appendage and the left superior pulmonary vein (LAA-LSPV region), as well as between the left inferior pulmonary vein and the mitral annulus (“mitral isthmus” region) were examined.ResultsAtrial coronary arteries extending to the LAA-LSPV region were found in 92 subjects (35%), while arteries crossing the mitral isthmus region were found in 119 subjects (46%). Atrial coronary arteries crossed the ablation line in about 69% of subjects overall.ConclusionThese results might suggest a risk of acute complications due to left atrial ablation. Alternatively, recurrence of atrial fibrillation might be caused by protected myocardium around the atrial arteries. We should note that atrial coronary arteries cross the ablation line in many patients.

QRS complex widening due to loss of left bundle branch capture: pitfall of para-Hisian pacing

During para-Hisian pacing, widening of the paced QRS complex usually indicates loss of His bundle capture. We describe a patient without any accessory pathways in whom widening of the paced QRS complex occurred due to loss of left bundle branch capture during para-Hisian pacing. After initial widening of the QRS complex, further widening was observed due to loss of His bundle capture. With the initial QRS widening, the stimulus-atrial interval and retrograde atrial activation sequence were almost unchanged, so the findings mimicked retrograde conduction over an accessory pathway. This may be a pitfall of the para-Hisian pacing technique.

Exact Location of the Branching Bundle in the Living Heart

Aims: The His bundle electrogram is believed to reflect the exact location of the His bundle. However, the distinction between distal His bundle potential and proximal right bundle branch potential is challenging. The aim of this study was to pinpoint the location of the branching point of the His bundle, and to compare that site with the site of recording of the largest His bundle electrogram (LH) during sinus rhythm.

Characterization of the novel mutant A78T-HERG from a long QT syndrome type 2 patient: Instability of the mutant protein and stabilization by heat shock factor 1

The human ether‐a‐go‐go‐related gene (HERG) encodes the α‐subunit of rapidly activating delayed‐rectifier potassium channels. Mutations in this gene cause long QT syndrome type 2 (LQT2). In most cases, mutations reduce the stability of the channel protein, which can be restored by heat shock (HS).

Stabilization of Kv1.5 channel protein by the inotropic agent olprinone

Olprinone is an inotropic agent that inhibits phosphodiesterase (PDE) III and causes vasodilation. Olprinone has been shown to be less proarrhythmic and possibly affect expression of functional Kv1.5 channels that confer the ultra-rapid delayed-rectifier K+ channel current (IKur) responsible for action potential repolarization. To reveal involvement of Kv1.5 channels in the less arrhythmic effect of olprinone, we examined effects of the agent on the stability of Kv1.5 channel proteins expressed in COS7 cells. Olprinone at 30-1000 nM increased the protein level of Kv1.5 channels in a concentration-dependent manner. Chase experiments showed that olprinone delayed degradation of Kv1.5 channels. Olprinone increased the immunofluorescent signal of Kv1.5 channels in the endoplasmic reticulum (ER) and Golgi apparatus as well as on the cell surface. Kv1.5-mediated membrane currents, measured as 4-aminopyridine-sensitive currents, were increased by olprinone without changes in their activation kinetics. A protein transporter inhibitor, colchicine, abolished the olprinone-induced increase of Kv.1.5-mediated currents. The action of olprinone was inhibited by 4-aminopyridine, and was not mimicked by the application of 8-Bromo-cAMP. Taken together, we conclude that olprinone stabilizes Kv1.5 proteins at the ER through an action as a chemical chaperone, and thereby increases the density of Kv1.5 channels on the cell membrane. The enhancement of Kv1.5 currents could underlie less arrhythmogenicity of olprinone.

Macroreentrant atrial tachycardia with an isolated pathway mimicking focal activation on three-dimensional electroanatomical mapping

A 76-year-old man with two different sustained atrial arrhythmias that occurred after coronary artery bypass grafting underwent electrophysiological studies. Macroreentrant atrial tachycardias were detected with an isolated slow pathway mimicking focal activation on three-dimensional electroanatomical mapping. The slow conduction pathway in the right atrial free wall was assumed to represent tissue damaged by right atrial cannulation during previous coronary artery bypass grafting.

Pre-ablation levels of brain natriuretic peptide are independently associated with the recurrence of atrial fibrillation after radiofrequency catheter ablation in patients with nonvalvular atrial fibrillation

Association between pre-ablation levels of biomarkers of cardiac and endothelial dysfunctions, CHADS2, CHA2DS2-VASc, and APPLE scores and the recurrence of atrial fibrillation (AF) after radiofrequency catheter ablation has not been fully studied. A total of 254 patients with nonvalvular AF were prospectively followed for AF recurrence after a single ablation procedure. During a two-year follow-up period, AF recurred in 65 (25.6%) patients. Patients with AF recurrence had significantly greater baseline ln brain natriuretic peptide (BNP) than those without AF recurrence (P < 0.01), whereas there were no significant differences in the levels of biomarkers of endothelial dysfunction and points of scoring systems. In the Cox regression analyses, the baseline ln BNP was significantly independently associated with AF recurrence (adjusted HR =1.286, 95% CI =1.000–1.655, P < 0.05). The baseline levels of ln BNP were significantly associated with rhythm at blood collection, age, sex, and left atrial diameter, and left ventricular ejection fraction (P < 0.05).The subgroup analysis showed a significant interaction on the risk of AF recurrence between ln BNP, sex difference, and rhythm at blood collection (P for interaction < 0.05). In conclusion, the results suggest that the pre-ablation levels of ln BNP are useful to evaluate the risk of AF recurrence after ablation therapy; however, there is a need to be careful while using BNP as a biomarker for the risk of AF recurrence by taking account of the effects of rhythm status at blood collection and sex difference.