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Background: Adequate catheter-to-myocardial contact force (CF) and catheter stability are important to create transmural lesions during catheter ablation of atrial fibrillation (AF). It is known that there are anatomical variations in left atrium (LA) and it is related to the outcome after the ablation. We tested any relationship between the CF and LA anatomical variations. Methods: Consecutive patients undergoing radiofrequency-based extensive encircling pulmonary vein (PV) isolation for the treatment of paroxysmal AF were dichotomized according to the LA anatomical variations; patients who had a PV-bifurcation region of LA ridge that was steep enough to enable a stable catheter-tip contact or a left common PV (group 1, the red arrows in Figure 1), or those who had neither (group 2, the blue arrows in Figure 1). The blinded operators carried out the procedure with the use of CARTO system, and the following VisiTag™ module setting was applied; a minimum time spent in an area of 5 seconds, a maximum distance the catheter has moved of 4mm, a force over time of 25%, and a minimum force of 10g. Low-CF tags was defined as ablation tags on CARTO map located at anterior aspect of left PVs that did not fulfill the pre-determined VisiTag™ criteria. The endpoints were the number of low-CF tags and freedom from AF 1 year after the ablation. Results: Patients in group 1 (n=31) had a smaller number of low-CF tags than those in group 2 (n=55, 2.8±2.1 vs. 5.9±3.8; p=0.013). Freedom from AF was more common in group 1 compared to group 2 (80.6% vs. 60%; p=0.04), and was independently associated with the number of low-CF of Conclusions: Contact of the catheter-tip with the tissue may predict outcome after AF ablation, and it may depend on LA anatomical variations.

The common SCN5A polymorphism, H558R (c.1673A>G,rs1805124), has been reported to be a genetic modulator of Brugada syndrome (BrS) carrying a SCN5A mutation. H558R has been known to improve the sodium channel activity in mutated channels by restoring the abnormal channel gating kinetics or membrane trafficking. The mechanisms by which H558R rescues the SCN5A mutations remain incompletely defined. We investigated the possible mechanism of why H558R modifies the effects brought by an SCN5A mutation. We investigated rs1805124 in 95 BrS patients (91 males, mean age 42 ± 14 years) and 1,875 normal controls (1546 male, mean age 54±18 years). We obtained the right atrial sections during aortic aneurysm operations from 21 patients and rs1805124 was also genotyped in them. Using cDNA of these patients, we examined the expression level of SCN5A by real time RT-PCR and whether splicing of exon 9 to exon 10 in SCN5A was correct by RT-PCR.and evaluate the difference between the genotypes of rs1805124. Additionally, we analyzed the expression ratio of the A allele and G allele separately by specific probes in heterozygous patients. H558R was less frequent in patients with BrS than in normal controls (4.7% vs. 10.3%, P = 0.01). We found strong Linkage disequibrium (LD) in c1141-3C>A (Intron 9) and H558R (r2=0.946). The genotype distribution of the rs1805124 of AA, AG, and GG genotypes in the 21 patients were 13 (61.9 %), 8 (38.1 %), and 0 (0%), respectively. The expression level of SCN5A was similar in the patients with and without H558R. There were not any splicing abnormalities of SCN5A despite of H558R existence. The A allele expression level was mean 1.38 fold higher than that for the G allele (P=0.004). The result suggested that the mutation effect was relieved if the heterozygous mutation rode on the risk allele G. We may have elucidated one reason why H558R modifies the effects brought on by SCN5A mutations.

Objective: Little is known about the clinical features in patients with cardiac sarcoidosis who receive cardiac resynchronization therapy (CRT). We aimed to clarify the clinical response to CRT in patients with cardiac sarcoidosis. Methods: We compared the clinical data on CRT between heart failure patients with cardiac sarcoidosis and those with other etiologies at 3 cardiovascular centers. The primary endpoint was composite outcome of cardiovascular death or hospitalization from worsening heart failure within 5 years after the CRT. Results: The patients with cardiac sarcoidosis (N=18) were more likely than those without cardiac sarcoidosis (N=141) to be female (83.3% vs. 22.7%; P Conclusions: Outcomes after the CRT may be acceptable in patients with cardiac sarcoidosis. A poor left ventricular reverse remodeling and higher occurrence of ventricular arrhythmias may characterize them.

Background: Previous study showed that number of yellow plaque in a coronary artery was associated with future risk of acute coronary syndrome. However, impact of intrastent yellow plaque has not fully understood. Purpose: This study was investigated to assess the association of the grade of intrastent yellow plaque observed by coronary angioscopy at late phase after drug-eluting stents (DES) implantation and clinical outcome. Methods: This study consisted of 97 patients tread with DES implantation (39 patients with sirolimus-eluting stents ; 9 patients with paclitaxel-eluting stents; 24 patients with everolimus-eluting stents; 6 patients with zotalolimus-eluting stents; 19 patients with biolimus-eluting stents ). Coronary angioscopy was performed 8 months after DES implantation. The plaque color at stent segment was grade as 0 (white), 1 (light yellow), 2 (yellow), 3 (bright yellow). The maximum color grade of the plaques in stent segment was assessed. We divided these patients into 2 groups (53 patients with yellow plaque grade 2 or 3; 44 patients with yellow plaque grade 0 or 1). We evaluated the incidence of revascularization, such as percutaneous coronary intervention or coronary artery bypass graft. Results: Kaplan-Meier curves for 7-year Revascularization free rate are shown in Figure. Revascularization free rate was tend to be higher in patients with yellow grade 0/1 than those with yellow grade 2/3. Conclusion: The presence of intrastent yellow plaque at late phase after stent implantation might be associated with the future revascularization in coronary artery disease.

Aim: Risk stratification of ventricular fibrillation (VF) in Brugada syndrome remains controversial and it is difficult to describe using one parameter. We investigated whether we are able to assess VF risk using our non-invasive scoring method of each Brugada syndrome patients. Methods: We enrolled 46 patients with Brugada syndrome (45 men, average age 42 ± 3 years). Thirteen of the subjects had VF history or subsequent VF events (VF+) after implantable cardioverter defibrillator implantation. The frequency of Type1 Brugada ECG and positive TWA were significantly higher in VF+ patients than those without (Type 1 ECG 50% vs 4.8%, P=0.0003 and positive TWA 73.3% vs 6.7%, P Conclusions: The new scoring method using previous reported non-invasive risk factors of VF in Brugada syndrome is useful for assessing risk stratification in daily medical practice.