Search

Previously, direct monitoring of local activation at the communicating vein (CV) has been reported to be useful for the ablation of ventricular arrhythmias (VAs) originating from the left ventricular (LV) summit. In this study, we evaluated the performance of the novel over-the-wire (OTW)-type decapolar catheter for VAs originating from the LV summit.Overall, 17 patients who underwent catheter ablation for idiopathic VAs originating from the LV summit were included in this study. Of these, seven patients underwent mapping of the epicardial LV outflow tract with the novel 2.7 Fr OTW-type decapolar catheter (EPstar FIX AIV), and ten underwent mapping with the standard 2.0 Fr octopolar catheter (EPstar FIX 2F) procedure (AIV group = EPstar FIX AIV and control group = EPstar FIX 2F).No significant differences in the baseline characteristics were observed between the two groups. In the AIV group, all patients achieved successful catheter positioning in the target CV, whereas in the control group, two patients failed to achieve the same. The novel catheter not only advanced to the target vessels using a 0.014-in guidewire but it was also used for contrast injection from the catheter lumen, which enabled accurate and safe positioning. As a result, the earliest activation time preceding QRS onset during the VA, recorded at the CV, was significantly earlier when compared with the control group (44.66 ± 11.23 ms vs. 32.16 ± 4.26 ms, P = 0.007).Compared with the conventional electrode catheter, this novel multipolar electrode catheter is more effective for mapping local activation at the CV.

Recently, conduction system pacing, including His bundle and left bundle branch area pacing (LBBAP), has emerged as an alternative pacing procedure for right ventricular (RV) pacing. The current study aimed to compare the clinical outcomes of LBBAP and conventional RV midseptal pacing (RVMSP) in patients with heart failure (HF) with preserved ejection fraction (HFpEF) and HF with midrange ejection (HFmrEF) requiring frequency RV pacing due to atrioventricular block (AVB).A total of 89 patients with HFpEF and HFmrEF requiring RV pacing due to symptomatic AVB were enrolled between September 2018 and April 2021, among whom 43 and 46 underwent LBBAP and RVMSP, respectively.No significant differences in baseline characteristics were observed between the two groups. The LBBAP group had a significantly shorter paced-QRS duration and paced left ventricular activation time (LVAT) compared to the RVMSP group (123.4 ± 10.4 ms vs. 152.3 ± 12.3 ms, p .001 and 68.3 ± 10.0 ms vs. 95.2 ± 12.3 ms, p .001, respectively). The LBBAP group had significantly lower N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels at the 6-month follow-up compared to the RVMSP group [459.6 pg/ml (240.4-678.7) vs. 972.7 pg/ml (629.5-1315.9), p = .01]. More patients in the LBBAP group exhibited a significant improvement in NT-proBNP, defined as a 50% decreased from baseline levels.LBBAP maintains physiological ventricular activation and contributes to greater improvement in NT-proBNP value 6 months after implantation in patients with HFpEF and HFmrEF compared to RVMSP.

Although recent echocardiographic studies have suggested that left atrial appendage (LAA) remodeling contributes to the development of LAA thrombus (LAAT), histological evidence is absent. The objective of this study was to examine clinical parameters and histological findings to clarify the factors involved in LAAT formation.A total of 64 patients (no atrial fibrillation [AF], N = 22; paroxysmal AF, N = 16; nonparoxysmal AF, N = 26) who underwent LAA excision during surgery were enrolled. Transthoracic and transesophageal echocardiography were performed before surgery. We evaluated the fibrosis burden (%) in the excised LAA sections with Azan-Mallory staining in patients with a LAAT compared with those without.Patients with paroxysmal and non-paroxysmal AF had a higher LAA fibrosis burden than those without AF (p = .005 and p .0001, respectively). Among the patients enrolled, 16 had a LAAT and 15 of them had nonparoxysmal AF. Among the nonparoxysmal AF patients, those with a LAAT had significantly higher LAA fibrosis burden than those without (23.8% [14.8%-40.3%] vs. 12.8% [7.4%-18.2%], p = .004) and echocardiographic parameters of the left atrial volume index (R = 0.543, p = .01), LAA depth (R = 0.452, p = .02), and LAA flow velocity (R = - 0.487, p = .01) were correlated with the LAA fibrosis burden.This study provided histological evidence that LAA fibrosis is related to LAAT formation. Echocardiographic parameters of LAA remodeling and function were correlated with the LAA fibrosis burden.

Focal atrial tachycardia (AT) originating from the left atrial appendage (LAA) is one of the rare supraventricular tachycardias and is likely to cause arrhythmia-induced heart failure. Surgical treatment could be an alternative therapy because antiarrhythmic drugs and catheter ablation therapy to focal AT originating from the distal portion of the LAA is still challenging. We report a case of successful operation of minimally invasive thoracoscopic appendectomy in a patient with poor left ventricular (LV) function due to drug-resistant AT originating from the LAA for the first time. A 51-year-old female who had AT with a poor LV function suffered from congestive heart failure. We diagnosed the ongoing AT as focal AT that originated from the distal portion of LAA by electrophysiological examination. Total thoracoscopic stand-alone appendectomy was performed safely. AT was terminated and restored to sinus rhythm immediately after appendectomy.

Background Urinary liver-type fatty acid-binding protein (L-FABP) has been known as a potential biomarker for acute kidney injury. It has also been suggested to have an effective predictive value for cardiovascular mortality in patients with diabetes or critically ill condition. Therefore, this study aimed to examine the ability of urinary L-FABP in predicting mid-term cardiovascular morbidity and mortality in patients with hypertension. Methods Urinary L-FABP levels in stable outpatients without diabetes who were treated with antihypertensive drugs were measured, and a 5-year follow-up was planned. The primary end-point was a combination of acute heart failure requiring hospitalization, myocardial infarction, stroke, and cardiovascular death. The secondary end-point was kidney disease progression defined as a relative decline in the estimated glomerular filtration rate of ≥30% from the baseline. Results A total of 197 patients were recruited. Primary and secondary end-points occurred in 24 (12.2%) and 42 (21.3%) patients, respectively, during a median follow-up of 5.7 years. Patients with urinary L-FABP levels higher than the upper limit (8.4 µg/g creatinine) were more likely to reach the primary (30.43% vs. 9.77%; P = 0.003) and secondary end-points (56.52% vs. 16.67%; P < 0.001) than those with urinary L-FABP levels within the normal limits. Urinary L-FABP level was independently associated with both primary (hazard ratio (HR) 1.21; P = 0.03) and secondary end-points (HR 1.19; P = 0.02). Conclusions This study demonstrated that increased urinary L-FABP levels may predict adverse cardiovascular events and renal dysfunction progression even among stable nondiabetic patients with hypertension.

Background Brugada syndrome (BrS) can be diagnosed by a type 1 BrS tracing in a 12-lead electrocardiogram (ECG). However, there are daily variations in the ECGs of BrS patients, which presents a challenge when diagnosing BrS. Although many susceptibility genes have been identified, the SCN5A gene is reportedly the main causative gene of BrS. However, most patients do not have an evidence of genetic predisposition to develop BrS. In addition, the diagnosis and risk stratification for ventricular fibrillation (VF) in patients with BrS presents some problems. Meanwhile, circulating micro RNAs (miRNAs) have drawn increased attention as potential biomarkers of various diseases. We hypothesize that circulating miRNAs may be potential diagnostic biomarkers for BrS. Methods We enrolled 70 Japanese BrS patients and 34 controls for the screening cohort. A total of 2,555 miRNA sequences were detected using the 3D-Gene miRNAs labeling kit and 3D-Gene Human miRNAs Oligo Chip. We compared the expression of the miRNAs between the BrS patients and the controls. We validated whether the miRNA were significantly up- or downregulated in the screening cohort using RT-PCR. We also enrolled 72 Japanese BrS patients and 56 controls to replicate these miRNAs. Results Eight miRNAs (hsa-miR-223-3p, hsa-miR-22-3p, hsa-miR-221-3p, hsa-miR-4485-5p, hsa-miR-550a-5p, hsa-miR-423-3p, hsa-miR-23a-3p, and hsa-miR-30d-5p) were downregulated, and one miRNA (hsa-miR-873-3p) was upregulated by more than 3-fold in BrS patients. The multivariate logistic regression analysis determined that hsa-miR-423-3p, hsa-miR-223-3p, and hsa-miR-23a-3p were independently associated with BrS (P < 0.0001). The AUC based on cross validation was 0.871 with a sensitivity and specificity of 83.5% and 81.1%, respectively. Conclusions The plasma miRNAs are potential noninvasive biomarkers of BrS, and the constructed logistic model was useful for discriminating BrS.

Background myBeat is a novel cutaneous patch device that continuously records electrocardiography and automatically detects atrial fibrillation (AF) by using a new algorithm based on RR intervals. We aimed to test the diagnostic ability of this novel device for screening silent AF in asymptomatic patients.Methods and Results:A multicenter randomized prospective clinical study was performed. To be eligible for inclusion in the study, patients had to be ≥65 years of age and have ≥1 of the following risk factors: hypertension, diabetes, heart failure, ischemic heart disease, stroke, and transient ischemic attack. Patients with prior AF, an implantable pacemaker, and previous palpitation or syncope were excluded. The 300 participants were divided into 2 groups, those using myBeat (n=150) or those undergoing 24-h Holter monitoring (control group; n=150), for AF screening. The rate of AF detection was significantly higher in the myBeat than control group (16 [10.7%] vs. 7 [4.7%], respectively; P=0.04). Multivariable logistic regression analysis revealed that prior heart failure was an independent predictor of silent AF (odds ratio 12.07; 95% confidence interval 1.67-86.27; P=0.01). A 7.7-fold difference in silent AF was found between subjects with CHA2DS2-VASc scores of 1 point and those with scores ≥4 points. Conclusions The novel patch device using an original algorithm was beneficial for screening of silent AF.

Genome-wide association studies have reported a strong association of the single nucleotide polymorphism (SNP) rs6817105 (T > C) on chromosome 4q25 with atrial fibrillation (AF), but phenotype alterations conferred by this SNP have not been described. We genotyped SNP rs6817105 and examined the relationships among rs6817105 genotype, clinical characteristics, echocardiographic parameters, and electrophysiological parameters in 574 AF patients and 1,554 non-AF controls. Further, multiple microRNAs (miRNAs) are reported to be involved in atrial remodeling and AF pathogenesis, so we investigated relationships between rs6817105 genotype and serum concentrations of 2555 miRNAs. The rs6817105 minor allele frequency was significantly higher in AF patients than non-AF controls (66% vs. 47%, odds ratio 2.12, p = 4.9 × 10−26). Corrected sinus node recovery time (CSRT) was longer and left atrial volume index (LAVI) was larger in AF patients with the rs6817105 minor allele than patient non-carriers (CSRT: CC 557 ± 315 ms, CT 486 ± 273 ms, TT 447 ± 234 ms, p = 0.001; LAVI: CC 43.6 ± 12.1, CT 42.4 ± 13.6, TT 39.8 ± 11.6, p = 0.030). There were no significant differences between rs6817105 genotype and the serum concentrations of miRNAs. These findings strongly implicate rs6817105 minor allele in sinus node dysfunction and left atrial enlargement.

A 51‐year‐old man with dextrocardia and complete situs inversus who presented with palpitation as a result of drug refractory paroxysmal atrial fibrillation (AF) was referred to our hospital for catheter ablation. Pulmonary vein isolation (PVI) was performed using the HotBalloon technique. We were able to accomplish AF ablation safely and easily using 180 degree‐inversed mirror images of X‐ray fluoroscopy. We have reported successful PVI for AF with dextrocardia using HotBalloon and mirror image of X‐ray fluoroscopy without any complication for the first time., We report a case of successful pulmonary vein isolation for atrial fibrillation with dextrocardia using HotBalloon and 180 degree‐inversed mirror image of X‐ray fluoroscopy for the first time.

Background Atrial fibrillation (AF) has a genetic basis, and environmental factors can modify its actual pathogenesis. Objective The purpose of this study was to construct a combined risk assessment method including both genetic and clinical factors in the Japanese population. Methods We screened a cohort of 540 AF patients and 520 non-AF controls for single nucleotide polymorphisms (SNPs) previously associated with AF by genome-wide association studies. The most strongly associated SNPs after propensity score analysis were then used to calculate a weighted genetic risk score (WGRS). We also enrolled 1018 non-AF Japanese subjects as a validation cohort and monitored AF emergence over several years. Finally, we constructed a logistic model for AF prediction combining WGRS and clinical risk factors. Results We identified 5 SNPs (in PRRX1, ZFHX3, PITX2, HAND2, and NEURL1) associated with AF after Bonferroni correction. There was a 4.92-fold difference in AF risk between the highest and lowest WGRS calculated using these 5 SNPs (P = 2.32 × 10−10). Receiver operating characteristic analysis of WGRS yielded an area under the curve (AUC) of 0.73 for the screening cohort and 0.72 for the validation cohort. The predictive logistic model constructed using a combination of WGRS and AF clinical risk factors (age, body mass index, sex, and hypertension) demonstrated better discrimination of AF than WGRS alone (AUC = 0.84; sensitivity 75.4%; specificity 80.2%). Conclusion This novel predictive model of combined AF-associated SNPs and known clinical risk factors can accurately stratify AF risk in the Japanese population.

Background Atrial fibrillation (AF) recurrence after radiofrequency catheter ablation (RFCA) still remains a serious issue. Ca2+ handling has a considerable effect on AF recurrence. The histidine-rich calcium-binding protein (HRC) genetic single nucleotide polymorphism (SNP), rs3745297 (T>G, Ser96Ala), is known to cause a sarcoplasmic reticulum Ca2+ leak. We investigated the association between HRC Ser96Ala and AF recurrence after RFCA in paroxysmal AF (PAF) patients. Methods and results We enrolled PAF patients who underwent RFCA (N = 334 for screening and N = 245 for replication) and were genotyped for HRC SNP (rs3745297). The patient age was younger and rate of diabetes and hypertension lower in the PAF patients with Ser96Ala than in those without (TT/TG/GG, 179/120/35; 64±10/60±12/59±13 y, P = 0.001; 18.5/ 9.2/8.6%, P = 0.04 and 66.1/50.0/37.1%, P = 0.001, respectively). During a mean 19 month follow-up, 57 (17.1%) patients suffered from AF recurrences. The rate of an Ser96Ala was significantly higher in patients with AF recurrence than in those without in the screening set (allele frequency model: odds ratio [OR], 1.80; P = 0.006). We also confirmed this significant association in the replication set (OR 1.74; P = 0.03) and combination (P = 0.0008). A multivariate analysis revealed that the AF duration, sinus node dysfunction, and HRC Ser96Ala were independent predictors of an AF recurrence (hazard ratio [HR], 1.04, P = 0.037; HR 2.42, P = 0.018; and HR 2.66, P = 0.007, respectively). Conclusion HRC SNP Ser96Ala is important as a new genetic marker of AF recurrence after RFCA.

Urinary liver-type fatty acid-binding protein (L-FABP) is a potential biomarker for acute kidney injury, and it in turn increases cardiovascular mortality. We tested whether the urinary L-FABP level predicted short- and mid-term outcomes in patients with acute heart failure.We enrolled consecutive patients with acute heart failure, and measured their urinary L-FABP levels before acute treatment. Worsening renal function (WRF), defined as both an absolute increase in the serum creatinine level of ≥0.3mg/dL and a ≥25% relative increase in its level from baseline, occurred in 37 (26.8%) of 138 patients. Patients with a urinary L-FABP level above the upper normal limit (8.4 µg/g creatinine) (n = 49; 35.5%) were more likely than those with a urinary L-FABP level within normal limits (n = 89; 64.5%) to develop WRF (n = 26 [53.1%] vs n = 11 [12.4%]; P.001). A urinary L-FABP level above the upper limit was independently associated with WRF (hazard ratio 1.8; P = .01). During 1 year of follow-up, 12 patients (8.7%) died, and urinary L-FABP level had no association with all-cause mortality. There was, however, a tendency toward a higher readmission rate in patients with a urinary L-FABP level above the upper normal limit who survived the index hospitalization (n = 46) than in those without an abnormal L-FABP level (n = 88; n = 13 [28.3%] vs n = 13 [14.8%]; log-rank P = .06).Increased urinary L-FABP level before treatment may predict WRF in patients with acute heart failure. Further investigation is warranted for its predictive ability of adverse outcomes.

Objective Very late stent thrombosis (VLST) remains an unresolved problem, and recent reports have indicated that VLST onset can occur in patients treated with both drug-eluting stents (DES) and bare metal stents (BMS). We evaluated the causes of VLST using optical coherence tomography (OCT). Methods OCT was performed in 22 patients (12 DES-treated patients, 10 BMS-treated patients). Because two instances of VLST occurred simultaneously in one case in the DES group, the DES group comprised 13 lesions, while the BMS group comprised 10 lesions. All struts were counted in each frame, and the proportion of uncovered or malapposed struts was calculated based on the overall number of struts in the stent. Results The interval from stent implantation to VLST onset was significantly longer in the BMS group. The proportion of uncovered struts and the ratio of malapposed struts were significantly higher in the DES group than in the BMS group. The OCT analysis demonstrated intimal hyperplasia or intimal disruption in all patients in the BMS group. However, in the DES group, severe hyperplasia and/or neoatherosclerosis was observed in only eight lesions (61.5%), while uncovered and malapposed struts were involved in the other lesions. Conclusion In most BMS-treated lesions, it appeared that VLST was caused by the occurrence of neoatherosclerosis after stent implantation. The causes of VLST in DES-treated lesions are more various and complicated than those observed for BMS-treated lesions.