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Achieving a favorable pacing threshold with a Micra transcatheter pacing system (Micra-TPS) is needed to reduce battery depletion. In some cases, the threshold increases shortly after the device is implanted, and a higher pacing threshold may be required. This study aims to identify the causes and predictors of the increase in pacing threshold observed shortly after Micra-TPS implantation.The study included 64 consecutive patients who underwent Micra-TPS implantation between 2017 and 2020. The patients were divided into two groups depending on their pacing threshold: the increased pacing threshold (IPT) group (threshold increased by ≥0.5 V/0.24 ms within 1 month of implantation) and the stable pacing threshold (SPT) group.Excluding four patients who could not be followed up, of the 60 remaining patients, nine (15%) were in the IPT group and 51 (85%) were in the SPT group. The IPT group had significantly lower implant impedance values and higher implant thresholds than the SPT group (582 ± 59 vs 755 ± 167 Ω [P .001] and 1.29 ± 0.87 vs 0.71 ± 0.40 V/0.24 ms [P = .014]). Implant impedance and threshold may serve as predictors of a threshold increase after implantation (area under the curve: 0.737-0.943 and 0.586-0.926, respectively).An IPT was noted shortly after Micra-TPS implantation owing to micro-dislodgement because of insufficient anchoring of the device to the myocardium. Impedance 660 Ω and threshold 1.0 V/0.24 ms may predict an increase in pacing threshold.

Acute megakaryoblastic leukemia (AMKL) in children without Down syndrome (DS) has an extremely poor outcome with 3-year survival of less than 40%, whereas AMKL in children with DS has an excellent survival rate. Recently, a novel recurrent translocation involving CBFA2T3 and GLIS2 was identified in about 30% of children with non-DS AMKL, and the fusion gene was reported as a strong poor prognostic factor in pediatric AMKL. We report the difficult clinical courses of pediatric patients with AMKL harboring the CBFA2T3-GLIS2 fusion gene.Down sendromu (DS) olmayan çocuklarda akut megakaryoblastik löseminin (AMKL) prognozu çok kötü ve 3 yıllık sağkalım %40’ın altında iken, DS’li çocuklarda AMKL’nin sağkalım oranı mükemmeldir. Yakın zamanda, DS olmayan AMKL’li çocukların yaklaşık %30’unda CBFA2T3 ve GLIS2’yi içeren yeni bir tekrarlayan translokasyon tanımlandı ve füzyon geninin pediatrik AMKL olgularında kötü prognoz ile ilişkili güçlü bir prognostik belirteç olduğu bildirildi. CBFA2T3-GLIS2 füzyon genini taşıyan AMKL tanılı pediatrik hastalarda sorunlu klinik seyri bildiriyoruz.

Background— We recently showed that the presence of early repolarization (ER) increases the risk of ventricular fibrillation occurrences in the early phase of acute myocardial infarction (AMI). This study aimed to clarify whether an association exists between ER and occurrences of ventricular tachyarrhythmias or sudden death in the chronic phase of AMI. Methods and Results— This study retrospectively enrolled 1131 patients (67±12 years; 862 men) with AMIs surviving 14 days post-AMI. The primary end point was the occurrence of sustained ventricular tachyarrhythmias or sudden death >14 days after the AMI onset. We evaluated the presence of ER from the predischarge ECG (mean 10±3 days post-AMI). ER was defined as an elevation of the terminal portion of the QRS complex of >0.1 mV in inferior or lateral leads. After a median follow-up of 26.2 months, 26 patients had an episode of ventricular tachyarrhythmias or sudden death. A multivariable Cox regression analysis revealed the presence of ER (hazard ratio, 5.37; 95% confidence interval, 2.27–12.69; P I (hazard ratio, 2.75; 95% confidence interval, 1.24–6.07; P =0.013), and a left ventricular ejection fraction of P Conclusions— ER observed at a mean of 10 days post-AMI may be a marker for a subsequent risk of ventricular tachyarrhythmias or sudden death.

We recently showed that the presence of J waves increases the risk of ventricular fibrillation (VF) occurrence in the early phase of an acute myocardial infarction (AMI). This study aimed to evaluate the clinical characteristics of VF occurrences in the early phase of an AMI between patients with and without J waves.This retrospective, observational study included 281 consecutive patients with an AMI (69 ± 12 years; 207 men) in whom 12-lead ECGs before AMI onset could be evaluated. The patients were classified based on a VF occurrence48 hours after AMI onset and the presence of J waves. J waves were electrocardiographically defined as an elevation of the terminal portion of the QRS complex of0.1 mV from baseline in at least 2 contiguous inferior or lateral leads. VF occurred in 24 patients, and J waves were present in 37. VF occurrence was more prevalent in the patients with than without J waves (27% vs. 6%; P0.001). Among the 244 patients without J waves, peak creatine kinase level (P0.01), number of diseased coronary arteries (P0.01), and male sex (P0.05) were higher in the patients with than without VF occurrence. However, among the 37 patients with J waves, there was no significant difference in these variables. There was no association between the location of J waves and the infarct area.In patients with AMI, those with J waves were more likely to develop VF and less likely to have high-risk clinical characteristics than those without J waves.

Background— Triple antithrombotic therapy increases the risk of bleeding events in patients undergoing percutaneous coronary intervention. However, it remains unclear whether good control of percent time in therapeutic range is associated with reduced occurrence of bleeding complications in patients undergoing triple antithrombotic therapy. Methods and Results— This study included 2648 patients (70±11 years; 2037 men) who underwent percutaneous coronary intervention with stent in the Ibaraki Cardiovascular Assessment Study registry and received dual antiplatelet therapy with or without warfarin. Clinical end points were defined as the occurrence of major bleeding complications (MBC), major adverse cardiac and cerebrovascular event, and all-cause death. Among these 2648 patients, 182 (7%) patients received warfarin. After a median follow-up period of 25 months (interquartile range, 15–35 months), MBC had occurred in 48 (2%) patients, major adverse cardiac and cerebrovascular event in 484 (18%) patients, and all-cause death in 206 (8%) patients. Multivariable Cox regression analysis revealed that triple antithrombotic therapy was the independent predictor for the occurrence of MBC (hazard ratio, 7.25; 95% confidence interval, 3.05–17.21; P P =0.7). However, the mean international normalized ratio of prothrombin time at the time of MBC occurrence was 3.3±2.1. Triple antithrombotic therapy did not have a predictive value for the occurrence of all-cause death ( P =0.1) and stroke ( P =0.2). Conclusions— Triple antithrombotic therapy predisposes patients to an increased risk of MBC regardless of the time in therapeutic range.