Heart rhythm最新文献

Background: The coagulation response during vascular injury with uninterrupted administration of direct oral anticoagulants has not been elucidated.

Objective: Our aim was to evaluate differences in coagulation responses after vascular injury between uninterrupted direct thrombin inhibitor and direct factor Xa inhibitor recipients.

Methods: Patients scheduled for catheter ablation for atrial fibrillation were randomly assigned to receive dabigatran or apixaban in this prospective, randomized, comparative, parallel-group study. Venous blood was collected 3 times: 180 minutes after taking the anticoagulant on the day before the procedure, before vascular punctures of the ablation procedure, and 10-15 minutes after the start of vascular punctures.

Results: Forty-two patients were enrolled. The prothrombin fragment 1+2 level, the primary end point, was much larger after vascular puncture in the uninterrupted dabigatran recipients (median, 83 pmol/L; interquartile range, 56-133 pmol/L) than in the uninterrupted apixaban recipients (median, 1 pmol/L; interquartile range, -3 to 19 pmol/L; P < .001). Antithrombin levels decreased after vascular puncture in dabigatran recipients, and both protein C and antithrombin levels decreased after vascular puncture in apixaban recipients.

Conclusion: Unlike uninterrupted apixaban, uninterrupted dabigatran does not inhibit thrombin generation in response to vascular injury.

The complexity of cardiac electrophysiology procedures has increased significantly during the past 3 decades. Anesthesia requirements of these procedures can differ on the basis of patient- and procedure-specific factors. This manuscript outlines various anesthesia strategies for cardiac implantable electronic devices and electrophysiology procedures, including preprocedural, procedural, and postprocedural management. A team-based approach with collaboration between cardiac electrophysiologists and anesthesiologists is required with careful preprocedural and intraprocedural planning. Given the recent advances in electrophysiology, there is a need for specialized cardiac electrophysiology anesthesia care to improve the efficacy and safety of the procedures.

Background: Many genetic nonischemic dilated cardiomyopathies (NICMs) cause ventricular tachycardias (VTs) originating from scar substrate identified as areas of low electrogram voltage. Substrate locations vary, and the causes of scar are not well defined.

Objective: This study evaluated VT substrate locations in genetic NICM patients undergoing VT ablation to evaluate spatial relationships between specific variants and substrate locations.

Methods: In this retrospective case series analysis, 32 patients (aged 55 ± 16 years; 94% male; left ventricular ejection fraction, 34% ± 13%) with genetic NICM referred for VT ablation between October 2018 and November 2022 at a single medical center were evaluated. Scar locations were defined as areas of low unipolar or bipolar voltage.

Results: Of the 32 patients evaluated, mutations in TTN (n = 11), LMNA (n = 6), PKP2 (n = 5), MYBPC3 (n = 3), DSP (n = 2), TTR (n = 1), FLNC (n = 1), AGL (n = 1), DES (n = 1), and DSG2 (n = 1) were observed. Substrates associated with mutations in TTN were observed only in basal subregions, predominantly anterior (100%) and septal (50%) regions. LMNA mutations were associated with fibrosis in mid inferolateral (60%) and apical inferolateral (60%) regions. Substrate location for individuals with PKP2 mutations was solely observed in the right ventricle, predominantly basal inferolateral regions.

Conclusion: Understanding spatial relationships between genetic variants causing NICM and VT substrate locations can help lead to generalizable regions in patients with genetically related NICM presenting in VT, which can be investigated during ablation procedures.

The subcutaneous implantable cardioverter-defibrillator (S-ICD) has emerged as a feasible alternative to the transvenous ICD in the treatment of ventricular tachyarrhythmias in patients without indications for pacing or cardiac resynchronization therapy. Since its introduction, numerous innovations have been made and clinical experience has been gained, leading to its adoption in current practice and preference in certain populations. Moreover, emerging technologies like the extravascular ICD and the combination of the S-ICD with the leadless pacemaker offer new possibilities for the future. These advancements underscore the evolving role of the S-ICD in management of ventricular tachyarrhythmias. This review outlines implantation considerations, patient selection, and troubleshooting advancements in the last 15 years and provides insights into future perspectives.

Recent studies have highlighted the critical role of calcium/calmodulin-dependent protein kinase II (CaMKII) overactivation in the pathogenesis of various cardiac arrhythmias. Ruxolitinib, a Janus kinase inhibitor widely used for the treatment of myelofibrosis and acute graft-vs-host disease, has expanded its research horizons to include its potential as a CaMKII inhibitor in the treatment of cardiac arrhythmias. This article reviews the basic pharmacologic properties of ruxolitinib and delves into the role of CaMKII in cardiac arrhythmias, including its structural fundamentals, activation mechanisms, and association with arrhythmic conditions. Furthermore, the current state of CaMKII inhibitor research is discussed, with a special focus on the advances and clinical potential of ruxolitinib in this field. Studies indicate that ruxolitinib effectively inhibits CaMKII activity and has therapeutic potential against cardiac arrhythmias in animal models and at the cellular level. In addition, we address the critical issues that need to be resolved before the clinical application of ruxolitinib in arrhythmia treatment, including dosage concerns, long-term inhibitory effects, potential impacts on the nervous system, and efficacy across different types of arrhythmias. Future research directions involve further exploration of the clinical application potential of ruxolitinib, particularly in diseases such as heart failure, hypertrophic cardiomyopathy, dilated cardiomyopathy, and ischemic arrhythmias. In summary, the efficacy, low toxicity, and safety profile of ruxolitinib as a CaMKII inhibitor in the treatment of cardiac arrhythmias suggest a promising future for its development as a therapeutic drug in this domain.