ACC/AHA Task Force Members Glenn N. Levine, MD, FACC, FAHA, Chair Patrick T. O’Gara, MD, MACC, FAHA, Chair-Elect Jonathan L. Halperin, MD, FACC, FAHA, Immediate Past Chair‡‡ Sana M. Al-Khatib, MD, ...MHS, FACC, FAHA Joshua A. Beckman, MD, MS, FAHA Kim K. Birtcher, PharmD, MS, AACC Biykem Bozkurt, MD, PhD, FACC, FAHA‡‡ Ralph G. Brindis, MD, MPH, MACC‡‡ Joaquin E. Cigarroa, MD, FACC Lesley H. Curtis, PhD, FAHA‡‡ Anita Deswal, MD, MPH, FACC, FAHA Lee A. Fleisher, MD, FACC, FAHA Federico Gentile, MD, FACC Samuel Gidding, MD, FAHA‡‡ Zachary D. Goldberger, MD, MSc, FACC, FAHA Mark A. Hlatky, MD, FACC, FAHA John Ikonomidis, MD, PhD, FAHA‡‡ José A. Joglar, MD, FACC, FAHA Laura Mauri, MD, MSc, FAHA‡‡ Mariann R. Piano, RN, PhD, FAHA Susan J. Pressler, PhD, RN, FAHA‡‡ Barbara Riegel, PhD, RN, FAHA‡‡ Duminda N. Wijeysundera, MD, PhD‡‡Former Task Force member; current member during the writing effort.Table of Contents Top 10 Take-Home Messages For the Management of Bradycardia and Cardiac Conduction Delaye53 Preamblee54 Introductione55 1.1.Methodology and Evidence Reviewe55 1.2.Organization of the Writing Committeee55 1.3.Document Review and Approvale55 1.4.Scope of the Guidelinee56 1.5.Class of Recommendation and Level of Evidencee56 1.6.Abbreviationse56 2. General Evaluation of Patients With Documented or Suspected Bradycardia or Conduction Disorderse61 4.1.History and Physical Examination of Patients With Documented or Suspected Bradycardia or Conduction Disorderse61 4.2.Noninvasive Evaluatione66 4.2.1.Resting ECG in Patients With Documented or Suspected Bradycardia or Conduction Disorderse66 4.2.2.Exercise Electrocardiographic Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorderse66 4.2.3.Ambulatory Electrocardiography in Patients With Documented or Suspected Bradycardia or Conduction Disorderse67 4.2.4.Imaging in Patients With Documented or Suspected Bradycardia or Conduction Disorderse69 4.2.5.Laboratory Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorderse70 4.2.6.Genetic Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorderse71 4.2.7.Sleep Apnea Evaluation and Treatment in Patients With Documented or Suspected Bradycardia or Conduction Disorderse72 4.3. In patients with a left ventricular ejection fraction between 36% to 50% and atrioventricular block, who have an indication for permanent pacing and are expected to require ventricular pacing >40% of the time, techniques that provide more physiologic ventricular activation (e.g., cardiac resynchronization therapy, His bundle pacing) are preferred to right ventricular pacing to prevent heart failure. Because conduction system abnormalities are common after transcatheter aortic valve replacement, recommendations on postprocedure surveillance and pacemaker implantation are made in this guideline. Using the principles of shared decision-making and informed consent/refusal, patients with decision-making capacity or his/her legally defined surrogate has the right to refuse or request withdrawal of pacemaker therapy, even if the patient is pacemaker dependent, which should be considered palliative, end-of-life care, and not physician-assisted suicide.
In patients with or without left bundle branch block, left bundle branch pacing (LBBP) can produce near normalization of QRS duration (QRSd). This has recently emerged as an alternative technique to ...His bundle pacing.
The purpose of this study was to characterize a novel approach for LBBP in patients with bradycardia indications for pacing and to assess implant success rate and midterm safety.
Patients with bradycardia indications for pacing underwent LBBP by a trans-ventricular-septal method in the basal ventricular septum. Procedural success, pacing parameters, and complications were assessed at implantation and at 3 months follow-up.
This prospective study evaluated 87 patients (sinus node dysfunction 67.8%; atrioventricular conduction disease 32.2%) undergoing pacemaker implantation. LBBP implantation succeeded in 80.5% (70/87) of patients and the remaining 17 patients received right ventricular septal pacing. The procedure time of LBBP implantation was 18.0 ± 8.8 minutes with a fluoroscopic exposure time of 3.9 ± 2.7 minutes. LBBP produced narrower electrocardiographic QRSd than did right ventricular septal pacing (113.2 ± 9.9 ms vs 144.4 ± 12.8 ms; P < .001). There were no major implantation-related complications. The pacing threshold was low (0.76 ± 0.22 V at implantation and 0.71 ± 0.23 V at 3 months), with no loss of capture or lead dislodgment observed.
This study demonstrates that in patients with standard bradycardia pacing indications, LBBP results in QRSd < 120 ms in most patients and can be performed successfully and safely in the majority of patients.
Downregulation of the pacemaking ion channel, HCN4 (hyperpolarization-activated cyclic nucleotide gated channel 4), and the corresponding ionic current,
, underlies exercise training-induced sinus ...bradycardia in rodents. If this occurs in humans, it could explain the increased incidence of bradyarrhythmias in veteran athletes, and it will be important to understand the underlying processes.
To test the role of HCN4 in the training-induced bradycardia in human athletes and investigate the role of microRNAs (miRs) in the repression of HCN4.
As in rodents, the intrinsic heart rate was significantly lower in human athletes than in nonathletes, and in all subjects, the rate-lowering effect of the HCN selective blocker, ivabradine, was significantly correlated with the intrinsic heart rate, consistent with HCN repression in athletes. Next-generation sequencing and quantitative real-time reverse transcription polymerase chain reaction showed remodeling of miRs in the sinus node of swim-trained mice. Computational predictions highlighted a prominent role for miR-423-5p. Interaction between miR-423-5p and HCN4 was confirmed by a dose-dependent reduction in HCN4 3'-untranslated region luciferase reporter activity on cotransfection with precursor miR-423-5p (abolished by mutation of predicted recognition elements). Knockdown of miR-423-5p with anti-miR-423-5p reversed training-induced bradycardia via rescue of HCN4 and
. Further experiments showed that in the sinus node of swim-trained mice, upregulation of miR-423-5p (intronic miR) and its host gene, NSRP1, is driven by an upregulation of the transcription factor Nkx2.5.
HCN remodeling likely occurs in human athletes, as well as in rodent models. miR-423-5p contributes to training-induced bradycardia by targeting HCN4. This work presents the first evidence of miR control of HCN4 and heart rate. miR-423-5p could be a therapeutic target for pathological sinus node dysfunction in veteran athletes.
An 82‐year‐old woman received pacemaker implantation for sick sinus syndrome. Two days after the implantation, electrocardiography showed 2:1 atrial pacing failure, followed by a ...bradycardia‐dependent increase in the atrial pacing threshold during a pacemaker examination. However, transient 1:1 atrial pacing capture recovered by adenosine triphosphate (ATP) administration, which was performed to evaluate the bradycardia‐dependent pacing failure mechanism. We considered this phenomenon to be caused by Phase 4 depolarization and avoided replacing this atrial lead. Three weeks later, the atrial pacing threshold had improved. We report the potential role of Phase 4 depolarization in a bradycardia‐dependent increase in pacing threshold by using ATP.
Background
Despite descriptions of various cardiovascular manifestations in patients with coronavirus disease 2019 (COVID‐19), there is a paucity of reports of new onset bradyarrhythmias, and the ...clinical implications of these events are unknown.
Methods
Seven patients presented with or developed severe bradyarrhythmias requiring pacing support during the course of their COVID‐19 illness over a 6‐week period of peak COVID‐19 incidence. A retrospective review of their presentations and clinical course was performed.
Results
Symptomatic high‐degree heart block was present on initial presentation in three of seven patients (43%), and four patients developed sinus arrest or paroxysmal high‐degree atrioventricular block. No patients in this series demonstrated left ventricular systolic dysfunction or acute cardiac injury, whereas all patients had elevated inflammatory markers. In some patients, bradyarrhythmias occurred prior to the onset of respiratory symptoms. Death from complications of COVID‐19 infection occurred in 57% (4/7) patients during the initial hospitalization and in 71% (5/7) patients within 3 months of presentation.
Conclusions
Despite management of bradycardia with temporary (3/7) or permanent leadless pacemakers (4/7), there was a high rate of short‐term morbidity and death due to complications of COVID‐19. The association between new‐onset bradyarrhythmias and poor outcomes may influence management strategies for acutely ill patients with COVID‐19.
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