Search

BACKGROUND: The safety of electronic control devices (ECDs) has been questioned. The goal of this study was to analyze in detail cases of loss of consciousness associated with ECD deployment. METHODS AND RESULTS: Eight cases of TASER X26 ECD-induced loss of consciousness were studied. In each instance, when available, police, medical, and emergency response records, ECD dataport interrogation, automated external defibrillator information, ECG strips, depositions, and autopsy results were analyzed. First recorded rhythms were ventricular tachycardia/fibrillation in 6 cases and asystole (after ~=30 minutes of nonresponsiveness) in 1 case. An external defibrillator reported a shockable rhythm in 1 case, but no recording was made. This report offers evidence detailing the mechanism by which an ECD can produce transthoracic stimulation resulting in cardiac electrical capture and ventricular arrhythmias leading to cardiac arrest. CONCLUSIONS: ECD stimulation can cause cardiac electrical capture and provoke cardiac arrest resulting from ventricular tachycardia/ventricular fibrillation. After prolonged ventricular tachycardia/ventricular fibrillation without resuscitation, asystole develops. [ABSTRACT FROM AUTHOR]

Which of your patients are at risk for sudden death? Who is a candidate for confirmatory testing, and what will you do with the results once you have them? Which treatments are most likely to prevent a fatal arrhythmia or other catastrophic outcome? [ABSTRACT FROM AUTHOR]

Introduction: Spatial segmentation is essential for the numerical simulation of excitation propagation in cardiac muscle. Methods and Results: This study evaluated the effects of spatial segmentation on action potential and on the velocity of propagation in a continuous one-dimensional model of cardiac muscle [intracellular and extracellular resistivities along (L) and transverse (T) to the muscle fibers: 402 cm (Ri, L), 3,620 cm (Ri, T), 48 cm (Re, L), and 126 cm (Re, T), J of Physiol 255:335-346, 1976) and either Luo-Rudy (L-R, Circ Res 68:1501-1526, 1991) or Beeler-Reuter (B-R, J Physiol 268:177-210, 1977) ionic currents. Related cable equations for active membrane are derived. Spatial segmentations of < 31.2 um (L, L-R), < 11.5 um (T, L-R), &lt ;44.7 um (L, B-R), and < 16.5 um (T, B-R) were required for < 1 % errors in the characteristic parameters of action potential. Similarly, spatial segmentations of < 54.5 um (L, L-R), <20.1 um (T, L-R), <84.3 um (L, B-R), and <31.2 um (T, B-R) were required for <1% errors in the velocity of conduction. Conclusion: In general, spatial segmentations of < 26.9% and <50.8% of the space constant of a fully activated membrane gave < 1.0% errors in the characteristic parameters of action potential and in the velocity of propagation, respectively, for both membranes. The action potential duration was relatively insensitive to the spatial segmentation. Our analysis suggests that [lamda]full is a better criterion for the selection of spatial segmentation in numerical simulation than the space constant of the resting membrane. [ABSTRACT FROM AUTHOR]

Introduction: Cytochalasin D In tissue bath superfusate inhibits the contraction of isolated thin trabeculae from canine right ventricle without affecting the intracellular action potential recorded with glass microelectrode. The purpose of this study was to test whether cytochalasin D could also be used to immobilize perfused wedges of ventricular muscle without affecting the action potential duration or propagation, and also to determine the optimal concentration and time duration of drug in the perfusate. Methods and Results: Using a membrane potential sensitive dye, di-4-ANEPPS, and a high-resolution photodiode optical mapping system at a rate of 1,000 frames/sec, we recorded action potentials on the transmural surface of arterially perfused wedges of muscle from the canine left ventricular free wall. We also recorded arterial pulse pressure as a surrogate for tissue contraction. Cytochalasin D at >= 20 [mu] mol/L in the perfusate for >= 6 minutes reduced the arterial pulse pressure to approximately one tenth of its initial value and significantly reduced or eliminated motion artifacts in the action potentials. A sustained concentration of 10 [mu]mol/L cytocbalasin D in the perfusate prevented contraction from recurring after the tissue was immobilized with an initial concentration of 25 [mu]mol/L. Cytochalasin D had little effect on the action potential duration and on its transmural gradient, and did not slow the transmural velocity of excitation propagation. Conclusion: Cytochalasin D can be used to uncouple excitation and contraction in perfused canine cardiac muscle for the fluorescent-optical mapping of action potentials without affecting action potential duration or slowing transmural propagation. [ABSTRACT FROM AUTHOR]

Atrial fibrillation is the most common sustained tachyarrhythmia and, as such, has become the recent focus of intense clinical and experimental interest. Because of its associated morbidity and mortality, there is a multidisciplinary effort to understand the pathophysiology that may ultimately lead to improved therapeutic options. This review concentrates on three aspects of atrial fibrillation that influence contemporary choices for treatment: an electrophysiologic basis for initiation of atrial fibrillation, anatomic and electrophysiologic remodeling, and concepts regarding its termination or prevention. [ABSTRACT FROM AUTHOR]

Atrioventricular dissociation during paroxysmal junctional tachycardia. We describe the rare occurrence of atrioventricular dissociation in three patients during paroxysmal junctional tachycardia. The mechanism of tachycardia was atrioventricular nodal reentry in two patients. The third patient had reentrant tachycardia that utilized the AV node for at least port of the reentrant circuit. This patient also had a nodoventricular pathway that may have participated in the reentrant circuit. In two patients, ventricular tachycardia was diagnosed prior to electrophysiologic assessment and medication to prevent tachycardia was not successful. After electrophysiological studies, treatment directed at suppressing AV nodal reentry prevented recurrent tachycardia. These case studies demonstrate the importance of detailed electrophysiological assessment of tachycardia in patients whose arrhythmia clues not respond to empirical antiarrhythmic therapy. [ABSTRACT FROM AUTHOR]

Background: Whether vigorous exercise increases risk of ventricular arrhythmias for individuals diagnosed and treated for congenital long QT syndrome (LQTS) remains unknown., Methods: The National Institutes of Health-funded LIVE-LQTS study (Lifestyle and Exercise in the Long QT Syndrome) prospectively enrolled individuals 8 to 60 years of age with phenotypic and/or genotypic LQTS from 37 sites in 5 countries from May 2015 to February 2019. Participants (or parents) answered physical activity and clinical events surveys every 6 months for 3 years with follow-up completed in February 2022. Vigorous exercise was defined as ≥6 metabolic equivalents for >60 hours per year. A blinded Clinical Events Committee adjudicated the composite end point of sudden death, sudden cardiac arrest, ventricular arrhythmia treated by an implantable cardioverter defibrillator, and likely arrhythmic syncope. A National Death Index search ascertained vital status for those with incomplete follow-up. A noninferiority hypothesis (boundary of 1.5) between vigorous exercisers and others was tested with multivariable Cox regression analysis., Results: Among the 1413 participants (13% <18 years of age, 35% 18-25 years of age, 67% female, 25% with implantable cardioverter defibrillators, 90% genotype positive, 49% with LQT1, 91% were treated with beta-blockers, left cardiac sympathetic denervation, and/or implantable cardioverter defibrillator), 52% participated in vigorous exercise (55% of these competitively). Thirty-seven individuals experienced the composite end point (including one sudden cardiac arrest and one sudden death in the nonvigorous group, one sudden cardiac arrest in the vigorous group) with overall event rates at 3 years of 2.6% in the vigorous and 2.7% in the nonvigorous exercise groups. The unadjusted hazard ratio for experience of events for the vigorous group compared with the nonvigorous group was 0.97 (90% CI, 0.57-1.67), with an adjusted hazard ratio of 1.17 (90% CI, 0.67-2.04). The upper 95% one-sided confidence level extended beyond the 1.5 boundary. Neither vigorous or nonvigorous exercise was found to be superior in any group or subgroup., Conclusions: Among individuals diagnosed with phenotypic and/or genotypic LQTS who were risk assessed and treated in experienced centers, LQTS-associated cardiac event rates were low and similar between those exercising vigorously and those not exercising vigorously. Consistent with the low event rate, CIs are wide, and noninferiority was not demonstrated. These data further inform shared decision-making discussions between patient and physician about exercise and competitive sports participation., Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02549664., Competing Interests: Dr Lampert reports honoraria and research support from Medtronic, Abbott-St. Jude, and Boston Scientific, as well as serving on the Advisory Board for Medtronic. Dr Day received consulting and grant funding from Lexicon Pharmaceuticals, grant funding from Bristol Myers Squibb, and DMC from Cytokinetics. L. Salberg consulted for Biomarin. Dr Tome Esteban consulted for BMS and Cytokinetics. Dr Abrams served on the Scientific Advisory Board for Thryv Therapeutics and consulted for Rocket Pharmaceuticals. Dr Aziz served on the Medtronic Advisory Committee. Dr Behr consulted for Boston Scientific. Dr Berul received research funding from Medtronic. Dr Cerrone provided teaching and CME activities for Abbott and Medtronic. Dr Erickson received funding from Integer. Dr Estes reports consulting for Boston Scientific and Medtronic. Dr Ethridge reports funding from Spauling Research (ECG reading) and UpToDate. Dr James was a consultant for Pfizer and Lexeo Therapeutics and received research funding from Lexeo Therapeutics and StrideBio. Dr Law was a consultant for Medtronic and St. Jude and a speaker for Boston Scientific. Dr Olshansky, AstraZeneca DSMB (Data Safety Monitoring Board). Dr Noseworthy and Mayo Clinic have filed patents related to the application of artificial intelligence to the ECG for diagnosis and risk stratification and have licensed several A-ECG algorithms to Anumana. Dr Noseworthy and Mayo Clinic have a relationship with AliveCor related to the measurement of the QT interval on the Kardia device. Dr Shah was a consultant for Medtronic and Tenaya. Dr Ware received research support and/or consultancy fees from MyoKardia, Bristol Myers Squibb, Foresite Labs, Pfizer, and Health Lumen. Dr Ware is supported by Medical Research Council (UK), British Heart Foundation (RE/18/4/34215), and the NIHR Imperial College Biomedical Research Centre. Dr Ackerman has served as a consultant for Abbott, BioMarin Pharmaceuticals, Boston Scientific, Bristol Myers Squibb, Daiichi-Sankyo, Illumina, Invitae, Medtronic, Tenaya Therapeutics, and UpToDate. Dr Ackerman and Mayo Clinic are involved in an equity/royalty relationship with AliveCor, Anumana, ARMGO Pharma, Pfizer, and Thryv Therapeutics. The other authors report no conflicts.

Competing Interests: Disclosures The author has no conflicts of interest to disclose. This article was selected by the Editor before Dr Zipes was asked to be the Section Editor of this series.

Importance: Whether vigorous intensity exercise is associated with an increase in risk of ventricular arrhythmias in individuals with hypertrophic cardiomyopathy (HCM) is unknown., Objective: To determine whether engagement in vigorous exercise is associated with increased risk for ventricular arrhythmias and/or mortality in individuals with HCM. The a priori hypothesis was that participants engaging in vigorous activity were not more likely to have an arrhythmic event or die than those who reported nonvigorous activity., Design, Setting, and Participants: This was an investigator-initiated, prospective cohort study. Participants were enrolled from May 18, 2015, to April 25, 2019, with completion in February 28, 2022. Participants were categorized according to self-reported levels of physical activity: sedentary, moderate, or vigorous-intensity exercise. This was a multicenter, observational registry with recruitment at 42 high-volume HCM centers in the US and internationally; patients could also self-enroll through the central site. Individuals aged 8 to 60 years diagnosed with HCM or genotype positive without left ventricular hypertrophy (phenotype negative) without conditions precluding exercise were enrolled., Exposures: Amount and intensity of physical activity., Main Outcomes and Measures: The primary prespecified composite end point included death, resuscitated sudden cardiac arrest, arrhythmic syncope, and appropriate shock from an implantable cardioverter defibrillator. All outcome events were adjudicated by an events committee blinded to the patient's exercise category., Results: Among the 1660 total participants (mean [SD] age, 39 [15] years; 996 male [60%]), 252 (15%) were classified as sedentary, and 709 (43%) participated in moderate exercise. Among the 699 individuals (42%) who participated in vigorous-intensity exercise, 259 (37%) participated competitively. A total of 77 individuals (4.6%) reached the composite end point. These individuals included 44 (4.6%) of those classified as nonvigorous and 33 (4.7%) of those classified as vigorous, with corresponding rates of 15.3 and 15.9 per 1000 person-years, respectively. In multivariate Cox regression analysis of the primary composite end point, individuals engaging in vigorous exercise did not experience a higher rate of events compared with the nonvigorous group with an adjusted hazard ratio of 1.01. The upper 95% 1-sided confidence level was 1.48, which was below the prespecified boundary of 1.5 for noninferiority., Conclusions and Relevance: Results of this cohort study suggest that among individuals with HCM or those who are genotype positive/phenotype negative and are treated in experienced centers, those exercising vigorously did not experience a higher rate of death or life-threatening arrhythmias than those exercising moderately or those who were sedentary. These data may inform discussion between the patient and their expert clinician around exercise participation.

Catheter ablation is an established treatment option for atrial fibrillation (AF), and pulmonary vein isolation (PVI) has become the gold standard in AF ablation. AF recurrence after PVI remains an important clinical problem. Recovery of conduction from the pulmonary veins (PVs) is considered the dominant mechanism for AF recurrence in paroxysmal AF. However, the underlying mechanism of AF recurrence after PVI is more complex in patients with persistent and longstanding persistent AF. Different ablation technologies and energy sources have been developed aimed at improving lesion quality and durability with an acceptable safety profile. Novel technologies are under evaluation which have a great potential to produce permanent PVI after a single ablation procedure. However, clinical value of these novel devices needs to be tested in adequately powered randomized controlled trials. In this article, we review the history of catheter ablation for AF and discuss the present and future ablation technologies.

Importance: The US Department of Justice (DOJ) conducted an investigation into implantable cardioverter-defibrillators (ICDs) not meeting the Centers for Medicare & Medicaid Services National Coverage Determination (NCD) criteria., Objective: To examine changes in the proportion of initial primary prevention ICDs that did not meet NCD criteria following the announcement of the DOJ investigation at hospitals that reached settlements (settlement hospitals) and those that did not (nonsettlement hospitals)., Design, Setting, and Participants: Multicenter, longitudinal, serial cross-sectional analysis of 300 151 initial primary prevention ICDs among Medicare beneficiaries from January 1, 2007, through December 31, 2015, at 1809 US hospitals in the National Cardiovascular Data Registry (NCDR) ICD Registry, of which 452 hospitals (with 99 591 primary prevention ICDs) reached settlements with the DOJ., Exposures: The DOJ investigation announcement in 2010., Main Outcomes and Measures: Proportion of initial primary prevention ICDs not meeting NCD criteria., Results: In January 2007, the proportion of initial ICDs not meeting NCD criteria was 25.8% (95% CI, 24.7% to 26.8%) at settlement hospitals and 22.8% (95% CI, 22.1% to 23.5%) at nonsettlement hospitals (P < .001). Over the study period, there was a 62.7% (95% CI, 59.2% to 66.1%) relative decrease and 16.1% (95% CI, 14.8% to 17.5%) absolute decrease in the proportion of ICDs not meeting NCD criteria at settlement hospitals compared with a 53.2% (95% CI, 50.4% to 56.0%) relative decrease and 12.1% (95% CI, 11.2% to 13.0%) absolute decrease in proportion at nonsettlement hospitals (P < .001 for both; P for interaction < .001). Trends significantly differed between hospital groups only in the period following the announcement of the DOJ investigation (January 2010-June 2011) [corrected], with larger and more rapid decreases at settlement hospitals (P for interaction = .01). Over the study period, there was a 32.8% (95% CI, 29.9% to 35.7%) relative decrease and a 1703 ICDs (95% CI, 1520 to 1886) absolute decrease in the volume of primary prevention ICDs implanted at settlement hospitals compared with a 17.4% (95% CI, 14.8% to 20.0%) relative decrease and a 1495 ICDs (95% CI, 1249 to 1741) absolute decrease in volume at nonsettlement hospitals (P < .001 for both; P for interaction < .001), with more modest decreases or slight increases in secondary prevention ICD volume. These patterns were similar when examining ICD utilization among non-Medicare beneficiaries., Conclusions and Relevance: From 2007 through 2015, the volume of primary prevention implantable cardioverter-defibrillators and the proportion of devices not meeting the Centers for Medicare & Medicaid Services National Coverage Determination criteria decreased at all hospitals with substantially larger decreases at hospitals that reached settlements in the US Department of Justice investigation. These patterns extended to implantable cardioverter-defibrillators placed in non-Medicare beneficiaries, which were not the focus of the US Department of Justice investigation.

Professional society recommendations to decrease sudden cardiac death in athletes, including eligibility requirements with disqualification for athletes with diagnosed disease as well as preparticipation screening and emergency preparedness, were updated in 2015. The update includes new sections on aortic disease, channelopathies, and sickle cell trait, as well as a change in format from the previous binary yes/no format to the more nuanced and contemporary "class and level of evidence" format. Eighty-four of the 246 recommendations now carry Class II designation-"reasonable," or "may be considered." New language in the document emphasizes counseling as part of the decision process. New data on athletes with implantable cardioverter-defibrillators, and on those with long QT syndrome, have led to a change from blanket restriction of competitive sports participation to a Class IIB "may be considered" recommendation.