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Infection with SARS-CoV-2, which causes COVID-19, is associated with adverse maternal outcomes. While it is known that severity of COVID-19 varies by viral strain, the extent to which this variation is reflected in adverse maternal outcomes, including nonpulmonary maternal outcomes, is not well characterized.To evaluate the associations of SARS-CoV-2 infection with severe maternal morbidities (SMM) in pregnant patients delivering during 4 pandemic periods characterized by predominant viral strains.This retrospective cohort study included patients delivering in a multicenter, geographically diverse US health system between March 2020 and January 2022. Individuals with SARS-CoV-2 infection were propensity-matched with as many as 4 individuals without evidence of infection based on demographic and clinical variables during 4 time periods based on the dominant strain of SARS-CoV-2: March to December 2020 (wild type); January to June 2021 (Alpha [B.1.1.7]); July to November 2021 (Delta [B.1.617.2]); and December 2021 to January 2022 (Omicron [B.1.1.529]). Data were analyzed from October 2021 to June 2022.Positive SARS-CoV-2 nucleic acid amplification test result during the delivery encounter.The primary outcome was any SMM event, as defined by the US Centers for Disease Control and Prevention, during hospitalization for delivery. Secondary outcomes were number of SMM, respiratory SMM, nonrespiratory SMM, and nontransfusion SMM events.Over all time periods, there were 3129 patients with SARS-CoV-2, with a median (IQR) age of 29.1 (24.6-33.2) years. They were propensity matched with a total of 12 504 patients without SARS-CoV-2, with a median (IQR) age of 29.2 (24.7-33.2) years. Patients with SARS-CoV-2 infection had significantly higher rates of SMM events than those without in all time periods, except during Omicron. While the risk of any SMM associated with SARS-CoV-2 infection was increased for the wild-type strain (odds ratio [OR], 2.74 [95% CI, 1.85-4.03]) and Alpha variant (OR, 2.57 [95% CI, 1.69-4.01]), the risk during the Delta period was higher (OR, 7.69 [95% CI, 5.19-11.54]; P for trend .001). The findings were similar for respiratory complications, nonrespiratory complications, and nontransfusion outcomes. For example, the risk of nonrespiratory SMM events for patients with vs without SARS-CoV-2 infection were similar for the wild-type strain (OR, 2.16 [95% CI, 1.40-3.27]) and Alpha variant (OR, 1.96 [95% CI, 1.20-3.12]), highest for the Delta variant (OR, 4.65 [95% CI, 2.97-7.29]), and not significantly higher in the Omicron period (OR, 1.21 [95% CI, 0.67-2.08]; P for trend .001).This cohort study found that the SARS-CoV-2 Delta variant was associated with higher rates of SMM events compared with other strains. Given the potential of new strains, these findings underscore the importance of preventive measures.

Eric S. Williams, MD, MACC, Chair Jonathan L. Halperin, MD, FACC, Co-Chair James A. Arrighi, MD, FACC Eric H. Awtry, MD, FACC Eric R. Bates, MD, FACC John E. Brush, Jr, MD, FACC Salvatore Costa, MD, FACC Lori Daniels, MD, MAS, FACC Akshay Desai, MD, FACC[‡][1] Douglas E. Drachman, MD

Background— Definitive diagnosis of bilateral bundle-branch delay/block may be made when catheter-induced right bundle-branch block (RBBB) develops in patients with baseline left bundle-branch (LBB) block. We hypothesized that a RBBB pattern with absent S waves in leads I and aVL will identify bilateral bundle-branch delay/block. Methods and Results— Fifty patients developing transient RBBB pattern in lead V1 during right heart catheterization were studied. Patients were grouped according to whether the baseline ECG demonstrated a normal QRS, left fascicular blocks, or LBB block pattern. The RBBB morphologies in each group were compared. The prevalence of bilateral bundle-branch delay/block pattern was examined in our hospital ECG database. All patients with baseline normal QRS complexes (n=30) or left fascicular blocks (4 anterior, 5 posterior) developed a typical RBBB pattern. Among the 11 patients with a baseline LBB block pattern, 7 developed an atypical RBBB pattern with absent S waves in leads I and aVL and the remaining 4 demonstrated a typical RBBB. The absence of S waves in leads I and aVL during RBBB was 100% specific and 64% sensitive for the presence of pre-existing LBB block. Among the consecutive 2253 hospitalized patients with RBBB, 34 (1.5%) had the bilateral bundle-branch delay/block pattern. Conclusions— An ECG pattern of RBBB in lead V1 with absent S wave in leads I and aVL indicates concomitant LBB delay. Pure RBBB and bifascicular blocks are associated with S waves in leads I and aVL.

More than 100,000 patients annually receive an implantable cardioverter-defibrillator (ICD) in the United States. Placement techniques for ICDs have evolved and become safer, and hospital length of stay has declined accordingly. Patients who receive an ICD electively now are routinely discharged the

Atrial fibrillation (AF) is an important and highly prevalent arrhythmia, which is associated with significantly increased morbidity and mortality, including a four- to five-fold increased risk for stroke,1,2 a two-fold increased risk for dementia,3,4 a three-fold risk for heart failure,2 a two-fold increased risk for myocardial infarction,5,6 and a 40–90% increased risk for overall mortality.2,7 The constantly increasing number of AF patients and recognition of increased morbidity, mortality, impaired quality of life, safety issues, and side effects of rhythm control strategies with antiarrhythmic drugs, and high healthcare costs associated with AF have spurred numerous investigations to develop more effective treatments for AF and its complications.8 Although AF treatment has been studied extensively, AF prevention has received relatively little attention, while it has paramount importance in the prevention of morbidity and mortality, and complications associated with arrhythmia and its treatment. Current evidence shows a clear association between the presence of modifiable risk factors and the risk of developing AF. By implementing AF risk reduction strategies aiming at risk factors such as obesity, hypertension, diabetes, and obstructive sleep ap-noea (OSA), which are interrelated, we impact upon the escalating incidence of AF in the population and ultimately decrease the healthcare burden of associated co-morbidities of AF. To address this issue, a Task Force was convened by the European Heart Rhythm Association and the European Association of Cardiovascular Prevention and Rehabilitation, endorsed by the Heart Rhythm Society and Asia-Pacific Heart Rhythm Society, with the remit to comprehensively review the published evidence available, to publish a joint consensus document on the prevention of AF, and to provide up-to-date consensus recommendations for use in clinical practice. In this document, our aim is to summarize the current evidence on the association of each modifiable risk factor with AF and the available data on the impact of possible interventions directed at these factors in preventing or reducing the burden of AF. While the evidence on AF prevention is still emerging, the topic is not fully covered in current guidelines and some aspects are still controversial. Therefore, there is a need to provide expert recommendations for professionals participating in the care of at-risk patients and populations, with respect to addressing risk factors and lifestyle modifications. Health economic considerations Atrial fibrillation is a costly disease, both in terms of direct, and indirect costs, the former being reported by cost of illness studies as per-patient annual costs in the range of US $2000–14200 in North America and of €450–3000 in Europe.9 In individuals with AF or at risk of developing AF, any effective preventive measure, intervention on modifiable risk factors or comorbidities, as well as any effective pharmacological or non-pharmacological treatment has the aim to reduce AF occurrence, thromboembolic events and stroke, morbidity and, possibly, mortality related to this arrhythmia. Apart from the clinical endpoints, achievement of these goals has economic significance, in terms of positive impact on direct and indirect costs and favourable cost–effectiveness at mid- or long-term, in the perspective of healthcare systems.10–12 In view of the epidemiological profile of AF and progressive aging of the population,13 an impressive increase of patients at risk of AF or affected by AF,14 also in an asymptomatic stage, is expected in the next decades, inducing a growing financial burden on healthcare systems, not only in Europe and North America, but also worldwide.15,16 In consideration of this emerging epidemiological threat due to AF, it is worth considering a paradigm shift, going beyond the conventional approach of primary prevention based on treatment of AF risk factors, but, instead, considering the potential for ‘primordial’ prevention, defined as prevention of the development of risk factors predisposing to AF in the first place.17 This approach, aimed at avoiding the emergence and penetration of risk factors into the population, has been proposed in general terms for the prevention of cardiovascular diseases17 and should imply combined efforts of policymakers, regulatory and social service agencies, providers, physicians, community leaders, and consumers, in an attempt to improve social and environmental conditions, as well as individual behaviours, in the pursuit of adopting healthy lifestyle choices.16 Since a substantial proportion of incident AF events can be attributable to elevated or borderline levels of risk factors for AF,18 this approach could be an effective way to reduce the financial burden linked to AF epidemiology. In terms of individual behaviour and adoption of a ‘healthy lifestyle’, it is worth considering that availability of full healthcare coverage (through health insurance or the healthcare system) may in some cases facilitate the unwanted risk of reducing, at an individual level, the motivation to adopt all the preventive measures that are advisable, in line with the complex concept of ‘moral hazard effect’.19 Patient education and patient empowerment are the correct strategies for avoiding this undesirable effect.

h i Sudden cardiac death due to ventricular arrhythmias in the setting of underlying disease remains a substantial problem both within the U.S. and worldwide. Nearly 300,000 individuals in the U.S. die suddenly each year. In many, the terminal event is the first manifestation of underlying cardiac disease, even though this is present in the majority of cases. It is estimated that only 30%–50% among those at risk for sudden cardiac death, meeting defined primary prevention guidelines for the implantation of an ICD, receive appropriate risk counseling and potentially life saving medical or device treatment. The substantially lower implant rates in women and minorities further underscore the disparities in ICD use within North America. The strongest evidence guiding clinical decision-making for these patients is based on the outcomes of large-scale, multi-center randomized clinical trials that examine the impact of drug and device therapy in patients with significant left ventricular (LV) dysfunction. The SCD-HeFT and ADIT II trials clearly demonstrated enhanced survival with device therapy in patients with either ischemic or non-ischemic disease and ventricular dysfunction indicated

Objectives The purpose of this study was to differentiate non–re-entrant junctional tachycardia (JT) and typical atrioventricular node re-entry tachycardia (AVNRT). Background JT may mimic AVNRT. Ablation of JT is associated with a lower success rate and a higher incidence of heart block. Electrophysiologic differentiation of these tachycardias is often difficult. Methods We hypothesized that JT can be distinguished from AVNRT based on specific responses to premature atrial complexes (PACs) delivered at different phases of the tachycardia cycle: when a PAC is timed to His refractoriness, any perturbation of the subsequent His indicates that anterograde slow pathway conduction is involved and confirms a diagnosis of AVNRT. A PAC that advances the His potential immediately after it without terminating tachycardia indicates that retrograde fast pathway is not essential for the circuit and confirms a diagnosis of JT. This protocol was tested in 39 patients with 44 tachycardias suggesting either JT or AVNRT based on a short ventriculo-atrial interval and apparent AV node dependence. Tachycardias were divided into 3 groups: clinically obvious AVNRT, clinically obvious JT, and clinically indeterminate rhythm. Results In the 26 cases of clinically obvious AVNRT, the sensitivity and specificity of the test were 61% and 100%, respectively. In the 9 cases of clinically obvious JT, the sensitivity and specificity were 100% and 100%, respectively. In the 9 cases of clinically indeterminate rhythm, the technique indicated AVNRT in 1 patient and JT in 7 patients, and the test was indeterminate in 1 patient. Conclusions The response to PACs during tachycardia can distinguish JT and AVNRT with 100% specificity in adult patients.

Introduction: Device recalls create problems for patients and physicians, for the risks associated with replacement may be greater than the device failure rate. In 2005, Medtronic, Guidant, and St. Jude had implantable cardioverter defibrillator (ICD) recalls on several of their devices. There were no national standards to guide physicians on the management of such patients. We report the reasons for and outcomes of ICD and pacemaker generator changes from our practice resulting from these advisories. Methods and Results: After an advisory was issued, the patients with an affected device were contacted, evaluated in the office by one of the electrophysiologists in our group, and a management plan was determined. Two hundred and twenty-two of 1,039 (Medtronic 273, Guidant 766) (21.4%) patients with advisory devices underwent device replacement. Nine minor complications occurred: hematoma managed conservatively (n = 6); local discomfort (n = 1); and incisional infections treated successfully with oral antibiotics (n = 2). Major complications occurred in nine patients (4.1%). Four atrial leads were damaged, two of which were repaired, one during the same procedure and the other at a later date. One patient required a reoperation to tighten a loose ventricular lead set screw. Hematoma requiring evacuation occurred in one patient, and pocket revision was necessary in two patients secondary to severe discomfort due to the positioning of the device in the pocket. One patient had a cerebrovascular accident preoperatively. There were no perioperative deaths or infections requiring system removal. Conclusion: Even with experienced operators complications can occur when replacing generators for a device recall. Careful risk assessment for each individual patient should be performed and efforts made to minimize generator changes.

DavidSlotwiner,MD, FHRS, FACC(Chair),Niraj Varma,MD,PhD, FRCP(Co-chair), JosephG.Akar,MD,PhD, George Annas, JD, MPH, Marianne Beardsall, MN/NP, CCDS, FHRS, Richard I. Fogel, MD, FHRS, Nestor O. Galizio, MD, Taya V. Glotzer, MD, FHRS, FACC, Robin A. Leahy, RN, BSN, CCDS, FHRS, Charles J. Love, MD, CCDS, FHRS, FACC, FAHA, Rhondalyn C. McLean, MD, Suneet Mittal, MD, FHRS, Loredana Morichelli, RN, MSN, Kristen K. Patton, MD, Merritt H. Raitt, MD, FHRS, Renato Pietro Ricci, MD, John Rickard, MD, MPH, Mark H. Schoenfeld, MD, CCDS, FHRS, FACC, FAHA, Gerald A. Serwer, MD, FHRS, FACC, Julie Shea, MS, RNCS, FHRS, CCDS, Paul Varosy, MD, FHRS, FACC, FAHA, Atul Verma, MD, FHRS, FRCPC, Cheuk-Man Yu, MD, FACC, FRCP, FRACP From the Hofstra School of Medicine, North Shore Long Island Jewish Health System, New Hyde Park, New York, Cleveland Clinic, Cleveland, Ohio, Yale University School of Medicine, New Haven, Connecticut, Boston University School of Public Health, Boston, Massachusetts, Southlake Regional Health Centre, Newmarket, Ontario, Canada, St. Vincent Medical Group, Indianapolis, Indiana, Favaloro Foundation University Hospital, Buenos Aires, Argentina, Hackensack University Medical Center, Hackensack, New Jersey, Sanger Heart & Vascular Institute, Carolinas HealthCare System, Charlotte, North Carolina, New York University Langone Medical Center, New York City, New York, University of Pennsylvania Health System, Philadelphia, Pennsylvania, The Arrhythmia Institute at Valley Hospital, New York, New York, Department of Cardiovascular Diseases, San Filippo Neri Hospital, Rome, Italy, University of Washington, Seattle, Washington, VA Portland Health Care System, Oregon Health & Science University, Knight Cardiovascular Institute, Portland, Oregon, Johns Hopkins University, Baltimore, Maryland, Yale University School of Medicine, Yale-New Haven Hospital Saint Raphael Campus, New Haven, Connecticut, University of Michigan Congenital Heart Center, University of Michigan Health Center, Ann Arbor, Michigan, Brigham and Women’s Hospital, Boston, Massachusetts, Veterans Affairs Eastern Colorado Health Care System, University of Colorado, Denver, Colorado, and Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.

Mechanism of Induction of Atrioventricular Node Reentry. Introduction: AV node reentry (AVNRT) is typically induced with anterograde (Ant) block over the fast pathway (FP) and conduction over the slow pathway (SP), with subsequent retrograde (Ret) conduction over the FP. Rarely, a premature atrial complex (PAC) conducts simultaneously over the FP and SP to induce AVNRT (2 for 1). This study investigates the mechanism of 2 for 1 induction. Methods and Results: Of 192 consecutive patients (pts) undergoing posteroseptal radiofrequency ablation to treat AVNRT, 4 pts (2%) had 2 for 1 AVNRT induction. All needed isoproterenol for AVNRT initiation, and Ant conduction was over the SP during AVNRT. Controls (n = 15) were randomly selected from the remaining 188 pts and required isoproterenol to induce AVNRT with Ant block over the FP. For 2 for 1 versus control, respectively, there was no difference in mean age (55 vs. 46 yr), AVNRT cycle length (420 vs. 320 ms), or the Ant effective refractory period of the FP (320 vs. 344 ms). Of note, the PAC that induced AVNRT had a significantly longer AH interval over the SP in pts with 2 for 1 versus control (470 vs. 320 ms, P = 0.016), even though the A1A2 interval for induction was longer for 2 for 1 (315 vs. 260 ms, P = 0.003). Ret conduction over the SP was relatively poor in the 2 for 1 group as evidenced by 4/4 pts with induction of AVNRT during incremental ventricular pacing versus only 1/15 control pts (P < 0.001). Conclusion: The unique induction of AVNRT by a PAC with simultaneous conduction over the FP and SP is best explained by minimal to no retrograde invasion of the SP from the anterogradely conducted fast pathway impulse, and consistent with this observation is the initiation of slow/fast AVN reentry during incremental RV pacing.

Introduction: Dofetilide is the newest drug approved by the United States Food and Drug Administration for the treatment of patients with atrial fibrillation (AF). Few data on the efficacy and safety of dofetilide in a diverse group of patients are available. The aim of this study was to evaluate the results of dofetilide in a consecutive series of 69 patients with AF. Methods and Results: Sixty-nine patients with persistent (n = 53) or paroxysmal (n = 16) AF were administered dofetilide in-hospital. Prior to starting dofetilide, all patients had been adequately anticoagulated, and concomitant agents contraindicated in the presence of dofetilide were discontinued. Heart rhythms were monitored continuously by telemetry in all patients. The initial dose, which was determined using the Cockroft-Gault calculated creatinine clearance, was 500 μg bid, 250 μg bid, and 125 μg bid in 51, 13, and 5 patients, respectively. Reductions in subsequent dosage occurred in 12 patients, 4 for QT prolongation. Dofetilide was discontinued in-hospital in 7 patients, 2 for adverse arrhythmic events and 3 for unacceptable QT prolongation. Twenty-seven (63%) of 43 patients in AF converted spontaneously to sinus rhythm. Fifty-eight patients were discharged receiving dofetilide treatment and were followed as outpatients for 21 ± 7 months. One third of patients continued to take dofetilide at 1 year. One patient had a cardiac arrest 1 day after hospital discharge. Conclusion: Dofetilide is a well-tolerated antiarrhythmic drug with a high conversion rate of AF to sinus rhythm. One third of patients maintained sinus rhythm at 1 year. Proarrhythmia can occur and initiation of therapy must be performed in-hospital. (J Cardiovasc Electrophysiol, Vol. 14, pp. S287-S290, December 2003, Suppl.)

ObjectivesThe aim of this study was to evaluate tecadenoson safety and efficacy during conversion of paroxysmal supraventricular tachycardia (PSVT) to sinus rhythm.BackgroundTecadenoson (CVT-510), a novel adenosine receptor (Ado R) agonist, selectively activates the A1Ado R and prolongs atrioventricular (AV) nodal conduction at doses lower than those required to cause A2Ado R-mediated coronary and peripheral vasodilation. Unlike adenosine, which non-selectively activates all four Ado R subtypes and produces unwanted effects, tecadenoson appears to terminate AV node-dependent supraventricular tachycardias without hypotension and bronchoconstriction.MethodsIn this open-label, multicenter, dose escalation study, tecadenoson was administered to 37 patients (AV node re-entrant tachycardia, n = 29; AV re-entrant tachycardia, n = 8) with inducible PSVT sustained for ≥1 min during an electrophysiology study. Seven regimens (0.3 to 15 μg/kg) of up to two identical tecadenoson intravenous bolus doses were administered.ResultsAfter the first or second bolus, PSVT converted to sustained sinus rhythm for ≥5 min in 86.5% (32/37) of the patients, with 91% (29/32) of the conversions occurring after the first bolus (most within 30 s), coincident with anterograde conduction block in the AV node. No effects on sinus cycle length (SCL) or systolic blood pressure were observed. The atrial-His (AH), but not the His-ventricular (HV) interval was prolonged up to 5 min after the final tecadenoson bolus, returning to baseline by 10 min. Tecadenoson was generally well tolerated.ConclusionsIn this study, tecadenoson rapidly terminated sustained PSVT by depressing AV nodal conduction without causing hypotension. After sinus rhythm restoration, there was minimal AH interval prolongation without HV interval or SCL prolongation.

The Heart Rhythm Society convened a research symposium on December 9–10, 2013, in Washington, DC, that focused on the prevention of atrial fibrillation (AF) as well as AF-related stroke and morbidity. Attendees sought to summarize advances in understanding AF since a 2008 National Institutes of Health (NIH) conference on this topic1 and to identify continued knowledge gaps and current research priorities. The research symposium also sought to identify key deficiencies and opportunities in research infrastructure, operations, and methodologies. The committee sought to identify both basic research targets and how clinical AF research could be improved in the current health care environment. This whitepaper summarizes our deliberations in an effort to accelerate progress toward preventing AF and its consequences. Although largely focused on primary prevention of AF, the paper also addresses some aspects of secondary prevention of recurrent AF due to the continuum of risk factors that contribute to arrhythmogenesis, permissive left atrial (LA) substrates, and the emergence of AF.

Patients electively receiving a primary prevention implantable cardioverter-defibrillator (ICD) are commonly observed overnight in the hospital; the prevalence, implementation, and associated outcomes of same-day discharge have not been characterized. Using data from the National Cardiovascular

OBJECTIVES The purpose of this study was to investigate whether clinical or electrophysiologic characteristics could predict initial and subsequent implantable cardioverter defibrillator (ICD) therapy. BACKGROUND Identification of markers to predict subsequent ICD therapy and symptoms after the first event could affect patient management. METHODS We analyzed baseline and follow-up data on 125 ICD patients followed for 408 ± 321 days. Medications and ICD programming were not changed after first ICD therapy. RESULTS Implantable cardioverter defibrillator therapy occurred in 58 patients (46%). Clinical features were as follows: mean left ventricular ejection fraction (LVEF) 29% ± 15%; coronary artery disease 84%; presenting arrhythmia with sustained monomorphic ventricular tachycardia (SMVT) in 68%. In a multivariate analysis the relative risk for ICD therapy in patients presenting with SMVT versus cardiac arrest (CA) was 2.57 (range, 1.32 to 5.01), and for patients with LVEF ≤25%, 1.95 (1.11 to 3.45), respectively (p CONCLUSIONS First ICD therapy tends to occur in patients presenting with SMVT and LVEF ≤25%. Subsequent therapy occurs sooner and is unpredictable, suggesting that antiarrhythmic drug therapy should be considered after the first symptomatic ICD therapy. Symptoms during first ICD therapy predict subsequent symptoms, and patients presenting with SMVT and asymptomatic first ICD therapy are at very low risk for future syncopal ICD therapy.

Sudden cardiac death continues to be a major health problem in the United States, accounting for ∼400,000 deaths per year. The last 10 yrs have seen major advances in the primary and secondary prevention of this problem. In patients who have survived an episode of cardiac arrest, the AVID study conclusively established the superiority of the implantable cardioverter defibrillator over empiric amiodarone. For patients with recurrent hemodynamically destabilizing ventricular tachycardia and ventricular fibrillation, intravenous amiodarone has emerged as a potent therapeutic agent, especially when other agents such as lidocaine and procainamide have not been effective. Finally, recent work has focused on the risk stratification of patients for sudden cardiac death. Both the MADIT and MUSTT studies suggest that patients with coronary artery disease, reduced ejection fraction, and nonsustained ventricular tachycardia who are inducible to a sustained ventricular arrhythmia at electrophysiology testing have improved survival with an implantable cardioverter defibrillator. (Crit Care Med 2000; 28[Suppl.]:N165–N169)

Background Intravenous amiodarone is effective for the acute suppression of recurrent hemodynamically destabilizing ventricular arrhythmias. There are no follow-up data on patients undergoing long-term therapy with intravenous amiodarone. The objective of this investigation was to evaluate long-term outcome. Methods and Results We reviewed the clinical courses of 245 patients given intravenous amiodarone for sustained ventricular tachyarrhythmias. Of the 107 survivors (84% men; mean age 64 years) released from the hospital taking oral amiodarone, 41 were discharged with an empiric prescription for oral amiodarone. For 64 patients a decision regarding further therapy was based on results of an electrophysiologic study. Two patients were treated empirically with oral amiodarone and an implantable cardioverter defibrillator. Clinical variables and survival curves were the same for the empirically treated group and the group whose treatment was based on electrophysiologic findings ( P = .89). Survival at 6, 12, and 18 months was 88%, 81% and 71%, respectively, for empirically treated patients, and 83%, 80% and 73%, respectively, for patients whose therapy was directed with an electrophysiologic study. Of the 64 patients who underwent electrophysiologic studies, 33 received an implantable cardioverter defibrillator. The Kaplan-Meier survival curves for patients with and patients without an implantable cardioverter defibrillator were similar ( P = .46). Conclusions Patients for whom recurrent ventricular tachycardia and fibrillation are suppressed with intravenous amiodarone and who are discharged receiving oral amiodarone have an 80% 1-year survival rate. Although not randomized, our data suggested that among such patients, electrophysiologic testing, implantation of a cardioverter defibrillator, or both may not be necessary. Ascertaining the best management strategy for these patients will require a prospective randomized trial.

OBJECTIVES To assess the clinical significance of inducible ventricular tachyarrhythmias among patients with unexplained syncope. BACKGROUND Induction of sustained ventricular arrhythmias at electrophysiology study in patients with unexplained syncope and structural heart disease is usually assigned diagnostic significance. However, the true frequency of subsequent spontaneous ventricular tachyarrhythmias in the absence of antiarrhythmic medications is unknown. METHODS In a retrospective case-control study, the incidence of implantable cardiac defibrillator (ICD) therapies for sustained ventricular arrhythmias among patients with unexplained syncope or near syncope (syncope group, n = 22) was compared with that of a control group of patients (n = 32) with clinically documented sustained ventricular tachycardia (VT). Sustained ventricular arrhythmias were inducible in both groups and neither group received antiarrhythmic medications. All ICDs had stored electrograms or RR intervals. Clinical variables were similar between groups except that congestive cardiac failure was more common in the syncope group. RESULTS Kaplan-Meier analysis of the time to first appropriate ICD therapy for syncope and control groups produced overlapping curves (p = 0.9), with 57 ± 11% and 50 ± 9%, respectively, receiving ICD therapy by one year. In both groups, the induced arrhythmia was significantly faster than spontaneous arrhythmias, but the cycle lengths of induced and spontaneous arrhythmias were positively correlated (R = 0.6, p CONCLUSIONS In patients with unexplained syncope, structural heart disease and inducible sustained ventricular arrhythmias, spontaneous sustained ventricular arrhythmias occur commonly and at a similar rate to patients with documented sustained VT. Thus, electrophysiologic testing in unexplained syncope can identify those at risk of potentially life-threatening tachyarrhythmias, and aggressive treatment of these patients is warranted.

We evaluated the incidence and energy dependence of atrial fibrillation/flutter (AF) induced by implantable ventricular defibrillator shocks in 63 patients tested in the operating room or electrophysiology laboratory.Defibrillator shocks were epicardial monophasic in 32 patients, and through an Endotak lead endocardial monophasic in 19 and biphasic in 12 patients. The epicardial and endocardial patient groups had similar clinical characteristics. A total of 517 defibrillator shocks were given. The epicardial group received 336 total defibrillator shocks and 10 +/- 6 shocks (mean +/- SD) per patient compared with the endocardial group, which received 181 total shocks and 6 +/- 4 defibrillator shocks per patient (P = 0.004). In the epicardial group, AF occurred in 13 (41%) patients and in 17 (5%) of the 336 shocks. No AF was induced with endocardial defibrillator shocks. The epicardial mean energy was 16 +/- 9 J, lower than the endocardial mean energy of 20 +/- 9 J (P0.004). In the epicardial monophasic group, energy correlated with AF induction. Each patient received 7 +/- 6 defibrillator shocks15 J and 4 +/- 2 shocksor = 15 J, yet AF occurred in only 2.3% versus 9.6% (P0.05) of defibrillator shocks15 J andor = 15 J, respectively. Of note, AF was not induced with energy4 J or31 J.In the epicardial configuration, AF induction is energy dependent, with an apparent lower and upper limit of vulnerability. AF induction by defibrillator shocks delivered through an Endotak lead is very rare, possibly related to an apparent upper limit of vulnerability of less energy, avoidance of thoracotomy, or different energy field distribution.

Recently, the American College of Cardiology Foundation in collaboration with the Heart Rhythm Society published appropriate use criteria (AUC) for implantable cardioverter-defibrillators and cardiac resynchronization therapy. These criteria were developed to critically review clinical situations that may warrant implantation of an implantable cardioverter-defibrillator or cardiac resynchronization therapy device, and were based on a synthesis of practice guidelines and practical experience from a diverse group of clinicians. When the AUC was drafted, the writing committee recognized that some of the scenarios that were deemed "appropriate" or "may be appropriate" were discordant with the clinical requirements of many payers, including the Medicare National Coverage Determination (NCD). To charge Medicare for a procedure that is not covered by the NCD may be construed as fraud. Discordance between the guidelines, the AUC, and the NCD places clinicians in the difficult dilemma of trying to do the "right thing" for their patients, while recognizing that the "right thing" may not be covered by the payer or insurer. This commentary addresses these issues. Options for reconciling this disconnect are discussed, and recommendations to help clinicians provide the best care for their patients are offered.

Background— Although cardiac resynchronization therapy (CRT) can improve left ventricular ejection fraction (LVEF), it is not known whether a specific level of improvement will predict future implantable cardioverter defibrillator (ICD) therapy. Methods and Results— CRT-defibrillator (CRT-D) was implanted in 423 patients at 1 institution between October 2, 2001 and January 19, 2007. A retrospective analysis was performed to evaluate the relationship between post–CRT-D LVEF and ICD therapy for ventricular tachyarrhythmias. A landmark population of 270 patients, with post–CRT-D LVEF measured and no ICD therapy within 1 year of device implantation, was followed for subsequent outcomes. Of these, 22 patients (8.2%) had subsequent appropriate ICD therapy over a median follow-up of 1.5 years. The estimated 2-year risk of appropriate ICD therapy is 3.0% (95% confidence interval [95% CI], 0%–6.3%), 2.1% (95% CI, 0%–5.0%), and 1.5% (95% CI, 0%–3.9%) for post–CRT-D LVEF of 45%, 50%, and 55%, respectively. In patients with a primary prevention indication for CRT-D, the estimated 2-year risk is 3.3% (95% CI, 0%–7.3%), 2.5% (95% CI, 0%–6.1%), and 1.9% (95% CI, 0%–5.1%) for post–CRT-D LVEF of 45%, 50%, and 55%, respectively. Conclusions— When a CRT responder demonstrates near normalization in LVEF to ≥45%, the incidence of ICD therapy for ventricular arrhythmias becomes low. Future studies are needed to determine whether an ICD is still needed in some of these patients at the time of generator replacement.

There are several methods available for the evaluation of patients with ventricular arrhythmia. The most effective approaches, however, involve the use of techniques that provide objective data. These include ambulatory monitoring and exercise testing (a noninvasive approach), and electrophysiologic testing (invasive). The information derived from these two approaches is complementary, and both are important for patient evaluation and management. These methods are useful for establishing the risk of arrhythmia occurrence in certain patient groups and for establishing the effect of antiarrhythmic agents. The signal-averaged ECG is of help in establishing risk in some patient groups, but it has no role for evaluating drug therapy.

Background: A properly placed stimulus on the T-wave during ventricular repolarization can result in ventricular fibrillation (VF). Initiation of VF with pacing on T-wave is a rare event with a few reported cases in the literature. We present a unique case of induced VF attributed to a pacing stimulus on T-wave during ventricular pacing threshold testing of a permanent pacemaker. Case Report: A 64-year-old woman with persistent atrial fibrillation (AF) and a permanent pacemaker for tachycardia–bradycardia syndrome presented with symptomatic AF with rapid ventricular response. Acute rate control was achieved with intravenous diltiazem. During ventricular pacing threshold testing, noncapture occurred followed by a pacing spike on T-wave initiating VF. Cardiopulmonary resuscitation and defibrillation converted the rhythm to rate-controlled AF. An acute prolongation of the QT was noted and normalized within 12 hours. No antiarrhythmic medications were used. Postevent laboratory values were within normal limits. She was free of ischemia and an echocardiogram revealed normal left ventricular function. She recovered from the event and was discharged with rate-controlled AF. No further pacing-induced arrhythmias have occurred during follow-up pacemaker interrogation and 12-lead electrocardiograms continued to show normal QT intervals. Conclusion: Pacemaker-induced VF is an extraordinarily rare complication of cardiac pacing. Alterations in ventricular repolarization with rapid slowing of the heart rate demonstrated by acute prolongation of QT intervals may play a role. This report should alert physicians to the possibility of QT prolongation and an increased risk of ventricular arrhythmias following acute rate control of AF.

Importance Atrial fibrillation is a common arrhythmia that affects more than 2.5 million people in the United States and causes substantial morbidity and mortality, especially regarding the increased risk of stroke. Objective To summarize atrial fibrillation treatment exclusive of stroke prevention. Evidence Review An Ovid MEDLINE comprehensive literature search was performed on atrial fibrillation therapy excluding anticoagulation and emphasizing studies published within the last 5 years through April 2015 (N = 5044 references). The 2014 atrial fibrillation guideline from the American Heart Association, the American College of Cardiology, and the Heart Rhythm Society also was reviewed. Findings Reversible causes of atrial fibrillation should be identified. Risk factor modification, including weight loss and treatment of hypertension, diabetes, and obstructive sleep apnea can reduce atrial fibrillation episodes. Appropriate anticoagulation is necessary for patients at substantial stroke risk regardless of rate or rhythm treatment strategy. Sinus rhythm is often needed to control symptoms; however, an alternative strategy for atrial fibrillation is appropriate rate control. Rate control is safe in older patients (those who are about age ≥65 years) followed up for a few years, but no such safety data exist for patients younger than 60 years or for those followed up for longer periods. Thus, selection of therapy is individualized, taking into account present and future medical problems for the patient. Choice of an antiarrhythmic drug is based on safety first vs efficacy. Catheter ablation is an effective nonpharmacological alternative that is often, but not always, the second-line treatment. Reduction of the frequency and duration of atrial fibrillation episodes that result in a significant improvement in quality of life is a good marker of drug treatment success and complete elimination of atrial fibrillation is not required in many patients. Rate control is usually achieved with a β-blocker or non–dihydropyridine calcium channel blockers. It is important to assess adequate rate control during both rest and activity. If the ventricular rate goes uncontrolled for a prolonged period, tachycardia-mediated cardiomyopathy can occur. Conclusions and Relevance Therapy for atrial fibrillation includes prevention and modification of inciting causes and appropriate anticoagulation. Rate control is necessary for all patients. Maintenance of sinus rhythm with drugs or catheter ablation should be considered based on the individual needs of each patient.

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Patients with ICDs are commonly advised to quit industrial jobs because of concerns that strong electromagnetic fields operating in the industrial environment might interfere with ICD functions. This study was done to assess interactions between industrial equipment and ICDs, and to devise a simple low risk screening protocol. We studied 18 patients carrying nine different ICD models who were met at their workplace by a clinical technician and were asked to walk through their workplace and perform typical duties while sensing status was monitored by listening to the ICD's beeper. All devices were interrogated at the completion of testing. At follow-up, patients were contacted by phone and were asked about employment status and history of ICD discharges or syncope. One hundred eighty-four contacts with 114 types of industrial equipment in 13 different industrial facilities (including 31 contacts with arc welding machines) were monitored. Interference with ICD's function occurred in only one contact (0.5%), when ICD therapy was temporarily suspended while a worker was attaching a huge electromagnet to a crane. At follow-up 46.0 +/- 6.0 months after testing, 7 patients (41%) are still holding the same job, 7 have retired because of reasons unrelated to their ICD, and 3 patients were transferred to a nonindustrial job. None of the patients had either an ICD shock or syncope during work. The use of a simple screening procedure can safely identify sources of electromagnetic interference that may affect ICD operation, and can predict long-term safety of working in an industrial workplace for ICD patients.

Late Occurrence of Heart Block.Introduction: There are few data regarding the occurrence of delayed heart block at least 24 hours after radiofrequency catheter ablation (RFCA) of AV nodal reentry or posteroseptal accessory pathways (APs). We investigated the late occurrence of heart block in this population, the clinical outcome, and whether findings at electrophysiologic study could have predicted its development. Methods and Results: Two of 418 patients with AV nodal reentry undergoing RFCA using a posterior approach and 1 of 54 patients with RFCA of a posteroseptal AP developed late heart block. Anterograde and retrograde AV nodal conduction before and after RFCA were normal. Patients received 12, 15, and 32 RFCA lesions, respectively, using a mean maximum power of 44 W. The RFCA sites were the posterior septum for posteroseptal AP and the posterior and mid-septum for patients with AV nodal reentry, with no His electrogram ever recorded at the ablation site. During RFCA, junctional tachycardia occurred with 1:1 VA conduction in the patient with a posteroseptal AP, but occasional intermittent single retrograde blocked complexes were present in both patients with AV nodal reentry. No rapid junctional tachycardia or > 1 consecutive retrograde blocked complex was ever observed during RFCA. Persistent high-degree AV block with junctional escape developed 2 days after RFCA in the posteroseptal AP patient. A permanent pacemaker was implanted, and normal conduction was noted 16 days after RFCA. Both patients with AV nodal reentry complained of fatigue, mainly on exertion, 3 to 4 days after RFCA, and ECG-documented exercise-induced variable AV block was obtained. Because heart block resolved in our initial patient, a prolonged monitoring period was allowed. Symptoms disappeared at 13 and 8 days, and a follow-up treadmill test showed normal PR interval and no heart block. No recurrence of heart block has been seen in any of these three patients. Conclusion: Late unexpected heart block after RFCA of AV nodal reentry and posteroseptal AP is rare, often resolves uneventfully in 1 to 2 weeks, and no specific electrophysiologic findings predicted its occurrence. Prolonged clinical observation is preferable to immediate pacemaker implantation in such patients.

We prospectively investigated in 55 pts characteristics of successful radiofrequency ablation (RFA) sites to cure AVN reentry (AVNRT) using a thermistor tipped catheter system with a posterior (slow pathway) approach. RFA success (S) was ≤ 0:2 AVNRT echos after RFA; only 1 pt had AVNRT at follow-up. There were 166 RFA [55 S; 111 failure (F)], with 3 ± 3/pt. Local atrial electrogram morphology was-A (low to isoelectric to high frequency); B (low to high frequency); and C(≥ 2 high frequency components). Differences with S vs F, respectively. are: atrial amplitude (396 ± 181 vs 357 ± 205 μV P l 0.001); ventricular amp. (3.0 ± 1.6 vs 2.7 ± 1.6 mV, p l 0.001); time to onset of junctional tachycardia (JT) (2.1 ± 1.9 vs 4.6 ± 6.1 sec, p l 0.05); duration of JT 1146 ± 8.6 vs 11.6 ± 7.7 sec, p l 0.001); CL of JT(481 ± 92vs 511 ± 120 ms, p l 0.0011; and change in CL of JT during RFA (–34 ± 113 vs + 23 ± 128 ms, p l 0.03). Of note, continuous JT was more common at S sites (46% vs 21%), and JT occurred in:≤ 7.5 sec at all S sites. No differences between Svs F were in: power(46.8 ± 7.5 vs 44.5 ± 8.6 W); catheter tip temp. (52.6 ± 4.6 vs 49.3 ± 5.5°C); atrial electrogram duration (66 ± 20 vs 66 ± 19 ms); ortype of local atrial electrogram. We conclude: 1) Successful RFA to cure AVNRT more frequently occurs with rapid onset of continuous junctional tachycardia with a CL that shortens before termination and, 2) there is no specific local atrial electrogram morphology that predicts success.

Many advances in the treatment of congestive heart failure (CHF) have resulted in improved survival, and a growing number of such patients are being seen by physicians. Although several interventions have reduced the number of patients dying from progressive CHF, sudden cardiac death remains a frequent and important problem in this patient population. It is now well established that ventricular premature beats (VPBs) and complex ventricular arrhythmia, particularly nonsustained ventricular tachycardia (VT), are commonly observed in these patients. It has been proposed that spontaneous ventricular arrhythmia, which results from underlying electrical instability of the myocardium, is a marker of an abnormal substrate capable of generating and sustaining arrhythmia. Additionally, spontaneous arrhythmia may serve as a trigger activating the mechanisms responsible for a sustained ventricular tachyarrhythmia.

It has been recognized that antiarrhythmic agents, although intended to prevent or limit arrhythmia, may actually cause an unexpected and unpredictable worsening of arrhythmia.’ Reported risk factors for this complication include significantly reduced left ventricular function, congestive heart failure and history of sustained ventricular tachyarrhythmia.2 The results of the Cardiac Arrhythmia Suppression Trial (CAST)3 increased concerns about arrhythmia aggravation, because 2 widely used an&-rhythmic agents resulted in an increased mortality when administered to patients with a recent myocardial infarction and no overt congestive heart failure who had frequent but only single ventricular premature beats. In CAST, the increase in mortality was observed in all patient groups analyzed, but was especially significant in those with several previous infarctions and a subendocardial infarction. In these patients, the risk of arrhythmia aggravation was as high (risk ratio 3.4) as that observed in those with more severe disease, sub stantial left ventricular dysfunction and history of serious arrhythmia. Furthermore, the occurrence of proarrhythmia, previously reported to be an early complication with antiarrhythmic drugs, was observed throughout the entire follow-up period and was also a late event. Patients exhibited “late” proarrhythmia despite initial suppression of spontaneous ventricular arrhythmia during the titration phase of the study. It is likely that during follow-up, myocardial remodeling and healing altered the underlying substrate, affecting the action of these drugs. One proposed hypothesis is that these patients had ongoing myocardial ischemia that further modified the underlying myocardial substrate, and transiently converted a stable myocardium into 1 that was unstable and potentially arrhythmogenic, capable of generating and supporting a reentrant arrhythmia. In the case of ischemia, the presence of antiarrhythmic drugs may further enhance this potential and is perhaps more likely to result in arrhythmia aggravation. It has been observed that during acute coronary occlusion, there is spatial heterogeneity of blood flow between ischemic and nonischemic tissue. Several investigators proposed that this can even occur in a normal heart, but to a such smaller degree. Marcus et al4 studied the spatial distribution of left ventricular perfusion in 24 awake dogs using radiolabeled microspheres. At the conclusion of the infusion, the left ventricular myo

The importance of ventricular arrhythmia is based on its association with sudden death. In certain groups of patients, ventricular arrhythmia--primarily runs of nonsustained ventricular tachycardia (NSVT)--is associated with an increased risk for sudden death. Although this relationship has been most often reported in patients with recent myocardial infarction, it has also been recognized in patients with dilated cardiomyopathy, regardless of etiology. Therefore, ventricular arrhythmia is common in patients with CHF due to cardiomyopathy. A number of studies have reported that 70-95% of patients with cardiomyopathy and congestive heart failure (CHF) have frequent ventricular premature beats, and 40-80% will manifest runs of NSVT. Many factors are responsible for ventricular arrhythmia in such patients, including structural abnormalities, electrolyte imbalance, hemodynamic impairment, activation of neurohormonal mechanisms, and pharmacologic therapy. Many studies have reported a high yearly mortality in patients with cardiomyopathy and CHF; greater than 40% of deaths are sudden, most often the result of sustained ventricular tachyarrhythmia. Most studies have noted an association between presence (and frequency) of NSVT and risk of sudden cardiac death in these patients. Unfortunately, other techniques--such as the signal-averaged electrocardiogram and electrophysiologic testing--are not helpful in identifying the individual at risk. Although several drug interventions will reduce mortality from progressive CHF, these drugs have not been shown to reduce sudden death and, indeed, have a variable effect on ventricular arrhythmia. Although NSVT is a marker for increased risk for sudden death, it is uncertain if antiarrhythmic drugs will prevent this outcome. Antiarrhythmic drugs have not been shown to be effective for preventing sudden death, although there are as yet no well-controlled randomized trials. Several studies suggest that amiodarone and beta blockers are beneficial, but this requires confirmation. For patients who have been resuscitated following an episode of sudden death due to a sustained ventricular tachyarrhythmia, antiarrhythmic therapy guided by invasive and noninvasive techniques appears to reduce risk of recurrent arrhythmia. However, the response rate to antiarrhythmic agents is low and side effects are common in patients with CHF. Especially important is the increased risk of precipitating CHF and aggravating the arrhythmia being treated. For many such patients who have had serious ventricular tachyarrhythmia, the automatic implantable cardioverter defibrillator may prove a better option. Other drugs used for management of CHF reduce overall mortality, but not risk of sudden death.

Ventricular arrhythmia (VA) in structurally normal hearts can be broadly considered under non-life-threatening monomorphic and life-threatening polymorphic rhythms. Monomorphic VA is classified on the basis of site of origin in the heart, and the most common areas are the ventricular outflow tracts and left ventricular fascicles. The morphology of the QRS complexes on electrocardiogram is an excellent tool to identify the site of origin of the rhythm. Although these arrhythmias are common and generally carry an excellent prognosis, rare sudden death events have been reported. Very frequent ventricular ectopy may also result in a cardiomyopathy in a minority of patients. Suppression of VA may be achieved using calcium-channel blockers, beta-adrenergic blockers, and class I or III antiarrhythmic drugs. Radiofrequency ablation has emerged as an excellent option to eliminate these arrhythmias, although certain foci including aortic cusps and epicardium may be technically challenging. Polymorphic ventricular tachycardia (VT) is rare and generally occurs in patients with genetic ion channel disorders including long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, and short QT syndrome. Unlike monomorphic VT, these arrhythmic syndromes are associated with sudden death. While the cardiac gross morphology is normal, suggesting a structurally normal heart, abnormalities exist at the molecular level and predispose them to arrhythmias. Another fascinating area, idiopathic ventricular fibrillation and early repolarization syndrome, are undergoing research for a genetic basis.

Discrimination between long RP tachycardias can be difficult but is essential when ablative therapy is contemplated. After diagnosis by EP study, we administered adenosine (Ad) 12 mg to pts during atrial (AT, n = 24) or atypical AV node (ATYP, n = 7) tachycardia (tc). Tc cycle length (CL) and component intervals were measured before and after Ad. Ad caused termination (term) in all AT without prior AV node block. In tc without substantial CL variability, first change (δ) in Cl after Ad was located in either H-H or A-A intervals. For cycles between δ and term in atrium (a) or ventricle (v), presence of CL oscillation (Osc) and net change of A-A were assessed and intervals were examined for Pearson rlinear correlation patterns. 1. Before Ad age (y) sex (m, f) CL (ms) A-H (ms) H-A (ms) AT 43 ± 17 2, 22 425 ± 94 82 ± 52 332 ± 107 ATYP 38 ± 20 3, 4 387 ± 107 113 ± 70 289 ± 86 p: ns l0.005 ns ns ns 2. After Ad δ(kk)(A-A, H-H) Osc(kk)(n) term(kk)[0,5-6](a, v) δ to term(kk)(cycles) net ΔAA(kk)(ms) AT 17 0 15 10 14 3.9 ± 14 2 ± 29 ATYP 2 2 6 2 5 3.5 ± 1.7 25 ± 24 p: ns ns ns ns ns ns ns 3. A-Avs A-H A-Avs H-A (term a) (term v) (term a) (term v) No. of Correlations AT 6/10 2/14 4/10 13/14 with p l 0.05 for r ATYP 1/2 1/5 2/2 3/5 P(AT vs ATYP): ns ns ns ns AT pts were predominantly female. Othervvise, AT and ATYP were not separated by tc CL or intervals before Ad, or by dynamic relationships of intervals analysed by linear correlation. Thus, Ad is not a useful pharmacologic probe for differentiation of AT from ATYP when tc terminates without prior AVnode block.