Inappropriate noise detection in Tendril family pacing leads.

INTRODUCTION: Noise oversensing encountered in patients with Abbott Tendril leads in our hospital triggered an internal investigation. METHODS: We retrospectively analyzed patients with a Tendril lead model 1688, 1788, 1888, and 2088. Most leads were connected to Abbott generators. To exclude a primary generator issue as the cause of noise oversensing, we enrolled a cohort of patients in whom Medtronic CapSureFix leads model 4076 and 5076 were prospectively connected to similar Abbott generators. RESULTS: A total of 1063 Tendril leads were implanted in 869 patients. Noise was encountered in 66 leads (6.2%) during a follow-up of 3.9 years. Most affected leads had normal impedance and only a few of these patients were symptomatic. Reprogramming was attempted in 44 of 66 (67%), and reduced oversensing in 34 of 44 (77%) of these patients. Seventeen malfunctioning leads (1.5%) were replaced, including 16 of 66 (24%) of those with noise. Of the four leads with noise extracted and returned to the manufacturer, lead to device abrasion was identified in two and inner insulation breach in one. None of the 145 Medtronic CapSureFix leads connected to Abbott generators had noise during a follow-up of 3.6 years. CONCLUSION: Noise oversensing was relatively common in Tendril leads, but was not detected in Medtronic leads despite connecting to Abbott generators. Although the majority of the affected leads did not show abnormal impedance, outer or inner insulation breach was identified in three of the four returned leads. As patients with affected leads are generally asymptomatic, most of them can be managed conservatively.

Spontaneous scar-based reentrant atrial flutter: Electrophysiologic characteristics and ablation outcome in a retrospective analysis.

BACKGROUND: The understanding of spontaneous scar-based reentrant atrial arrhythmia is limited. We aim to characterize the electrophysiologic and mapping features of spontaneous scar-based atrial flutter (AFL) and outcomes of catheter ablation. METHODS: Consecutive patients with a diagnosis of AFL who underwent catheter ablation from January 2012 to June 2015 were screened. Scars were detected in 12 patients and were included in this study. All had negative coronary angiography. These patients were divided into right AFL (seven patients) and left AFL groups (five patients) based on electrophysiologic mappings. RESULTS: Compared to patients with right AFL, the size of right atrium (RA) was smaller and left atrium (LA) was larger in the left AFL group. The proportion of the scar area was 11.1 ± 11.7 % in the RA AFL group and 7.8 ± 2.8 % in the LA AFL group. The difference was significant (P = 0.001). The acute success rates of ablation were 85.7% and 100%, respectively, in patients with right and left AFL (P = 0.304). During the follow-up, expansion of the scar area was noted in three patients with recurrent right AFL. No scar expansion was noted in one patient with recurrent left AFL. In addition, three patients with right AFL required permanent pacemaker implantation for sinus node dysfunction, and no one required pacemaker in patients with left AFL. CONCLUSIONS: Spontaneous scar could serve as substrate for AFL in RA or LA. Compared to left AFL, there was a higher rate of recurrence and pacemaker implantation in patients with right AFL.

Bundle Branch Re-Entrant Ventricular Tachycardia: Novel Genetic Mechanisms in a Life-Threatening Arrhythmia.

OBJECTIVES: This study sought to investigate for an underlying genetic etiology in cases of apparent idiopathic bundle branch re-entrant ventricular tachycardia (BBRVT). BACKGROUND: BBRVT is a life-threatening arrhythmia occurring secondary to macro-re-entry within the His-Purkinje system. Although classically associated with dilated cardiomyopathy, BBRVT may also occur in the setting of isolated, unexplained conduction system disease. METHODS: Cases of BBRVT with normal biventricular size and function were recruited from 6 North American centers. Enrollment required a clinically documented wide complex tachycardia and BBRVT proven during invasive electrophysiology study. Study participants were screened for mutations within genes associated with cardiac conduction system disease. Pathogenicity of identified mutations was evaluated using in silico phylogenetic and physicochemical analyses and in vitro biophysical studies. RESULTS: Among 6 cases of idiopathic BBRVT, each presented with hemodynamic compromise and 2 suffered cardiac arrests requiring resuscitation. Putative culprit mutations were identified in 3 of 6 cases, including 2 in SCN5A (Ala1905Gly [novel] and c.4719C>T [splice site mutation]) and 1 in LMNA (Leu327Val [novel]). Biophysical analysis of mutant Ala1905Gly Nav1.5 channels in tsA201 cells revealed significantly reduced peak current density and positive shifts in the voltage-dependence of activation, consistent with a loss-of-function. The SCN5A c.4719C>T splice site mutation has previously been reported as disease-causing in 3 cases of Brugada syndrome, whereas the novel LMNA Leu327Val mutation was associated with a classic laminopathy phenotype. Following catheter ablation, BBRVT was noninducible in all cases and none experienced a clinical recurrence during follow-up. CONCLUSIONS: Our investigation into apparent idiopathic BBRVT has identified the first genetic culprits for this life-threatening arrhythmia, providing further insight into its underlying pathophysiology and emphasizing a potential role for genetic testing in this condition. Our findings also highlight BBRVT as a novel genetic etiology of unexplained sudden cardiac death that can be cured with catheter ablation.

Management of functional Sprint Fidelis leads at cardiac resynchronization therapy-defibrillator generator replacement: a novel option for preventing inappropriate shocks from lead failure in fragile patients with high risk of sudden death.

AIMS: In patients with a functional Sprint Fidelis lead at generator replacement, the manufacturer recommended to either continue to use the existing lead or replace it with a new lead. For those patients who continue to use a functional Fidelis lead, the risk of inappropriate shocks remains present if the lead fails in the future. We evaluated the feasibility of an alternative approach at the time of cardiac resynchronization therapy-defibrillator (CRT-D) generator replacement in patients with a functional bipolar left ventricular (LV) lead for prevention of inappropriate shocks from future Fidelis lead failure. METHODS AND RESULTS: During the procedure, the pace/sense IS-1 connection pin of the functional Fidelis lead was intentionally inserted into the LV port of the new CRT-D generator, while the existing bipolar LV lead IS-1 connection pin was inserted into the right ventricular (RV) pace/sense port. After such switching, the existing bipolar LV lead was used for functional LV pacing/sensing, while the Fidelis lead was used for functional RV pacing and high voltage shock only and could no longer be used for the purpose of sensing and detecting. This approach precluded oversensing and inappropriate shocks should the functional Fidelis lead fail in the future. Six fragile patients, who were not considered suitable candidates for lead replacement, underwent the alternative approach. During a follow-up of 35 ± 23 months, the CRT-D system functioned normally in five patients. The Fidelis lead fractured in one patient 7 months after generator replacement. The malfunction was detected promptly and the defected lead was replaced. No inappropriate detections or shock was triggered. CONCLUSIONS: In CRT-D patients with a functional Fidelis lead and a bipolar LV lead, switching of the Fidelis lead pace/sense IS-1 pin with the bipolar LV lead IS-1 pin at generator replacement did not affect normal system function. This novel approach may be valuable in fragile patients with high risk of sudden death for prevention of inappropriate shocks triggered by oversensing from a malfunctioning Fidelis lead.

Normalization of Left Ventricular Ejection Fraction and Incidence of Appropriate Antitachycardia Therapy in Patients With Implantable Cardioverter Defibrillator for Primary Prevention of Sudden Death.

BACKGROUND: Patients with severely depressed left ventricular ejection fractions (LVEFs) receive implantable cardioverter-defibrillators (ICDs) for the primary prevention of sudden death. In some patients, however, LVEF may improve or even normalize over time. Limited data are available on the incidence of appropriate antitachycardia therapy, including pacing and shock, in these patients. METHODS AND RESULTS: We retrospectively identified consecutive patients at our institution with an ICD for primary prevention who had LVEF measurement available at initial implantation and at the time of generator replacement. None of these patients had ever received appropriate antitachycardia therapy before generator replacement. The incidence of appropriate antitachycardia therapy after generator replacement was assessed. Of the 125 patients who received generator replacement, 53 (42%) received an ICD and 72 (58%) a cardiac resynchronization therapy-defibrillator (CRT-D). Among them, 30 (21%) had LVEF normalized to ≥50%, 25 (17%) had LVEF partially improved to 36%-49%, and 70 (63%) had LVEF that remained depressed at ≤35%. During an overall follow-up period of 25 ± 18 months, none of the individuals with normalized LVEF experienced appropriate antitachycardia therapy regardless of ICD or CRT-D. Meanwhile, 20% of patients with LVEF at 36%-49% and 14% of patients with LVEF at ≤35% received appropriate ICD therapy. The omnibus P value for any differences among the 3 LVEF groups was 0.046 for the entire cohort, 0.01 for ICD, and 0.15 for CRT-D patients. CONCLUSIONS: These preliminary data suggest that patients with reduced LVEF and primary-prevention ICDs who normalize their LVEF over time may be at lower risk of appropriate antitachycardia therapy.

Atrial flutter with 1:1 conduction in undiagnosed Wolff-Parkinson-White syndrome.

BACKGROUND: Atrial flutter with 1:1 atrioventricular conduction via an accessory pathway is an uncommon presentation of Wolff-Parkinson-White syndrome not previously reported in the emergency medicine literature. Wolff-Parkinson-White syndrome, a form of ventricular preexcitation sometimes initially seen and diagnosed in the emergency department (ED), can present with varied tachydysrhythmias for which certain treatments are contraindicated. For instance, atrial fibrillation with preexcited conduction needs specific consideration of medication choice to avoid potential degeneration into ventricular fibrillation. CASE REPORT: We describe an adult female presenting with a very rapid, regular wide complex tachycardia successfully cardioverted in the ED followed by a normal electrocardiogram (ECG). Electrophysiology study confirmed atrial flutter with 1:1 conduction and revealed an accessory pathway consistent with Wolff-Parkinson-White syndrome, despite lack of ECG findings of preexcitation during sinus rhythm. Why should an emergency physician be aware of this? Ventricular tachycardia must be the first consideration in patients with regular wide complex tachycardia. However, clinicians should consider atrial flutter with 1:1 conduction related to an accessory pathway when treating patients with the triad of very rapid rate (>250 beats/min), wide QRS complex, and regular rhythm, especially when considering pharmacologic treatment. Emergency physicians also should be aware of electrocardiographically concealed accessory pathways, and that lack of delta waves does not rule out preexcitation syndromes such as Wolff-Parkinson-White syndrome.

Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation.

INTRODUCTION: The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. METHODS: Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. RESULTS: The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22-3.21; p = 0.03). CONCLUSION: Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents.

Continuing warfarin therapy is superior to interrupting warfarin with or without bridging anticoagulation therapy in patients undergoing pacemaker and defibrillator implantation.

BACKGROUND: Current guidelines recommend stopping oral anticoagulation and starting bridging anticoagulation with intravenous heparin or subcutaneous enoxaparin when implanting a pacemaker or defibrillator in patients at moderate or high risk for thromboembolic events. A limited body of literature suggests that device surgery without cessation of oral anticoagulation may be feasible. OBJECTIVE: The purpose of this study was to evaluate the safety of device surgery in orally anticoagulated patients without interrupting warfarin therapy. METHODS: We performed a retrospective study of 459 consecutive patients on chronic warfarin therapy who underwent device surgery from April 2004 to September 2008. Warfarin was continued in 222 patients during the perioperative period. Warfarin was temporarily held and bridging therapy administered in 123 patients. Warfarin was temporarily held without bridging therapy in 114 patients. RESULTS: There were no significant differences with regard to age, sex, or risk factors for thromboembolism in the three groups. Patients who continued taking warfarin had a lower incidence of pocket hematoma (P = .004) and a shorter hospital stay (P <.0001) than did patients in the bridging group. Holding warfarin without bridging is associated with a higher incidence of transient ischemic attacks (P = .01). CONCLUSION: Temporarily interrupting anticoagulation is associated with increased thromboembolic events, whereas cessation of warfarin with bridging anticoagulation is associated with a higher rate of pocket hematoma and a longer hospital stay. Continuing warfarin with a therapeutic international normalized ratio appears to be a safe and cost-effective approach when implanting a pacemaker or defibrillator in patients with moderate to high thromboembolic risk.

Predictors of appropriate therapy in patients with implantable cardioverter-defibrillator for primary prevention of sudden cardiac death.

The purpose of this study was to evaluate predictors of appropriate therapy in patients with implantable cardioverter-defibrillators (ICD) for primary prevention of sudden cardiac death. A retrospective cohort of 321 patients with systolic heart failure undergoing ICD placement for primary prevention of sudden cardiac death was queried with a mean follow-up period of 2.6 years. Appropriate ICD therapy was defined as therapy delivered for termination of a ventricular tachyarrhythmia. Appropriate ICD therapy was delivered in 142 (44%) of the patients. In a multivariate model, body mass index ≥28.8 kg/m(2), chronic kidney disease, left ventricular ejection fraction ≤20% and metabolic syndrome were found to be independent predictors of appropriate ICD therapy. Appropriate ICD therapy was associated with higher cardiovascular mortality. These findings show the importance of identification of risk factors, especially metabolic syndrome, in patients following ICD implantation as aggressive treatment of these co-morbidities may decrease appropriate ICD therapy and cardiovascular mortality.

Sudden cardiac arrest in apical hypertrophic cardiomyopathy.

We present two cases of cardiac arrest, presumably attributable to apical hypertrophic cardiomyopathy(HCM). The first case was a 37-year-old Asian man known to have an apical HCM and was successfully resuscitated from an "out of hospital" ventricular fibrillation arrest. He underwent an electrophysiological study that was unable to induce tachyarrhythmias, which may not be surprising. He did receive an automated internal cardioverter defibrillator (AICD) in compliance with his class I indication for an implantable defibrillator. The second patient was an 86-year-old Caucasian woman with a cardiac history significant for apical HCM, coronary artery disease, diastolic heart failure, and monomorphic ventricular tachycardia. She underwent electrophysiological testing for frequent dizziness and monomorphic ventricular tachycardia of a right ventricular origin was induced. She received an AICD for sudden cardiac death prevention. Though lethal ventricular arrhythmias have been reported in patients with apical HCM, the prevailing consensus is that the prognosis of apical HCM is benign. Whether these accounts are truly exceptional occurrences for this rare and conventionally regarded benign condition or whether they represent an under-appreciated risk for sudden cardiac arrest is an intriguing question.

The potential mechanisms of bradyarrhythmias associated with AngioJet thrombectomy.

The AngioJet Rheolytic Thrombectomy System (Possis Medical, Inc., Minneapolis, Minnesota) is an effective thrombectomy device, but it may cause bradycardias ranging from mild bradycardia to asystole and hypotension in some patients. The incidence appears to be higher with the proximity of the device to the heart. Several hypotheses have attempted to explain and attenuate this phenomenon.