Prognostic value of late-gadolinium enhancement on cardiac magnetic resonance in patients with cardiac sarcoidosis.

BACKGROUND: Late-gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) is a predictor of adverse events in patients with cardiac sarcoidosis (CS), but available studies had small sample sizes and did not consider all relevant endpoints. OBJECTIVE: To evaluate the association between LGE on CMR in patients with CS and mortality, ventricular arrhythmias (VA) and sudden cardiac death (SCD), and heart failure (HF) hospitalization. METHODS: A literature search was conducted for studies reporting the association between LGE in CS and the study endpoints. The endpoints were mortality, VA and SCD, and HF hospitalization. The search included the following databases: Ovid MEDLINE, EMBASE, Web of Science, and Google Scholar. The search was not restricted to time or publication status. The minimum follow-up duration was 1 year. RESULTS: A total of 17 studies and 1915 CS patients (595 with LGE vs. 1320 without LGE) were included; mean follow-up was 3.3 years (ranging between 17 and 84 months). LGE was associated with increased all-cause mortality (OR 6.05, 95% CI 3.16-11.58; p < .01), cardiovascular mortality (OR 5.83, 95% CI 2.89-11.77; p < .01), and VA and SCD (OR 16.48, 95% CI 8.29-32.73; p < .01). Biventricular LGE was associated with increased VA and SCD (OR 6.11, 95% CI 1.14-32.68; p = .035). LGE was associated with an increased HF hospitalization (OR 17.47, 95% CI 5.54-55.03; p < .01). Heterogeneity was low: df = 7 (p = .43), I2 = 0%. CONCLUSIONS: LGE in CS patients is associated with increased mortality, VA and SCD, and HF hospitalization. Biventricular LGE is associated with an increased risk of VA and SCD.

QT interval measurement in ventricular pacing: Implications for assessment of drug effects and pro-arrhythmia risk.

QT interval prolongation is a known risk factor for development of malignant ventricular arrhythmias. Measurement of the QT interval is difficult in the setting of ventricular pacing (VP), which can prolong depolarization and increase the QT interval, overestimating repolarization time. VP and cardiac resynchronization therapies have become commonplace in modern cardiac care and may contribute to repolarization heterogeneity and subsequent increased risk for ventricular arrhythmias including Torsades de Pointes. It is imperative for the clinician caring for acutely ill cardiac patients to understand the relationship between QT interval prolongation, both drug-induced and pacing-induced, and repolarization changes with subsequent ventricular arrhythmia risk. In this review, we discuss the components of QT interval assessment for arrhythmogenic risk including arrhythmogenic QT prolongation, methods for adjusting the QT interval to identify repolarization changes, methods to adjust for heart rate, and propose a framework for medication management to assess for drug-induced long QT syndrome in patients with VP.

Wearable Cardioverter-Defibrillator after Myocardial Infarction.

BACKGROUND: Despite the high rate of sudden death after myocardial infarction among patients with a low ejection fraction, implantable cardioverter-defibrillators are contraindicated until 40 to 90 days after myocardial infarction. Whether a wearable cardioverter-defibrillator would reduce the incidence of sudden death during this high-risk period is unclear. METHODS: We randomly assigned (in a 2:1 ratio) patients with acute myocardial infarction and an ejection fraction of 35% or less to receive a wearable cardioverter-defibrillator plus guideline-directed therapy (the device group) or to receive only guideline-directed therapy (the control group). The primary outcome was the composite of sudden death or death from ventricular tachyarrhythmia at 90 days (arrhythmic death). Secondary outcomes included death from any cause and nonarrhythmic death. RESULTS: Of 2302 participants, 1524 were randomly assigned to the device group and 778 to the control group. Participants in the device group wore the device for a median of 18.0 hours per day (interquartile range, 3.8 to 22.7). Arrhythmic death occurred in 1.6% of the participants in the device group and in 2.4% of those in the control group (relative risk, 0.67; 95% confidence interval [CI], 0.37 to 1.21; P=0.18). Death from any cause occurred in 3.1% of the participants in the device group and in 4.9% of those in the control group (relative risk, 0.64; 95% CI, 0.43 to 0.98; uncorrected P=0.04), and nonarrhythmic death in 1.4% and 2.2%, respectively (relative risk, 0.63; 95% CI, 0.33 to 1.19; uncorrected P=0.15). Of the 48 participants in the device group who died, 12 were wearing the device at the time of death. A total of 20 participants in the device group (1.3%) received an appropriate shock, and 9 (0.6%) received an inappropriate shock. CONCLUSIONS: Among patients with a recent myocardial infarction and an ejection fraction of 35% or less, the wearable cardioverter-defibrillator did not lead to a significantly lower rate of the primary outcome of arrhythmic death than control. (Funded by the National Institutes of Health and Zoll Medical; VEST ClinicalTrials.gov number, NCT01446965 .).

Impact of wearable cardioverter-defibrillator compliance on outcomes in the VEST trial: As-treated and per-protocol analyses.

BACKGROUND: Vest Prevention of Early Sudden Death Trial did not demonstrate a significant reduction in arrhythmic death with the wearable cardioverter-defibrillator (WCD), but compliance with the device may have substantially affected the results. ThePletcher influence of WCD compliance on outcomes has not yet been fully evaluated. METHODS: Using linear and pooled logistic models, we performed as-treated analyses omitting person-time in the hospital and adjusted for correlates of WCD compliance. To assess the impact of early stopping of WCD, we performed a per-protocol Kaplan-Meier analysis, censoring after the last day the WCD was worn. Interactions of potential effect modifiers with treatment assignment and WCD compliance on outcomes were investigated. Finally, we used linear models to identify predictors of WCD compliance. RESULTS: A per-protocol analysis demonstrated a significant reduction in total (P < .001) and arrhythmic (P = .001) mortality. Better WCD compliance was independently predicted by cardiac arrest during index myocardial infarction (MI), higher Cr, diabetes, prior heart failure, EF ≤ 25%, Polish enrolling center and number of WCD alarms, while worse compliance was predicted by being divorced, Asian race, higher body mass index, prior percutaneous coronary intervention, or any WCD shock. Neither excluding time in hospital from the as-treated analysis nor adjustment for factors affecting WCD compliance materially changed the results. No variable demonstrated a significant interaction in either the intention-to-treat or as-treated analysis. CONCLUSION: Robust sensitivity analyses of as-treated and per-protocol analyses suggest that the WCD is protective in compliant patients with ejection fraction less than or equal to 35% during the first 3 months post-MI.

Very early administration of glucose-insulin-potassium by emergency medical service for acute coronary syndromes: Biological mechanisms for benefit in the IMMEDIATE Trial.

AIMS: In the IMMEDIATE Trial, intravenous glucose-insulin-potassium (GIK) was started as early as possible for patients with suspected acute coronary syndrome by ambulance paramedics in communities. In the IMMEDIATE Biological Mechanism Cohort substudy, reported here, we investigated potential modes of GIK action on specific circulating metabolic components. Specific attention was given to suppression of circulating oxygen-wasting free fatty acids (FFAs) that had been posed as part of the early GIK action related to averting cardiac arrest. METHODS: We analyzed the changes in plasma levels of FFA, glucose, C-peptide, and the homeostasis model assessment (HOMA) index. RESULTS: With GIK, there was rapid suppression of FFA levels with estimated levels for GIK and placebo groups after 2 hours of treatment of 480 and 781 µmol/L (P<.0001), even while patterns of FFA saturation remained unchanged. There were no significant changes in the HOMA index in the GIK or placebo groups (HOMA index: placebo 10.93, GIK 12.99; P = .07), suggesting that GIK infusions were not countered by insulin resistance. Also, neither placebo nor GIK altered endogenous insulin secretion as reflected by unchanging C-peptide levels. CONCLUSION: These mechanistic observations support the potential role of FFA suppression in very early cardioprotection by GIK. They also suggest that the IMMEDIATE Trial GIK formula is balanced with respect to its insulin and glucose composition, as it induced no endogenous insulin secretion.

Risk of Appropriate Implantable Cardioverter-Defibrillator Therapies and Sudden Cardiac Death in Patients With Heart Failure With Improved Left Ventricular Ejection Fraction.

BACKGROUND: The benefit of implantable cardioverter-defibrillator (ICD) therapy is controversial in patients who have heart failure with improved left ventricular ejection fraction (EF) to >35% after implantation (HFimpEF). METHODS: Databases (Ovid MEDLINE, EMBASE, Web of Science, and Google Scholar) were queried for studies in patients with ICD that reported the association between HFimpEF and arrhythmic events (AEs), defined as the combined incidence of ventricular arrhythmias, appropriate ICD intervention, and sudden cardiac death (primary composite end point). RESULTS: A total of 41 studies and 38,572 patients (11,135 with HFimpEF, 27,437 with persistent EF ≤35%) were included; mean follow-up was 43 months. HFimpEF was associated with decreased AEs (odds ratio [OR] 0.39, 95% confidence interval [CI] 0.32 to 0.47; annual rate [AR] 4.1% vs 8%, p <0.01). Super-responders (EF ≥50%) had less risk of AEs than did patients with more modest reverse remodeling (EF >35% and <50%, OR 0.25, 95% CI 0.14 to 0.46, AR 2.7% vs 6.2%, p <0.01). Patients with HFimpEF who had an initial primary-prevention indication had less risk of AEs (OR 0.43, 95% CI 0.3 to 0.61, AR 5.1% vs 10.3%, p <0.01). Among patients with primary prevention who had never received appropriate ICD therapy at the time of generator change, HFimpEF was associated with decreased subsequent AEs (OR 0.26, 95% CI 0.12 to 0.59, AR 1.6% vs 4.8%, p <0.01). In conclusion, HFimpEF is associated with reduced, but not eliminated, risk for AEs in patients with ICDs. The decision to replace an ICD in subgroups at less risk should incorporate shared decision making based on risks for subsequent AEs and procedural complications.

Effect of Implanted Defibrillator on Mortality in Patients With Chronic Kidney Disease.

The beneficial role of implantable cardioverter defibrillators (ICDs) in patients with chronic kidney disease (CKD) is controversial. This meta-analysis aimed to evaluate the effect of ICD on mortality in patients with CKD. A literature search was conducted for studies reporting the effect of ICD on all-cause mortality in patients with CKD (estimated glomerular filtration rate <60 ml/min/1.73 m2). The search was not restricted to time or publication status. The search included the following databases: Ovid MEDLINE, EMBASE, Scopus, Web of Science, Google Scholar, and EBSCO CINAHL. The primary end point was all-cause mortality. The minimum duration of follow-up required for inclusion was 1 year. The literature search identified 834 studies, of which 14 studies with 70,661 patients were included. Mean follow-up was 39 months (12 to 81 months). For all patients with CKD, ICD was associated with lower all-cause mortality (log hazard ratio [HR] -0.247, standard error [SE] 0.101, p = 0.015). Heterogeneity: degree of freedom = 13 (p <0.01), I2 = 97.057; test for overall effect: Z = -2.431 (p = 0.015). When further stratified based on dialysis, patients with CKD without the need for dialysis had significantly lower mortality (log HR -0.211, SE 0.095, p = 0.026), with a similar trend in patients who underwent dialysis (log HR -0.262, SE 0.134, p = 0.051). ICD implantation is associated with a significant mortality benefit in patients with CKD.

Association of late gadolinium enhancement in cardiac magnetic resonance with mortality, ventricular arrhythmias, and heart failure in patients with nonischemic cardiomyopathy: A systematic review and meta-analysis.

Background: Late gadolinium enhancement (LGE) on cardiac magnetic resonance is a predictor of adverse events in patients with nonischemic cardiomyopathy (NICM). Objective: This meta-analysis evaluated the correlation between LGE and mortality, ventricular arrhythmias (VAs) and sudden cardiac death (SCD), and heart failure (HF) outcomes. Methods: A literature search was conducted for studies reporting the association between LGE in NICM and the study endpoints. The primary endpoint was mortality. Secondary endpoints included VA and SCD, HF hospitalization, improvement in left ventricular ejection fraction (LVEF) to >35%, and heart transplantation referral. The search was not restricted to time or publication status. The minimum follow-up duration was 1 year. Results: A total of 46 studies and 10,548 NICM patients (4610 with LGE, 5938 without LGE) were included; mean follow-up was 3 years (range 13-71 months). LGE was associated with increased mortality (odds ratio [OR] 2.9; 95% confidence interval [CI] 2.3-3.8; P < .01) and VA and SCD (OR 4.6; 95% CI 3.5-6.0; P < .01). LGE was associated with an increased risk of HF hospitalization (OR 3.4; 95% CI 2.3-5.0; P < .01), referral for transplantation (OR 5.1; 95% CI 2.5-10.4; P < .01), and decreased incidence of LVEF improvement to >35% (OR 0.2; 95% CI 0.03-0.85; P = .03). Conclusion: LGE in NICM patients is associated with increased mortality, VA and SCD, and HF hospitalization and heart transplantation referral during long-term follow up. Given these competing risks of mortality and HF progression, prospective randomized controlled trials are required to determine if LGE is useful for guiding prophylactic implantable cardioverter-defibrillator placement in NICM patients.

Effects of GLP-1 Agonists on mortality and arrhythmias in patients with Type II diabetes.

Background: Glucagon-like Peptide-1 Receptor Agonists (GLP-1 RA) are frequently used for the management of diabetes. The impact of GLP-1 RA on cardiovascular outcomes is unclear. We aim to assess the effect of GLP-1 RA on mortality, atrial and ventricular arrhythmias, and sudden cardiac death in patients with type II diabetes. Methods: We searched databases including Ovid MEDLINE, EMBASE, Scopus, Web of Science, Google Scholar and CINAHL, from inception to May 2022, for randomized controlled trials reporting the relationship between GLP-1 RA (including albiglutide, dulaglutide, exenatide, liraglutide, lixisenatide, and semaglutide) and mortality, atrial arrhythmias, and the combined incidence of ventricular arrhythmias and sudden cardiac death. The search was not restricted to time or publication status. Results: A total of 464 studies resulted from literature search, of which 44 studies, including 78,702 patients (41,800 GLP-1 agonists vs 36,902 control), were included. Follow up ranged from 52 to 208 weeks. GLP-1 RA were associated with lower risk of all-cause mortality (odds ratio 0.891, 95% confidence interval 0.837-0.949; P < 0.01) and reduced cardiovascular mortality (odds ratio 0.88, 95% confidence interval 0.881-0.954; P < 0.01). GLP-1 RA were not associated with increased risk of atrial (odds ratio 0.963, 95% confidence interval 0.869-1.066; P 0.46) or ventricular arrhythmias and sudden cardiac death (odds ratio 0.895, 95% confidence interval 0.706-1.135; P 0.36). Conclusion: GLP-1 RA are associated with decreased all-cause and cardiovascular mortality, and no increased risk of atrial and ventricular arrhythmias and sudden cardiac death.

Study design for the Immediate Myocardial Metabolic Enhancement During Initial Assessment and Treatment in Emergency Care (IMMEDIATE) Trial: A double-blind randomized controlled trial of intravenous glucose, insulin, and potassium for acute coronary syndromes in emergency medical services.

BACKGROUND: Experimental studies suggest that metabolic myocardial support by intravenous (IV) glucose, insulin, and potassium (GIK) reduces ischemia-induced arrhythmias, cardiac arrest, mortality, progression from unstable angina pectoris to acute myocardial infarction (AMI), and myocardial infarction size. However, trials of hospital administration of IV GIK to patients with ST-elevation myocardial infarction (STEMI) have generally not shown favorable effects possibly because of the GIK intervention taking place many hours after ischemic symptom onset. A trial of GIK used in the very first hours of ischemia has been needed, consistent with the timing of benefit seen in experimental studies. OBJECTIVE: The IMMEDIATE Trial tested whether, if given very early, GIK could have the impact seen in experimental studies. Accordingly, distinct from prior trials, IMMEDIATE tested the impact of GIK (1) in patients with acute coronary syndromes (ACS), rather than only AMI or STEMI, and (2) administered in prehospital emergency medical service settings, rather than later, in hospitals, after emergency department evaluation. DESIGN: The IMMEDIATE Trial was an emergency medical service-based randomized placebo-controlled clinical effectiveness trial conducted in 13 cities across the United States that enrolled 911 participants. Eligible were patients 30 years or older for whom a paramedic performed a 12-lead electrocardiogram to evaluate chest pain or other symptoms suggestive of ACS for whom electrocardiograph-based acute cardiac ischemia time-insensitive predictive instrument indicated a ≥75% probability of ACS, and/or the thrombolytic predictive instrument indicated the presence of a STEMI, or if local criteria for STEMI notification of receiving hospitals were met. Prehospital IV GIK or placebo was started immediately. Prespecified were the primary end point of progression of ACS to infarction and, as major secondary end points, the composite of cardiac arrest or in-hospital mortality, 30-day mortality, and the composite of cardiac arrest, 30-day mortality, or hospitalization for heart failure. Analyses were planned on an intent-to-treat basis, on a modified intent-to-treat group who were confirmed in emergency departments to have ACS, and for participants presenting with STEMI. CONCLUSION: The IMMEDIATE Trial tested whether GIK, when administered as early as possible in the course of ACS by paramedics using acute cardiac ischemia time-insensitive predictive instrument and thrombolytic predictive instrument decision support, would reduce progression to AMI, mortality, cardiac arrest, and heart failure. It also tested whether it would provide clinical and pathophysiologic information on GIK's biological mechanisms.

Rhythm versus rate control for atrial fibrillation in heart failure with preserved ejection fraction.

Background: There are few prospective studies assessing the benefits of rhythm control of atrial fibrillation (AF) in patients with heart failure and preserved ejection fraction (HFpEF), which accounts for 50% of all heart failure patients. Objective: Conduct a meta-analysis to assess the effects of rhythm control (ablation and/or antiarrhythmic medications) vs rate control on all-cause mortality in AF patients with HFpEF. Methods: Databases were searched for studies reporting the effect of rhythm control vs rate control on mortality in patients with HFpEF (Ovid MEDLINE, EMBASE, Scopus, Web of Science, Google Scholar, and EBSCO CINAHL). The search was not restricted to time or publication status. The primary endpoint was all-cause mortality. The minimum duration of follow-up required for inclusion was 1 year. Results: The literature search identified 1210 candidate studies; 5 studies and 16,825 patients were included. The study population had 57% men with a mean age of 71± 2.5 years. Rhythm control for AF was associated with lower all-cause mortality (odds ratio 0.735, 95% confidence interval 0.665-0.813; P < .001) as compared to rate control. Conclusion: Rhythm control for AF in patients with HFpEF was associated with decreased all-cause mortality.

Identification and Endocardial Ablation of the Ligament of Marshall for Pulmonary Vein Isolation.

OBJECTIVES: The aims of this study were to establish criteria for identifying ligament of Marshall (LOM) connections that are responsible for pulmonary vein isolation (PVI) failure, assess their incidence, and determine if they can be targeted by focal endocardial ablation at the anterior carina of the left superior pulmonary vein (LSPV). BACKGROUND: Wide antral ablation of the left pulmonary veins (PVs) may not achieve PVI, sometimes requiring empirical ablation of the PV carina. The mechanism could be due to epicardial conduction along the LOM, which courses adjacent to the anterior carina. METHODS: In patients undergoing radiofrequency ablation for atrial fibrillation, if wide ablation of the left PV did not achieve isolation, bidirectional mapping was performed. A presumptive LOM connection was diagnosed if the earliest entrance was mapped to the anterior LSPV, while the earliest exit was mapped inferior to the left inferior PV. Focal ablation at the LSPV anterior carina was performed, even if not at the site of earliest entrance activation. The primary endpoint was successful PVI immediately after ablation. RESULTS: The study included 455 consecutive patients who underwent 570 procedures, of which 364 were first-time ablations. Presumptive LOM connections were identified in 48 procedures (8.4%) and in 41 patients (11.2%) undergoing first-time ablation and were successfully ablated at the anterior carina of the LSPV in 47 of 48 procedures (98%). CONCLUSIONS: LOM connections may be a common cause of PVI failure and can be easily identified and reliably ablated with focal endocardial ablation at the anterior LSPV carina.

Electrical Storm in a Case of Bilateral Pheochromocytomas.

BACKGROUND Pheochromocytomas are catecholamine-secreting tumors that develop within the chromaffin cells of the adrenal glands. They most commonly present with hypertension, and the classic triad of symptoms is headaches, palpitations, and diaphoresis. Electrical storm (ES) is defined as at least 3 sustained episodes of ventricular tachycardia (VT), ventricular fibrillation (VF), or appropriate shocks from an implanted cardioverter-defibrillator (ICD) within 24 h. We discuss the case of a 63-year-old man with known bilateral pheochromocytomas who presented with ES prompting multiple ICD shocks, possibly exacerbated by catecholamine surge from his adrenal tumors. CASE REPORT The patient was a 63-year-old man with an extensive medical history including ischemic cardiomyopathy and congestive heart failure with reduced ejection fraction presented with multiple syncopal episodes secondary to persistent monomorphic ventricular tachycardia (MMVT), polymorphic ventricular tachycardia (PMVT), and VF requiring ICD shocks. He had known bilateral pheochromocytomas. ES was attributed to catecholamine excess in the setting of these tumors, so VT ablation was deferred pending tumor removal. Alpha blockade was initiated preoperatively, and the patient subsequently underwent bilateral adrenalectomy; however, he continued to sustain tachyarrhythmias and eventually died despite resuscitative efforts. CONCLUSIONS Bilateral pheochromocytomas are rare adrenal tumors. In even more infrequent situations, they can cause ES secondary to adrenergic stimulation from catecholamine surges. It is worth considering pheochromocytoma in patients with refractory ES, as treating these tumors could potentially reduce the frequency of this dangerous arrhythmia.

Electrophysiological effects of late percutaneous coronary intervention for infarct-related coronary artery occlusion: the Occluded Artery Trial-Electrophysiological Mechanisms (OAT-EP).

BACKGROUND: The Occluded Artery Trial-Electrophysiological Mechanisms (OAT-EP) tested the hypothesis that opening a persistently occluded infarct-related artery by percutaneous coronary intervention and stenting (PCI) after the acute phase of myocardial infarction compared with optimal medical therapy alone reduces markers of vulnerability to ventricular arrhythmias. METHODS AND RESULTS: Between April 2003 and December 2005, 300 patients with an occluded native infarct-related artery 3 to 28 days (median, 12 days) after myocardial infarction were randomized to PCI or optimal medical therapy. Ten-minute digital Holter recordings were obtained before randomization, at 30 days, and at 1 year. The primary end point was the change in alpha1, a nonlinear heart rate variability parameter, between baseline and 1 year. Major secondary end points were the changes in the filtered QRS duration on the signal-averaged ECG and variability in T-wave morphology (T-wave variability) between baseline and 1 year. There were no significant differences in the changes in alpha1 (-0.04; 95% CI, -0.12 to 0.04), filtered QRS (2.2 ms; 95% CI, -1.4 to 5.9 ms), or T-wave variability (3.0 microV; 95% CI, -4.8 to 10.7 microV) between the PCI and medical therapy groups (medical therapy change minus PCI change). Multivariable analysis revealed that the results were unchanged after adjustment for baseline clinical variables and medication treatments during the Holter recordings. CONCLUSIONS: PCI with stenting of a persistently occluded infarct-related artery during the subacute phase after myocardial infarction compared with medical therapy alone had no significant effect on changes in heart rate variability, the time-domain signal-averaged ECG, or T-wave variability during the first year after myocardial infarction. These findings are consistent with the lack of clinical benefit, including no reduction in sudden death, with PCI for stable patients with persistently occluded infarct-related arteries after myocardial infarction in the main OAT.

Acute defibrillation performance of a novel, non-transvenous shock pathway in adult ICD indicated patients.

OBJECTIVES: The purpose of this study was to evaluate the efficacy of a totally subcutaneous, anteroposterior defibrillation shock pathway using a long time-constant shock waveform that emulates a proposed device having approximately twice the capacitance and thus twice the available energy of traditional transvenous devices. BACKGROUND: A non-transvenous defibrillation system potentially offers advantages over a transvenous system including simplification of the implant procedure and reduction of the impact of device complications by eliminating the need to place a lead within the heart. Previous non-transvenous defibrillation efficacy studies have been reported using anterolateral and anterior-anterior shock vectors. An external anteroposterior shock vector has demonstrated superior efficacy compared to anterolateral shock vectors but a prospective study on an anteroposterior shock vector with implanted electrodes has not been previously reported. METHODS: The non-transvenous shock vector consisted of an anterior low pectorally-placed active can emulator electrode and a posterior subcutaneous coil electrode. The shock waveform was a biphasic with 50% tilt per phase and a time constant of decay of 12 ms. Defibrillation efficacy was characterized using a step-down defibrillation threshold protocol (35 J, 25 J, 15 J). RESULTS: A total of 33 patients with standard ICD indications were enrolled in the study with 32 fully completing the protocol. The patient population was 69% male, with a mean age of 59 +/- 12 years. Mean ejection fraction was 27 +/- 12%. Of the 32 patients tested, 26 patients (81%) were successfully defibrillated at 35 J or less, 18 patients were defibrillated at 25 J or less and 9 patients were successfully defibrillated at 15 J. CONCLUSIONS: Defibrillation using a long time-constant waveform delivered through an anteroposterior non-transvenous pathway including a pectoral active can emulator electrode and a posterior subcutaneous coil electrode is feasible with over 80% of patients defibrillated successfully using 35 J or less.