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Introduction: Device-related infection is estimated to occur in 1.9% of the Medicare patients with de novo transvenous (TV) implantable cardioverter-defibrillators (ICD) within 2 years post-implant. TV-ICD infection is a serious complication that frequently requires complete device removal for attempted cure, which can be associated with patient morbidity and mortality. The objective of this study is to expand on limited published data and assess mortality risk associated with TV-ICD infection in a large Medicare population with de novo TV-ICD implants. Methods: A survival analysis was conducted using 100% fee-for-service Medicare facility-level claims data to identify patients who underwent de novo TV-ICD implantation between 7/2016 and 1/2018. TV-ICD infection within 2 years of implantation was identified using ICD-10 and CPT codes. Baseline patient risk factors associated with mortality were identified using the Charlson Comorbidity Index categories. Infection was treated as a time-dependent variable in a multivariate Cox proportional hazards model to account for immortal time bias. Results: Among 26,742 Medicare patients with de novo TV-ICD, 518 (1.9%) had a device-related infection. The overall number of decedents was 4,721 (17.7%) over 2 years, with 4,555 (17%) in the non-infection group and 166 (32%) in the infection group. After adjusting for baseline patient demographic characteristics and various comorbidities, the presence of TV-ICD infection was associated with an increase of 2.4 [95% CI: 2.08-2.85] times in the mortality hazard ratio (see attached Figure). Most of the baseline patient risk factors were also associated with higher risk of mortality in the Cox model. Conclusion: The rate of de novo TV-ICD infection and associated mortality in a large, real-world Medicare population is noteworthy. The positive association between device-related infection and risk of mortality further highlights the need to reduce infections.

Background: Implantable cardioverter-defibrillator (ICD) therapy prevents sudden cardiac death in selected patients with heart failure. When a primary prevention ICD arrives at elective replacement interval (ERI), conventional management is to replace the device. However, the effectiveness of ICDs in patients with nonischemic and ischemic cardiomyopathy (NICM and ICM, respectively) whose left ventricular ejection fraction (LVEF) improved to ≥50% before replacement is unclear. Hypothesis: The therapeutic benefit of primary prevention ICD for NICM is attenuated by the recovery of LVEF at the time of ERI. Methods: Consecutive patients presenting for first time primary prevention ICD battery change-out at a single quaternary care center between 1/1/2008 and 6/27/2019 were included. The primary endpoint was the rate of ICD therapy (ICD discharge and anti-tachycardia pacing) according to LVEF recovery at ERI. Results: During the study period 6851 ICDs were placed, of which 310 underwent battery change-out, of whom 100 did not receive therapy from the first ICD, of whom 44 had NICM. The demographics of the NICM cohort are in the table. Following ERI, 0 (0%) with NICM and recovered LVEF had received ICD therapy, whereas 13 (30%) with persistently low LVEF had received therapy (p = 0.07). Furthermore, among patients without recovered LVEF, the NICM group had a lower rate of therapy (4, 12%) than the ICM group (12, 32%) (p=0.04). Conclusion: Rates of ICD therapy provided by primary prevention ICD after first battery change out trended towards a significantly lower rate in NICM patients with LVEF that recovered to ≥50% than those without LVEF recovery. No other patient demographic significantly predicted therapy-free survival but the analysis was limited by sample size. A prospective study with a larger cohort would be necessary to better estimate therapy-free survival.

Introduction: Practice guidelines recommend use of subcutaneous implantable cardioverter-defibrillators (ICD) in patients (pts) at risk of sudden cardiac death and high risk for infection. This has prompted a need to better identify pts at high risk of infection to assist in de novo device selection. The objective of this study is to estimate infection incidence in de novo transvenous (TV) ICD implants and assess risk factors associated with infection in a large Medicare population. Methods: A retrospective cohort study was conducted using 100% Medicare administrative and claims data to identify pts who underwent de novo TV-ICD implantation between 7/2016 and 1/2018. Device-related infection within 2 years of implantation was identified using ICD-10 diagnosis and procedure codes. Baseline pt factors associated with infection were identified by univariable logistic regression analysis of all variables of interest, including factors in Charlson and Elixhauser comorbidity indices, followed by stepwise selection criteria with a p≤0.25 for inclusion in a multivariable model and a backwards, stepwise elimination process with p≤0.1 to remain in the model. A time-to-event analysis was also conducted. Results: Among 26,742 pts with de novo TV-ICD, 519 (1.9%) had a device-related infection over 2 years. The mean pt age with and without infection was 68 and 71 years, respectively. While more than half (54%) of infections occurred within 90 days post implant, infections continued to be diagnosed with 16% of infections occurring between years 1 and 2. Multivariable analysis revealed several significant predictors of infection (Figure) including age Conclusion: The rate of de novo TV-ICD infection in a large real-world Medicare population is clinically significant. The factors associated with increased infection risk identified here can be used to help determine device selection.

Introduction: Patients with end stage renal disease (ESRD) often progress to hemodialysis (HD), where permanent access such as arteriovenous fistula (AVF) is needed. Due to associated cardiovascular comorbidities, several of these patients also require cardiac implantable electronic devices (CIEDs) for pacing or defibrillation needs. HD vascular access is their lifeline, yet prolonged use is fraught with complications which often necessitate the eventual use of both upper extremities. Conventional CIEDs require placement of leads through subclavian veins which limits the ability to use that extremity for AVF. Novel devices such as subcutaneous defibrillator and leadless pacemakers do not require placement of leads in the upper extremity and may offer an advantage in HD patients to preserve both upper extremities for AVF. Objective: To compare the incidence of successful use of contralateral upper extremity for AVF following HD access failure in patients with novel and conventional devices. Methods: This study included all patients who underwent placement of novel leadless and conventional devices during the last 10 years at the Ohio State University. Incidence of successful use of contralateral upper extremity for AVF following HD access failure was assessed as the primary outcome. Incidence of initial HD access failure was assessed as a secondary outcome. Results: A total of 58 patients with novel devices (subcutaneous defibrillator: 30 and leadless pacemaker: 28) comprised the interventional group, while a total of 25 patients with conventional devices comprised the control group. The primary outcome occurred in 18% of the interventional group and 0% of the control group (p < 0.01). Incidence of initial access failure was 46% in the interventional group and 40% in the control group (p= 0.2). Conclusion: Patients on HD have a high incidence of access failure and often require use of the contralateral upper extremity for AVF. Presence of novel devices provides the option for contralateral access compared to conventional transvenous devices. Where possible and clinically indicated, novel devices should be preferred over conventional transvenous devices in ESRD and HD patients.

Background— The most frequent complications associated with implantable cardioverter-defibrillators (ICDs) involve the transvenous leads. A subcutaneous implantable cardioverter-defibrillator (S-ICD) has been developed as an alternative system. This study evaluated the safety and effectiveness of the S-ICD System (Cameron Health/Boston Scientific) for the treatment of life-threatening ventricular arrhythmias (ventricular tachycardia/ventricular fibrillation). Methods and Results— This prospective, nonrandomized, multicenter trial included adult patients with a standard indication for an ICD, who neither required pacing nor had documented pace-terminable ventricular tachycardia. The primary safety end point was the 180-day S-ICD System complication-free rate compared with a prespecified performance goal of 79%. The primary effectiveness end point was the induced ventricular fibrillation conversion rate compared with a prespecified performance goal of 88%, with success defined as 2 consecutive ventricular fibrillation conversions of 4 attempts. Detection and conversion of spontaneous episodes were also evaluated. Device implantation was attempted in 321 of 330 enrolled patients, and 314 patients underwent successful implantation. The cohort was followed for a mean duration of 11 months. The study population was 74% male with a mean age of 52±16 years and mean left ventricular ejection fraction of 36±16%. A previous transvenous ICD had been implanted in 13%. Both primary end points were met: The 180-day system complication-free rate was 99%, and sensitivity analysis of the acute ventricular fibrillation conversion rate was >90% in the entire cohort. There were 38 discrete spontaneous episodes of ventricular tachycardia/ventricular fibrillation recorded in 21 patients (6.7%), all of which successfully converted. Forty-one patients (13.1%) received an inappropriate shock. Conclusions— The findings support the efficacy and safety of the S-ICD System for the treatment of life-threatening ventricular arrhythmias. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01064076.

Introduction: Cystic fibrosis is among the most common inherited disorders, with ∼ 3% of Caucasians being heterozygous for the common CFTR ΔF508 mutation. Cardiomyopathy is a major cause of morbidity and mortality. While a small preliminary study suggested that cardiomyopathy patients heterozygous for the CFTR ΔF508 mutation have poorer outcomes, the finding has not been replicated and it is not known whether the poor outcomes are related to sudden death and/or heart failure progression. Methods: We screened 1347 Caucasian cardiomyopathy subjects (EF 21%, 82% male, 75% ischemic) with implantable cardioverter defibrillators (ICDs) from the prospective, multicenter, NIH-funded Genetic Risk Assessment of Defibrillator Events (GRADE) study. CFTR ΔF508 alleles were discriminated by real time fluorescence PCR. GRADE subjects were followed for up to 5 years to the primary endpoint of freedom from appropriate ICD shocks and the secondary endpoints of death and death/heart transplant/VAD placement. The results were compared by genotype using Kaplan-Meier analysis and Log Rank testing. Results: Genotyping revealed 33 CFTR ΔF508 heterozygotes (allele frequency 2.4%). ΔF508 carriers were older (68 vs 64 yrs, p=0.03); more likely to be diabetic (55 vs 34%, p=0.02), to have had an MI (77 vs 57%, p=0.02), and to have a RBBB on ECG (18 vs 7%, p=0.03); and had lower EFs (19 vs 21%, p=0.01). CFTR ΔF508 carriers had markedly higher rates of death (HR>2; p Conclusion: We have confirmed that carrying one CFTR ΔF508 allele is associated with an increased mortality in cardiomyopathy patients, and that this is likely not due to increased arrhythmic death. These findings may have implications for the treatment of this high risk heart failure subgroup. Future studies are needed to determine whether the increased mortality stems from a cardiac and/or pulmonary etiology.

Heart failure (HF) is a chronic disease resulting in abnormal prolongation and instability of ventricular repolarization. IKCa has been suggested to stabilize repolarization in HF as IKca blockade has shown pro-arrhythmic effects in the failing ventricle. We tested the hypothesis that an SK channel (IKCa) agonist CyPPA, would shorten and stabilize ventricular repolarization in HF ventricular myocytes. Methods: A tachypacing - induced 4 month HF canine model was used (LVFS: 15.9 ± 2.5%), and LV midwall myocytes were isolated and compared to normal controls. Action potential duration at 50 (APD50), and 90% (APD90) repolarization and APD instability (beat to beat variability of repolarization, a measure of arrhythmia risk) were measured before and after the application of CyPPA (0.001nM-20uM) in control ventricular, and in 4 months HF ventricular myocytes (n=10-15 per group). Results: In control myocytes, CyPPA shortened action potential APD50 and APD90 in a concentration dependent manner (0.001nM-20uM, p

Mutations that disrupt the coding sequence of Nav1.5, the cardiac Na+ channel encoded by SCN5A, cause inherited arrhythmias and cardiomyopathy. Changes in Nav1.5 splice isoforms, localization and function have also been associated with prognosis in acquired heart disease. However, the role of genetic variants in SCN5A gene regulatory sequences (e.g. those modulating expression) remains poorly understood. MicroRNAs (miRs) have emerged as vital gene regulators in heart, having roles in cardiogenesis, contractile function, and disease. These small non-coding RNAs are loaded into Argonaute proteins to direct post-transcriptional gene suppression by base-pairing with target transcripts, and genetic variants altering miR binding sequences may influence disease. Here, we used high-throughput biochemical means (HITS-CLIP) to generate the first transcriptome-wide map of miR binding events in human heart (4000 sites across >2200 genes). Our query of the data uncovered >500 common SNPs residing in or nearby miR target sites. Among these, we identified a synonymous SNP (rs1805126, T/C) which alters a conserved miR-24 binding site in the terminal coding exon of SCN5A. We hypothesized that this SNP affects Nav1.5 expression and contributes to clinical outcomes in heart failure. In vitro experiments showed that miR-24 suppresses Na+ current on patch clamp analysis (~5-fold; p1800 subjects with EFs≤30% and implantable cardioverter defibrillators (ICDs) from GRADE, a prospective multicenter study of genetic modulators of heart failure outcomes. We found that CC homozygotes had worse survival rates than T-allele carriers (HR=1.5, p=0.001), but no change in appropriate ICD shocks, a surrogate for sudden death. Together, these data reveal a novel miR-24:SCN5A:SNP regulatory axis that points to a surprising link between cardiac Na+ channel levels and non-arrhythmic death in heart failure. Overall, this work represents a key advance in exploring the interface of cardiac miRs with genetics and disease, perhaps signifying a broader functional relevance for “silent” SNPs.

Background — Brugada syndrome is a form of idiopathic ventricular fibrillation characterized by a right bundle-branch block pattern and ST elevation (STE) in the right precordial leads of the ECG. Sodium channel blockers increase STE. Mutations of the cardiac sodium channel SCN5A cause the disorder, and an implantable cardioverter-defibrillator is often recommended for affected individuals. Mutations in other genes have not been identified, and it is not known if the efficacy of drug testing or the malignancy of arrhythmias correlates to the gene defect. Methods and Results — We performed histories, physical examinations, ECGs, and drug testing on a large multigenerational family with Brugada syndrome. DNA isolated from blood samples, polymorphic genomic markers, and polymorphisms within candidate sodium channels were used for a genome-wide screen, fine mapping, and linkage analysis. We identified 12 affected individuals (right bundle-branch block, ≥1-mm STE) with an autosomal dominant inheritance pattern characterized by incomplete penetrance that appeared to be dependent on age and sex. Four affected individuals had syncope and 2 had documented ventricular arrhythmias, but there was minimal family history of sudden death. Procainamide infusions did not identify additional affected individuals. Linkage was present to an ≈15-cM region on chromosome 3p22-25 (maximum LOD score=4.00). The sodium channel genes SCN5A , SCN10A , and SCN12A on chromosome 3 were excluded as candidates (LOD scores ≤−2). Conclusions — A Brugada syndrome locus distinct from SCN5A is associated with progressive conduction disease, a low sensitivity to procainamide testing, and a relatively good prognosis in a single large pedigree.

Introduction: The cornerstone of atrial fibrillation (AF) radiofrequency ablation (RFA) is pulmonary vein (PV) isolation. A recently described technique directs RFA to electrical rotors identified by computational analyses of 64-electrode basket catheter (BC) endocardial recordings of AF. Hypothesis: The purpose of this study was to develop and then to assess the ability of a novel analysis method, CartoFinder™ (CF), incorporated into a 3D mapping system, CARTO (Biosense Webster, CA, USA) to identify rapid activation patterns (RAP). Methods: 20 patients who were undergoing RFA AF utilizing CARTO mapping and who consented were enrolled. 1 minute BC maps of the right (RA) and left (LA) were obtained after creation of a 3D virtual anatomic shell prior to and after RFA around the PV. In each atria, 2 BC recordings were obtained at the same location, separated by 5 minutes. Results: Unipolar signals from the BC were recorded by CARTO and analyzed offline. The signal was processed to filter out far-field ventricular activity and the remaining signals were analyzed to create dynamic 3D activation maps and visually identify RAP. CF labels the leading edge of activation with a red color. Of these 20 patients, CF recordings were complete in 14 pts (mean age 59; 12 with persistent AF). There were 2.8 RAP / pt. (mean 1.3 RA; 1.6 LA). No RAP were recorded in 2 pts. The correlation of the BC separated by 5 minutes to identify the same RAP was 12/15 in RA and 15/18 in LA (total: 27/33, 82%). Conclusions: CF is a newly developed online technique to identify RAP incorporated into a conventional 3D mapping system. RAPs can be identified in the majority of patients undergoing RFA AF with approximately 80% reproducibility.

Introduction: Computational analysis of 64-electrode basket catheter (BC) recordings of atrial fibrillation (AF) have been used to generate visually-identified electrical rotors and focal sources that are then targeted for radiofrequency ablation (RFA). Hypothesis: The purpose of this study was to assess BC maps of right (RA) and left (LA) atria during AF in humans using a novel software, CartoFinder™ (CF) (Biosense Webster, CA, USA), which was developed to identify rapid activation patterns (RAP) and incorporate them into a 3D mapping system, CARTO. Methods: 20 patients who were undergoing RFA AF utilizing CARTO mapping and who consented were enrolled. 1 minute BC maps of the RA and LA were obtained after creation of a 3D virtual anatomic shell prior to and after RFA around the pulmonary veins (PV). There were no complications. BC maps were analyzed by CF post procedure. CF annotates the leading edge of RAP with red color (see figure). Results: Of these 20 patients, CF recordings were complete in 14 pts (mean age 59; 12 persistent AF). There were 2.8 RAP / pt. The RA RAP were located septum (n = 9), anterolateral (n=5), and posterior (n = 3) walls. The LA RAP were located anterior (n = 8), roof (n=7), and posterior (n = 7) walls. RFA was delivered on top of (n=10), within 5mm (n = 4), or distant (n=10) from any RAP. Post PV isolation, there was a 45% reduction in RAP vs pre-RFA; and, 11 pts converted to sinus (n=7) or transitioned to flutter (n=4). Conclusions: CF is a novel software algorithm incorporated into CARTO that identifies RAP in the RA and LA. RFA around the PV only results in 45% reduction of RAP, suggesting that RFA beyond traditional PV isolation is required to eliminate the bulk of RAP.

Background Atrial fibrillation (AF) shortens the atrial effective refractory period (ERP) and predisposes to further episodes of AF. The purpose of this study was to determine the effect of verapamil and procainamide on these manifestations of AF-induced electrical remodeling. Methods and Results In adult patients without structural heart disease, the atrial ERP was measured before and after AF after pharmacological autonomic blockade and administration of verapamil (17 patients), procainamide (10 patients), or saline (20 patients). AF was then induced by rapid pacing. Immediately on AF conversion, the post-AF ERP was measured at alternating drive cycle lengths of 350 and 500 ms. In the saline group, the pre-AF and first post-AF ERPs at the 350-ms drive cycle length were 206±19 and 179±27 ms ( P P P =.8) or 500-ms (230±17 versus 232±20 ms, P =.6) drive cycle length. During determinations of the post-AF ERP, 105 secondary episodes of AF were unintentionally induced in 12% of verapamil patients compared with 90% and 80% of saline and procainamide patients ( P Conclusions Pretreatment with the calcium channel antagonist verapamil, but not the sodium channel antagonist procainamide, markedly attenuates acute, AF-induced changes in atrial electrophysiological properties. These data suggest that calcium loading during AF may be at least partially responsible for AF-induced electrical remodeling.

Background The probability of successful defibrillation has been determined in normal animals but not in patients undergoing defibrillator implantation. Therefore, the purpose of this prospective study was to determine the probability of successful defibrillation in humans on the basis of a step-down defibrillation energy requirement. Methods and Results Fifty-three consecutive patients underwent five separate inductions of ventricular fibrillation after the defibrillation energy requirement was determined with the use of small decrements and a step-down protocol (20, 15, 12, 10, 8, 6, 5, 4, 3, 2, 1, and 0.8 J). The first shock energy for defibrillation was either 1.0, 1.3, 1.5, 1.7, or 2.0 times the defibrillation energy requirement, and the likelihoods of successful defibrillation were 70±27%, 84±12%, 86±25%, 80±29%, and 88±32%, respectively ( P =.03). The frequencies of uniformly successful defibrillation (5 of 5 defibrillation attempts) were 30%, 27%, 60%, 64%, and 73%, respectively ( P =.01). Seven patients in whom the defibrillation energy requirement was P =.002). The likelihood of successful defibrillation at twice the defibrillation energy requirement was 98% in the 46 patients with a defibrillation energy requirement of >4 J and 67% in the 7 patients with a defibrillation energy requirement of P =.17). An absolute safety margin of 7 J was associated with a 96% probability of successful defibrillation. Conclusions The probability of successful defibrillation is 70% at the defibrillation energy requirement. The probability plateaus at 88%, at twice the defibrillation energy requirement. A 96% probability of successful defibrillation is achieved at an absolute safety margin of 7 J, and a 98% success rate is achieved at energies that are twice the defibrillation energy requirement if the defibrillation energy requirement is >4 J. If the defibrillation energy requirement is

Background Concealed entrainment has been useful in guiding catheter ablation of monomorphic ventricular tachycardia in patients with coronary artery disease. However, not all sites with concealed entrainment result in successful ablation of the targeted ventricular tachycardia. The purpose of this prospective study was to identify factors at sites that demonstrate concealed entrainment that differentiate effective from ineffective target sites. Methods and Results In 14 consecutive patients with hemodynamically stable monomorphic ventricular tachycardia and coronary artery disease, radiofrequency ablation of 26 ventricular tachycardias was performed. Ablation was attempted at 46 sites that demonstrated concealed entrainment. Twenty-five of the targeted ventricular tachycardias (96%) were successfully ablated. The positive predictive value of concealed entrainment for successful ablation was 54%; it increased to 72% in the presence of a stimulus-QRS interval/ventricular tachycardia cycle length ratio of ≤70%, to 82% in the presence of a match of the stimulus-QRS and electrogram-QRS interval, and to 89% in the presence of isolated middiastolic potentials that could not be dissociated from ventricular tachycardia during entrainment. Conclusions The positive predictive value of concealed entrainment for identification of successful ablation sites in patients with sustained ventricular tachycardia and coronary artery disease can be significantly enhanced by the presence of associated mapping criteria, particularly an isolated mid diastolic potential that cannot be dissociated from the tachycardia.

Background Radiofrequency catheter modification of AV conduction can be used to control the ventricular rate during atrial fibrillation both in the baseline state and during exercise. Slow-pathway ablation has been suggested to be the mechanism for this response. The purpose of this study was to determine the effect of slow-pathway ablation on the ventricular rate in atrial fibrillation during autonomic blockade and sympathetic stimulation in patients with AV nodal reentrant tachycardia (AVNRT). Methods and Results Thirty-five patients undergoing slow-pathway radiofrequency ablation for AVNRT were assigned to autonomic blockade (0.2 mg/kg propranolol and 0.04 mg/kg atropine; n=14) or isoproterenol (2 μg/min; n=21). Atrial fibrillation was induced before and after slow-pathway radiofrequency ablation. During autonomic blockade, the mean ventricular cycle length (448±34 versus 525±103 ms, P P =.04) were prolonged after ablation, whereas the minimum ventricular cycle length did not change significantly (361±42 versus 403±83 ms, P =.05). During isoproterenol infusion, the mean ventricular cycle length (375±52 versus 390±61 ms, P =.2), maximum ventricular cycle length (520±88 versus 537±106 ms, P =.3), and minimum ventricular cycle length (307±59 versus 298±33 ms, P =.4) did not change significantly after slow-pathway ablation. Conclusions Slow-pathway ablation slows the ventricular rate during atrial fibrillation under conditions of autonomic blockade but not during sympathetic stimulation. Therefore, slow-pathway ablation alone cannot account for the clinical results obtained with radiofrequency modification of AV conduction in patients with atrial fibrillation.

Background— Brugada syndrome is a rare, autosomal-dominant, male-predominant form of idiopathic ventricular fibrillation characterized by a right bundle-branch block and ST elevation in the right precordial leads of the surface ECG. Mutations in the cardiac Na + channel SCN5A on chromosome 3p21 cause ≈20% of the cases of Brugada syndrome; most mutations decrease inward Na + current, some by preventing trafficking of the channels to the surface membrane. We previously used positional cloning to identify a new locus on chromosome 3p24 in a large family with Brugada syndrome and excluded SCN5A as a candidate gene. Methods and Results— We used direct sequencing to identify a mutation (A280V) in a conserved amino acid of the glycerol-3-phosphate dehydrogenase 1–like ( GPD1-L ) gene. The mutation was present in all affected individuals and absent in >500 control subjects. GPD1-L RNA and protein are abundant in the heart. Compared with wild-type GPD1-L, coexpression of A280V GPD1-L with SCN5A in HEK cells reduced inward Na + currents by ≈50% ( P P =0.01). Conclusions— GPD1-L is a novel gene that may affect trafficking of the cardiac Na + channel to the cell surface. A GPD1-L mutation decreases SCN5A surface membrane expression, reduces inward Na + current, and causes Brugada syndrome.

Background Because it is not clear which technique is less expensive, the purpose of this study was to compare the cost of radiofrequency modification and ablation of the atrioventricular (AV) node in drug-refractory patients with atrial fibrillation and an uncontrolled ventricular rate. Methods and Results The initial nominal charges for a successful procedure were compared in 10 patients with chronic atrial fibrillation who underwent modification of the AV node ($13 109±2002) and 14 similar patients who underwent ablation and pacemaker implantation ($28 302±2023, P P Conclusions The initial charges generated by AV node modification are significantly lower than for AV node ablation in patients with chronic atrial fibrillation. Even when adjusted for higher failure and recurrence rates, the modification procedure retains a major cost advantage over ablation during long-term follow-up.

Background Implantable cardioverter-defibrillator (ICD) therapy is integral to current therapy for ventricular tachycardia. Patients with an ICD frequently require concomitant antiarrhythmic drug therapy. Despite this, some patients still receive frequent ICD therapies for ventricular tachycardia. Therefore, the purpose of this prospective study was to determine the utility of ablation of ventricular tachycardia in patients with an ICD who experience frequent ICD therapies. Methods and Results Twenty-one consecutive patients with frequent ICD therapies despite antiarrhythmic drug therapy were the subjects of this study. The mean age was 69±6 years, and 17 were men. The mean ejection fraction was 0.22±0.08, and all patients had coronary artery disease. During the 36±51 days (range, 4 days to 7 months) preceding the ablation procedures, the patients received 34±55 ICD therapies for the clinical ventricular tachycardia, or a mean of 25±88 ICD therapies per month. The patients underwent radiofrequency ablation of the presumed clinical ventricular tachycardia by inducing the tachycardia and mapping according to endocardial activation, continuous electrical activity, pace mapping, concealed entrainment, or mid-diastolic potentials. Ablation of the clinical arrhythmia was successful in 76% of patients during 1.4±0.6 (range, 1 to 3) ablation procedures and required 12.5±9.2 applications of energy. During 11.8±10.0 months of follow-up, the frequency of ICD therapies per month decreased from 60±80 before successful ablation to 0.1±0.3 ICD therapies per month after ablation ( P =.01). A quality-of-life assessment demonstrated a significant improvement after successful ( P =.02) but not unsuccessful ablation ( P =.9). Conclusions Radiofrequency ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and an ICD has a reasonable success rate, significantly reduces ICD therapies, and appears to be associated with an improved quality of life.

Background Ventricular pace mapping is performed by comparing the QRS morphology of ventricular paced complexes to that of a template arrhythmia, either a premature ventricular depolarization or a QRS complex during ventricular tachycardia. The objective of this study was to evaluate the effect of coupling interval and pacing cycle length on QRS morphology. Methods and Results The study population consisted of 20 patients (mean age, 38±16 years) undergoing a clinically indicated electrophysiology procedure. In the first 10 patients, the effect of coupling interval on the morphology of single paced ventricular complexes was evaluated visually and by signal processing techniques. Visually apparent differences in QRS morphology occurred in a mean of 4/12 electrocardiographic leads with a change in coupling interval of ≥100 ms. In the next 10 patients, the QRS complex morphology during ventricular overdrive pacing at cycle lengths of 600 and 300 ms was found to differ significantly in a mean of 4/12 leads. The QRS morphology during overdrive pacing differed significantly from that of a single paced complex whenever the pacing cycle length differed from the coupling interval of the single paced complex by >80 ms. Conclusions The morphology of single paced QRS complexes may vary, depending on coupling interval, and the QRS morphology during overdrive pacing is affected by the pacing cycle length. During ventricular pace mapping, the coupling interval or cycle length of the template arrhythmia should be matched during pacing. If not, rate-dependent changes in QRS morphology that are independent of the pacing site may confound the results of pace mapping.