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The Resynchronization-Defibrillation for Ambulatory Heart Failure Trial (RAFT) showed a greater benefit with respect to mortality at 5 years among patients who received cardiac-resynchronization therapy (CRT) than among those who received implantable cardioverter-defibrillators (ICDs). However, the effect of CRT on long-term survival is not known. We randomly assigned patients with New York Heart Association (NYHA) class II or III heart failure, a left ventricular ejection fraction of 30% or less, and an intrinsic QRS duration of 120 msec or more (or a paced QRS duration of 200 msec or more) to receive either an ICD alone or a CRT defibrillator (CRT-D). We assessed long-term outcomes among patients at the eight highest-enrolling participating sites. The primary outcome was death from any cause; the secondary outcome was a composite of death from any cause, heart transplantation, or implantation of a ventricular assist device. The trial enrolled 1798 patients, of whom 1050 were included in the long-term survival trial; the median duration of follow-up for the 1050 patients was 7.7 years (interquartile range, 3.9 to 12.8), and the median duration of follow-up for those who survived was 13.9 years (interquartile range, 12.8 to 15.7). Death occurred in 405 of 530 patients (76.4%) assigned to the ICD group and in 370 of 520 patients (71.2%) assigned to the CRT-D group. The time until death appeared to be longer for those assigned to receive a CRT-D than for those assigned to receive an ICD (acceleration factor, 0.80; 95% confidence interval, 0.69 to 0.92; P = 0.002). A secondary-outcome event occurred in 412 patients (77.7%) in the ICD group and in 392 (75.4%) in the CRT-D group. Among patients with a reduced ejection fraction, a widened QRS complex, and NYHA class II or III heart failure, the survival benefit associated with receipt of a CRT-D as compared with ICD appeared to be sustained during a median of nearly 14 years of follow-up. (RAFT ClinicalTrials.gov number, NCT00251251.).

Atrial fibrillation (AF) is prevalent in aging populations; however not all individuals age at the same rate. Instead, individuals of the same chronological age can vary in health status from fit to frail. Our objective was to determine the impacts of age and frailty on atrial function and arrhythmogenesis in mice using a frailty index (FI). Aged mice were more frail and demonstrated longer lasting AF compared to young mice. Consistent with this, aged mice showed longer P wave duration and PR intervals; however, both parameters showed substantial variability suggesting differences in health status among mice of similar chronological age. In agreement with this, P wave duration and PR interval were highly correlated with FI score. High resolution optical mapping of the atria demonstrated reduced conduction velocity and action potential duration in aged hearts that were also graded by FI score. Furthermore, aged mice had increased interstitial fibrosis along with changes in regulators of extracellular matrix remodelling, which also correlated with frailty. These experiments demonstrate that aging results in changes in atrial structure and function that create a substrate for atrial arrhythmias. Importantly, these changes were heterogeneous due to differences in health status, which could be identified using an FI.

In patients with ischemic cardiomyopathy and an implantable cardioverter–defibrillator who had ventricular tachycardia, catheter ablation was associated with a lower rate of death, ventricular tachycardia storm, or ICD shock at 28 months than an escalation in antiarrhythmic drugs. Ventricular tachycardia caused by the scarring that occurs after myocardial infarction carries a substantial risk of death, a risk that is significantly reduced by the placement of an implantable cardioverter–defibrillator (ICD). 1 ICDs are implanted in more than 100,000 patients annually in the United States. Of these patients, 15% are initially treated with concomitant antiarrhythmic drug (AAD) therapy, 2 and up to 38% receive an appropriate shock for ventricular arrhythmia within 5 years. 3 ICDs effectively terminate ventricular tachycardia, but recurrent arrhythmias and ICD shocks may cause impairment in the quality of life, 4 are associated with an increased risk of death, heart failure, . . .

Background There is clear evidence that patients with prior myocardial infarction and a reduced ejection fraction benefit from implantation of a cardioverter-defibrillator (ICD). It is unclear whether this benefit is altered by whether or not revascularization is performed prior to ICD implantation. Methods This was a retrospective cohort study following patients who underwent ICD implantation from 2002 to 2014. Patients with ischemic cardiomyopathy and either primary or secondary prevention ICDs were selected for inclusion. Using the electronic medical record, cardiac catheterization data, revascularization status (percutaneous coronary intervention or coronary bypass surgery) were recorded. The outcomes were mortality and ventricular arrhythmia. Results There were 606 patients included in the analysis. The mean age was 66.3 ± 10.1 years, 11.9% were women, and the mean LVEF was 30.5 ± 12.0, 58.9% had a primary indication for ICD, 82.0% of the cohort had undergone coronary catheterization prior to ICD implantation. In the overall cohort, there were fewer mortality and ventricular arrhythmia events in patients who had undergone prior revascularization. In patients who had an ICD for secondary prevention, revascularization was associated with a decrease in mortality (HR 0.46, 95% CI (0.24, 0.85) p  = 0.015), and a trend towards fewer ventricular arrhythmia (HR 0.62, 95% CI (0.38, 1.00) p  = 0.051). There was no association between death or ventricular arrhythmia with revascularization in patients with primary prevention ICDs. Conclusion Revascularization may be beneficial in preventing recurrent ventricular arrhythmia, and should be considered as adjunctive therapy to ICD implantation to improve cardiovascular outcomes.

Patients with ventricular tachycardia and ischemic cardiomyopathy are at high risk for adverse outcomes. Catheter ablation is commonly used when antiarrhythmic drugs do not suppress ventricular tachycardia. Whether catheter ablation is more effective than antiarrhythmic drugs as a first-line therapy in patients with ventricular tachycardia is uncertain. In an international trial, we randomly assigned in a 1:1 ratio patients with previous myocardial infarction and clinically significant ventricular tachycardia (defined as ventricular tachycardia storm, receipt of appropriate implantable cardioverter-defibrillator [ICD] shock or antitachycardia pacing, or sustained ventricular tachycardia terminated by emergency treatment) to receive antiarrhythmic drug therapy or to undergo catheter ablation. All the patients had an ICD. Catheter ablation was performed within 14 days after randomization; sotalol or amiodarone was administered as antiarrhythmic drug therapy according to prespecified criteria. The primary end point was a composite of death from any cause during follow-up or, more than 14 days after randomization, ventricular tachycardia storm, appropriate ICD shock, or sustained ventricular tachycardia treated by medical intervention. A total of 416 patients were followed for a median of 4.3 years. A primary end-point event occurred in 103 of 203 patients (50.7%) assigned to catheter ablation and in 129 of 213 (60.6%) assigned to drug therapy (hazard ratio, 0.75; 95% confidence interval, 0.58 to 0.97; P = 0.03). Among patients in the catheter ablation group, adverse events within 30 days after the procedure included death in 2 patients (1.0%) and nonfatal adverse events in 23 patients (11.3%). Among the patients assigned to drug therapy, adverse events that were attributed to antiarrhythmic drug treatment included death from pulmonary toxic effects in 1 patient (0.5%) and nonfatal adverse events in 46 patients (21.6%). Among patients with ischemic cardiomyopathy and ventricular tachycardia, an initial strategy of catheter ablation led to a lower risk of a composite primary end-point event than antiarrhythmic drug therapy. (Funded by the Canadian Institutes of Health Research and others; VANISH2 ClinicalTrials.gov number, NCT02830360.).

Ventricular tachycardia (VT) is an abnormal rapid heart rhythm that most commonly occurs in the setting of ventricular scar. In patients with ischaemic cardiomyopathy and VT, the most common mechanism is re-entry of electrical activation through narrow channels of diseased myocardium manifesting on the ECG as a regular sustained wide-complex tachycardia that can present clinically with sudden cardiac death (SCD).Implantable cardioverter-defibrillators (ICDs) are proven to reduce the risk of SCD, but do not prevent VT; they treat it when it occurs. Although antiarrhythmic drug therapy has a long history of use to suppress VT, recurrence rates remain high and adverse effects are not negligible. Significant advances have been made over the past decades in catheter-based techniques for VT suppression. Improvements in both mapping accuracy and ablation efficacy have resulted in recent studies demonstrating improved outcomes of catheter ablation of VT. Patient selection for a procedural approach will be important for achieving optimal clinical outcomes.This review provides a comprehensive overview of randomised trials of catheter ablation for VT as well as contemporary VT ablation techniques, and aims to understand which patients should undergo VT ablation, when is the ideal timing for intervention, and how best to achieve freedom from recurrent VT.

Recurrent ventricular tachycardia (VT) in patients with prior myocardial infarction is associated with adverse quality of life and clinical outcomes, despite the presence of implanted defibrillators (ICDs). Suppression of recurrent VT can be accomplished with antiarrhythmic drug therapy or catheter ablation. The Ventricular Tachycardia Antiarrhythmics or Ablation In Structural Heart Disease 2 (VANISH2) trial is designed to determine whether ablation is superior to antiarrhythmic drug therapy as first line therapy for patients with ischemic cardiomyopathy and VT. The VANISH2 trial enrolls patients with prior myocardial infarction and VT (with one of: ≥1 ICD shock; ≥3 episodes treated with antitachycardia pacing (ATP) and symptoms; ≥5 episodes treated with ATP regardless of symptoms; ≥3 episodes within 24 hours; or sustained VT treated with electrical cardioversion or pharmacologic conversion). Enrolled patients are classified as either sotalol-eligible, or amiodarone-eligible, and then are randomized to either catheter ablation or to that antiarrhythmic drug therapy, with randomization stratified by drug-eligibility group. Drug therapy, catheter ablation procedures and ICD programming are standardized. All patients will be followed until two years after randomization. The primary endpoint is a composite of mortality at any time, appropriate ICD shock after 14 days, VT storm after 14 days, and treated sustained VT below detection of the ICD after 14 days. The outcomes will be analyzed according to the intention-to-treat principle using survival analysis techniques The results of the VANISH2 trial are intended to provide data to support clinical decisions on how to suppress VT for patients with prior myocardial infarction. Clinicaltrials.gov registration NCT02830360.

We have previously developed an automated localization method based on multiple linear regression (MLR) model to estimate the activation origin on a generic left-ventricular (LV) endocardial surface in real time from the 12-lead ECG. The present study sought to investigate whether machine learning—namely, random-forest regression (RFR) and support-vector regression (SVR)—can improve the localization accuracy compared to MLR. For 38 patients the 12-lead ECG was acquired during LV endocardial pacing at 1012 sites with known coordinates exported from an electroanatomic mapping system; each pacing site was then registered to a generic LV endocardial surface subdivided into 16 segments tessellated into 238 triangles. ECGs were reduced to one variable per lead, consisting of 120-ms time integral of the QRS. To compare three regression models, the entire dataset (\\[n=1012\\]) was partitioned at random into a design set with 80% and a test set with the remaining 20% of the entire set, and the localization error—measured as geodesic distance on the generic LV surface—was assessed. Bootstrap method with replacement, using 1000 resampling trials, estimated each model’s error distribution for the left-out sample (\\[n\\simeq 371\\]). In the design set (\\[n=810\\]), the mean accuracy was 8.8, 12.1, and 12.9 mm, respectively for SVR, RVR and MLR. In the test set (\\[n=202\\]), the mean value of the localization error in the SVR model was consistently lower than the other two models, both in comparison with the MLR (11.4 vs. 12.5 mm), and with the RFR (11.4 vs. 12.0 mm); the RFR model was also better than the MLR model for estimating localization accuracy (12.0 vs. 12.5 mm). The bootstrap method with 1,000 trials confirmed that the SVR and RFR models had significantly higher predictive accurate than the MLR in the bootstrap assessment with the left-out sample (SVR vs. MLR (\\[p<0.01\\]), RFR vs. MLR (\\[p < 0.01\\])). The performance comparison of regression models showed that a modest improvement in localization accuracy can be achieved by SVR and RFR models, in comparison with MLR. The “population” coefficients generated by the optimized SVR model from our dataset are superior to the previously-derived “population” coefficients generated by the MLR model and can supersede them to improve the localization of ventricular activation on the generic LV endocardial surface.

BackgroundContact force-sensing technology has become a widely used addition to catheter ablation procedures. Neither the optimal contact force required to achieve adequate lesion formation in the ventricle, nor the impact of left ventricular access route on contact force has been fully clarified.Patients and methodsConsecutive patients (n = 24) with ischemic cardiomyopathy who underwent ablation for scar-related ventricular tachycardia were included in the study. All ablations (n = 25) were performed using irrigated contact force-sensing catheters (Smart Touch, Biosense Webster). Effective lesion formation was defined as electrical unexcitability post ablation at sites which were electrically excitable prior to ablation (unipolar pacing at 10 mA, 2 ms pulse width). We explored the contact force which achieved effective lesion formation and the impact of left ventricular access route (retrograde aortic or transseptal) on the contact force achieved in various segments of the left ventricle. Scar zone was defined as bipolar signal amplitude < 0.5 mV.ResultsAmong 427 ablation points, effective lesion formation was achieved at 201 points (47.1%). Contact force did not predict effective lesion formation in the overall group. However, within the scar zone, mean contact force ≥ 10 g was significantly associated with effective lesion formation [OR 3.21 (1.43, 7.19) P = 0.005]. In the 12-segment model of the left ventricle, the retrograde approach was associated with higher median contact force in the apical anterior segment (31 vs 19 g; P = 0.045) while transseptal approach had higher median force in the basal inferior segment (25 vs 15 g; P = 0.021). In the 4-segment model, the retrograde approach had higher force in the anterior wall (28 vs 16 g; P = 0.004) while the transseptal approach had higher force in the lateral wall (21 vs 18 g; P = 0.032). There was a trend towards higher force in the inferior wall with the transseptal approach, but this was not statistically significant (20 vs 15 g; P = 0.063).ConclusionsIn patients with ischemic cardiomyopathy, a mean contact force of 10 g or more within the scar zone had the best correlation with electrical unexcitability post ablation in our study. The retrograde aortic approach was associated with better contact force over the anterior wall while use of a transseptal approach had better contact force over the lateral wall.