Identification of 2 Distinct Boundaries Distinguishes Critical From Noncritical Isthmuses in Ablating Atypical Atrial Flutter.

BACKGROUND: Atypical atrial flutters often involve complex circuits. Classic methods of identifying ablation targets, including detailed electroanatomical mapping and entrainment within a well-defined isthmus, may not always be sufficient to allow the critical isthmus to be delineated and ablated, with flutter termination and prevention of reinduction. OBJECTIVES: This study sought a systematic method to classify conduction barriers and isthmuses as critical or noncritical that would improve understanding and ablation success. We also sought a construct unifying single- and dual-loop re-entry. Re-entrant circuits are bounded on 2 sides, although these are not consistently identified. We hypothesized 2 distinct critical boundaries, and a critical isthmus could be consistently defined without requiring entrainment, and ablation connecting these 2 boundaries would terminate tachycardia. METHODS: Activation maps were created electroanatomically. Conduction barriers were classified as noncritical barriers or critical boundaries. Critical boundaries showed sequential activation around the barrier, spanning ≥90% of the cycle length. Noncritical barriers showed nonsequential, parallel, or colliding activation or <90% of the cycle length. Only tissue separating the 2 critical boundaries defined a critical isthmus (CI); all others were considered noncritical. The effect of ablation across a CI was assessed. RESULTS: Complete maps were obtained in 128 cases in 121 patients (28 atypical right atrial, 100 left atrial). In all cases, 2 distinct critical boundaries were identified. Ablation across a CI connecting these critical boundaries terminated tachycardia in 123 of 128 cases (96.1%). Failures were due to inability to achieve block across the isthmus. CONCLUSIONS: Activation mapping of atypical atrial flutter allows consistent identification of 2 critical boundaries. Successful ablation connecting the 2 critical boundaries reliably results in termination of atypical atrial flutter.

The effect of catheter ablation for ventricular arrhythmias originating from the left ventricular papillary muscles on mitral valve function.

BACKGROUND: Ablation of ventricular arrhythmias (VA) originating from the left ventricular (LV) papillary muscles (PM) has the potential to damage the mitral valve apparatus resulting in mitral regurgitation (MR). This study sought to evaluate the effect of radiofrequency (RF) ablation of a PM on MR severity. METHODS: Patients with pre- and postablation transthoracic echocardiograms who underwent PM ablation for treatment of VA were retrospectively identified and compared to similar patients who underwent VA ablation at non-PM sites. MR severity was evaluated pre- and postablation in both groups and graded as none/trace (Grade 0); mild/mild-to-moderate (Grade 1); moderate (Grade 2); moderate-to-severe/severe (Grade 3). RESULTS: A total of 45 and 49 patients were included in the PM and non-PM groups, respectively. There were no significant baseline demographic differences. The PM group had longer RF ablation times (22.3 vs. 13.3 min, p < .01) compared to the non-PM group. Most patients had low-grade MR in both groups at baseline. Change in pre- versus postablation MR within the PM group was not statistically significant by Wilcoxon rank-sum test (Figure 2, p = .46). MR severity following ablation was also evaluated using logistic regression models. The odds ratio for worsening MR in the PM group compared to non-PM was 0.19 (95% confidence interval: 0.008-4.18, p = .29) after adjusting for comorbidities, LV ejection fraction, and LV internal end-diastolic diameter. CONCLUSION: RF ablation of VA originating from PM under intracardiac echocardiography guidance did not result in clinically or statistically significant worsening of MR.

Occurrence, mortality and predictors of complicated cardiac perforation in patients with CRT-D: Based on the National Inpatient Sample registry.

BACKGROUND: Cardiac Resynchronization Therapy Defibrillator (CRT-D) has been one of the most important therapies for patients with cardiomyopathy over the last decades. Cardiac perforation occurs infrequently but can be fatal. The occurrence of cardiac perforation after CRT-D implantation has not been studied well. The aim of study is to investigate the occurrence, mortality and predictors of cardiac perforation in patients receiving CRT-D during the index hospitalization. METHODS: Data were obtained from the National Inpatient Sample, the largest all-player inpatient dataset in the United States. Patients who received CRT-D from 2002 to 2012 were identified using ICD-9 codes. Multivariate analyses were used to identify predictors of cardiac perforation. Complications including in-hospital death and cardiac perforation were identified using ICD-9 codes. RESULTS: A total of 77,827 patients with CRT-D implantation were included into our analysis. After the CRT-D implantation, the in-hospital and rate of cardiac perforation was between 0.24 and 0.48% and had increased significantly (p = 0.02). Although occurrence of cardiac perforation is rare (0.32%), the mortality was 10.6% among those patients with cardiac perforation. In Multivariate analysis identified female as independent risk factors for cardiac perforation (OR: 2.628, 95% CI 1.926-3.585, p < 0.0001). CONCLUSION: Despite rapid progress of the tools and skills for CRT-D implantation, the occurrence of cardiac perforation has not improved. While cardiac perforation is rare, it carries the highest rate of mortality, especially in female patients. Implanting physicians should be familiar with the comorbidities and patient demographics that put them at a higher risk for complications.

Wolff-Parkinson-White, Brugada phenocopy, and flecainide toxicity: All in one patient.

Accessory pathway Wolff-Parkinson-white is sometimes not manifested till later in life, as the conduction properties of AV node become slower, other mechanisms are also possible. Brugada pattern on EKG can be associated with various underlying clinical conditions, such as mechanical compression of RVOT by tumors. It is essential to have high index of suspicion for flecainide toxicity when encountering arrhythmias in patients taking the drug.

The Occurrence of Implantable Cardioverter Defibrillator Therapies After Generator Replacement in Patients Who No Longer Meet Primary Prevention Indications.

INTRODUCTION: At the time of generator replacement, after ICD implantation for primary prevention, many patients may no longer meet implantation criteria. We investigated the occurrence of ICD therapy after generator replacement in patients initially implanted ICD for primary prevention. METHODS: Patients from 3 hospitals undergoing ICD generator replacement, who were initially implanted for primary prevention, were retrospectively evaluated for occurrence of appropriate ICD therapy after generator replacement. Patients were categorized as to whether or not they had appropriate ICD therapy during their first battery life, and by their left ventricular ejection fraction (LVEF) before generator replacement. RESULTS: Data from 168 patients were analyzed, with average follow-up after generator replacement of 41.2 ± 26.5 months. Seventy-six (45.2%) patients had ventricular arrhythmia episodes (>180 beats per minutes) and 63 (37.5%) received appropriate ICD therapy during the first battery life. Among 105 patients without ICD therapy before generator replacement, those with an LVEF ≤35% before ICD replacement had higher occurrence of ICD therapy after generator replacement than patients with an LVEF ≥36%. Patients who no longer met primary prevention ICD indications (no ICD therapy and LVEF ≥36% before generator replacement) showed a lower risk for ICD therapy after generator replacement (11.6% over 5-year follow-up). CONCLUSIONS: In patients without ICD therapy before generator replacement, low LVEF (≤35%) contributed to future ICD therapy. In patients initially undergoing ICD implantation for primary prevention, history of ICD therapy during the first battery life and LVEF should be utilized for risk stratification at the time of generator replacement.

Routine Implant of Biventricular Devices Guided by an Electroanatomic Mapping System - Ready for Prime-Time?

Biventricular devices play an important adjunctive role in the treatment of heart failure. However, biventricular device implantation is associated with significant radiation exposure and a high proportion of non-response to cardiac resynchronization therapy (CRT). The use of electroanatomic mapping (EAM) during biventricular device implantation may help overcome these issues. This article will review the literature on the role of EAM in biventricular device implantation.

Electrophysiology procedures: weighing the factors affecting choice of anesthesia.

Invasive electrophysiologic procedures have evolved and increased in frequency significantly over the past 2 decades. The complexity and nature of the various procedures offered have also changed, and complex ablations for atrial fibrillation and ventricular tachycardia have become commonplace. These procedures often require the services of an anesthesiologist. An understanding of the specific nature and challenges of these procedures may be helpful in planning the optimal anesthetic and patient management. A paired review of these issues has been written from the standpoint of a practicing anesthesiologist. This review is written from the viewpoint of a cardiac electrophysiologist and will focus on the intra-procedural management of patients undergoing both cardiac implantable device implantation as well as catheter-based ablations, with a specific focus on the catheter ablation of atrial fibrillation. Ultimately, the proper management of these patients will facilitate successful procedural outcomes while maintaining a high degree of patient safety.

Predictors of response to cardiac resynchronization therapy in the Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy (MADIT-CRT).

BACKGROUND: We hypothesized that combined assessment of factors that are associated with favorable reverse remodeling after cardiac resynchronization-defibrillator therapy (CRT-D) can be used to predict clinical response to the device. METHODS AND RESULTS: The study population comprised 1761 patients enrolled in the Multicenter Automatic Defibrillator Implantation Trial With Cardiac Resynchronization Therapy (MADIT-CRT). Best-subset regression analysis was performed to identify factors associated with echocardiographic response (defined as percent reduction in left ventricular end-diastolic volume 1 year after CRT-D implantation) and to create a response score. Cox proportional hazards regression analysis was used to evaluate the CRT-D versus defibrillator-only reduction in the risk of heart failure or death by the response score. Seven factors were identified as associated with echocardiographic response to CRT-D and made up the response score (female sex, nonischemic origin, left bundle-branch block, QRS ≥150 milliseconds, prior hospitalization for heart failure, left ventricular end-diastolic volume ≥125 mL/m(2), and left atrial volume <40 mL/m(2)). Multivariate analysis showed a 13% (P<0.001) increase in the clinical benefit of CRT-D per 1-point increment in the response score (range, 0-14) and a significant direct correlation between risk reduction associated with CRT-D and response score quartiles: Patients in the first quartile did not derive a significant reduction in the risk of heart failure or death with CRT-D (hazard ratio=0.87; P=0.52); patients in the second and third quartiles derived 33% (P=0.04) and 36% (P=0.03) risk reductions, respectively; and patients in the upper quartile experienced a 69% (P<0.001) risk reduction (P for trend=0.005). CONCLUSION: Combined assessment of factors associated with reverse remodeling can be used for improved selection of patients for cardiac resynchronization therapy. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT00180271.

Left atrial mechanical responses to right ventricular pacing in heart failure patients: implications for atrial fibrillation.

BACKGROUND: RV pacing (RVP), even with preserved atrioventricular (AV) synchrony, may lead to left atrial (LA) enlargement and atrial fibrillation. However, inciting events are unknown. We hypothesized that RVP acutely impairs LA function by mechanisms affecting atrial contraction and/or ventricular diastole. METHODS: LA function in ICD patients (n = 31, LVEF ≤ 40%) and controls (n = 14, LVEF > 50%) was contrasted between intrinsic conduction versus RVP during asynchronous (ICD, n = 17, control, n = 7), and synchronous (ICD, n = 14, control, n = 14) pacing at long (LAVd, 107 ±16 ms) and short (SAVd, 31 ± 5 ms) AV delays. LA maximal volume (LA(Max)), minimal volume (LA(Min)), and emptying fraction {LA(EmF) = (LA(Max) -LA(Min))/LA(Max)} were measured echocardiographically. Six-segment mean mitral annular tissue doppler E' (global E') assessed diastolic recoil during baseline and LAVd. RESULTS: In the ICD group, LA(Min) increased by 42% (P < 0.0009) during VVI, by 31% (P = 0.0002) during SAVd, and by 17% (P < 0.0007) during LAVd. LA(EmF) decreased by 44% (P < 0.0008), 27% (P < 0.0001), and by 15% (P = 0.003) during VVI, SAVd, and LAVd respectively. LA(Max) was unaltered. Global E' was reduced by 12%. In control, LA(Min) increased and LA(EmF) decreased significantly during VVI (82 and 58%) and SAVd (46 and 41%), but not during LAVd. CONCLUSION: In patients with LV dysfunction, RVP acutely impaired LA emptying, and increased minimal volume, most prominently when atrial contraction was impeded (VVI, DDD-SAVd) but also when completed (DDD-LAVd), indicating impaired diastolic recoil as an important mechanism. When LV function was normal, similar changes were present when atrial filling is impeded (VVI, SAVd), but not when completed (LAVd).

Pericardial fat is independently associated with human atrial fibrillation.

OBJECTIVES: The purpose of this study was to investigate the association between atrial fibrillation (AF) and pericardial fat. BACKGROUND: Pericardial fat is visceral adipose tissue that possesses inflammatory properties. Inflammation and obesity are associated with AF, but the relationship between AF and pericardial fat is unknown. METHODS: Pericardial fat volume was measured using computed tomography in 273 patients: 76 patients in sinus rhythm, 126 patients with paroxysmal AF, and 71 patients with persistent AF. RESULTS: Patients with AF had significantly more pericardial fat compared with patients in sinus rhythm (101.6 +/- 44.1 ml vs. 76.1 +/- 36.3 ml, p < 0.001). Pericardial fat volume was significantly larger in paroxysmal AF compared with the sinus rhythm group (93.9 +/- 39.1 ml vs. 76.1 +/- 36.3 ml, p = 0.02). Persistent AF patients had a significantly larger pericardial fat volume compared with paroxysmal AF (115.4 +/- 49.3 ml vs. 93.9 +/- 39.1 ml, p = 0.001). Pericardial fat volume was associated with paroxysmal AF (odds ratio: 1.11; 95% confidence interval: 1.01 to 1.23, p = 0.04) and persistent AF (odds ratio: 1.18, 95% confidence interval: 1.05 to 1.33, p = 0.004), and this association was completely independent of age, hypertension, sex, left atrial enlargement, valvular heart disease, left ventricular ejection fraction, diabetes mellitus, and body mass index. CONCLUSIONS: Pericardial fat volume is highly associated with paroxysmal and persistent AF independent of traditional risk factors including left atrial enlargement. Whether pericardial fat plays a role in the pathogenesis of AF requires future investigation.

Electroanatomic mapping of postpacing intervals clarifies the complete active circuit and variants in atrial flutter.

BACKGROUND: Typical atrial flutter is characterized by cavotricuspid isthmus dependence and activation sequentially around the tricuspid annulus (TA), usually counterclockwise. However, analysis of the upper portion of the annulus by postpacing interval after entrainment sometimes suggests it is outside the circuit. Details on the true active circuit are limited, particularly in the upper portions. OBJECTIVE: The purpose of this study was to define the full active circuit in atrial flutter. METHODS: In 26 patients with isthmus-dependent atrial flutter, we created detailed electroanatomic maps of postpacing intervals throughout the entire right atrium. Postpacing intervals within 20 ms of the flutter cycle length were defined as within the circuit. RESULTS: Creating postpacing interval maps allowed characterization of the full active circuit in all patients, and revealed significant variations despite similar counterclockwise or clockwise patterns with activation mapping. In 8, the active circuit was solely around the TA. In 14, an oblique course between the anterior and posterior borders was found, with the upper circuit off the annulus, posterior to the right atrial appendage base. Of these, 8 coursed anterior to the SVC, 5 behind the SVC and 1 bifurcated the SVC. In 4 others, bifurcation of the upper circuit was seen around the right atrial appendage (n = 3), or around the combined right atrial appendage-superior vena cava (n = 1). CONCLUSION: Despite similar activation around the TA, creating electroanatomic postpacing interval maps distinguishes the active flutter circuit from passively activated myocardium. Significant variability exists in the active circuit, with only a minority around the TA. Most commonly, the circuit courses not around a single barrier but obliquely between anterior and posterior borders.

Prospective study of cardiac sarcoid mimicking arrhythmogenic right ventricular dysplasia.

INTRODUCTION: Case studies indicate that cardiac sarcoid may mimic the clinical presentation of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C); however, the incidence and clinical predictors to diagnose cardiac sarcoid in patients who meet International Task Force criteria for ARVD/C are unknown. METHODS AND RESULTS: Patients referred for evaluation of left bundle branch block (LBBB)-type ventricular arrhythmia and suspected ARVD/C were prospectively evaluated by a standardized protocol including right ventricle (RV) cineangiography-guided myocardial biopsy. Sixteen patients had definite ARVD/C and four had probable ARVD/C. Three patients were found to have noncaseating granulomas on biopsy consistent with sarcoid. Age, systemic symptoms, findings on chest X-ray or magnetic resonance imaging (MRI), type of ventricular arrhythmia, RV function, ECG abnormalities, and the presence or duration of late potentials did not discriminate between sarcoid and ARVD/C. Left ventricular dysfunction (ejection fraction <50%) was present in 3/3 patients with cardiac sarcoid, but only 2/17 remaining patients with definite or probable ARVD/C (P = 0.01). CONCLUSIONS: In this prospective study of consecutive patients with suspected ARVD/C evaluated by a standard protocol including biopsy, the incidence of cardiac sarcoid was surprisingly high (15%). Clinical features, with the exception of left ventricular dysfunction and histological findings, did not discriminate between the two entities.

A blended sensor restores chronotropic response more favorably than an accelerometer alone in pacemaker patients: the LIFE study results.

BACKGROUND: Adaptive rate sensors used in permanent pacemakers incorporate an accelerometer (XL) to increase heart rate with activity. Limited data exists regarding the relative benefit of a blended sensor (BS) (XL and minute ventilation) versus XL alone in restoring chronotropic response (CR) in chronotropically incompetent (CI) patients. METHODS: One thousand five hundred thirty-eight patients from the limiting chronotropic incompetence for pacemaker recipients (LIFE) study were implanted with a pacemaker and 1,256 patients had data collected at 1 month. Patients performed a treadmill test 1-month postimplant while programmed in nonrate responsive mode (DDD-60) to determine CI. Only patients who completed at least three exercise stages and achieved a peak perceived exertion >or=16 were included in the analyses. The metabolic chronotropic relationship (MCR) slope was used to evaluate CR in 547 patients. Patients were randomized to XL or BS with a conservative fixed rate response factor (XL = 8, MV = 4). CI patients performed a follow-up 6-month treadmill test. RESULTS: CI prevalence in this patient population (n = 547) was 34%. No differences in baseline characteristics existed between groups. Although both groups showed significant within-group improvements in MCR slope from 1 to 6 months (both P < 0.001), the BS group had a significantly higher MCR slope at 6 months compared to the XL group (P = 0.011). Improvement in quality of life (QOL) did not differ between groups. CONCLUSIONS: In this general pacemaker population with CI, a BS programmed empirically restores CR more favorably than an XL sensor programmed nominally. Further studies are needed to determine if individual sensor optimization would lead to improvement in functional capacity, higher MCR slopes, and QOL.

Endothelial dysfunction in heart failure identifies responders to cardiac resynchronization therapy.

BACKGROUND: The presence of endothelial dysfunction is associated with increased heart failure mortality. Cardiac resynchronization therapy (CRT) improves heart failure outcomes; however, current guidelines do not adequately identify responders to CRT. OBJECTIVE: The purpose of this study was to determine whether endothelial dysfunction can predict response to CRT. METHODS: Brachial artery flow-mediated dilation, a measure of endothelial function, was measured at baseline preimplant and 90 days postimplant in 33 patients undergoing CRT (age 64.2 +/- 16.8 years, left ventricular ejection fraction [LVEF] 25% +/- 9%, QRS duration 158 +/- 25 ms, New York Heart Association class III-IV). RESULTS: Of the 33 patients, 19 (58%) were responders to CRT. Baseline flow-mediated dilation was 4.6% +/- 4.5% in responders and 8.6% +/- 4.2% in nonresponders (P <.01). After 90 days of CRT, responders had significant improvement in LVEF (23% +/- 8% to 30% +/- 9%, P = .03), 6-minute walk distance (756 +/- 213 feet to 1,089 +/- 242 feet, P = .04), and quality of life (52 +/- 22 to 31 +/- 28, P <.005), whereas nonresponders did not show improvement in these measures. The presence of baseline endothelial dysfunction correlated with impaired baseline functional capacity (r = 0.39, P = .03), and improvement in flow-mediated dilation correlated with improvement in 6-minute walk distance (r = 0.34, P = .05). Logistic regression analysis showed that every 1% reduction in baseline flow-mediated dilation correlated with an approximately 5% increased likelihood of response to CRT. The predictive value of baseline endothelial dysfunction was independent of QRS duration, LVEF, or dyssynchrony and provided additive prognostic value. CONCLUSION: The presence of endothelial dysfunction independently identifies CRT responders and provides additive prognostic value for predicting response over current criteria. Addition of endothelial function assessment to current selection criteria may improve the ability to identify CRT responders.

Prospective study of atrial fibrillation termination during ablation guided by automated detection of fractionated electrograms.

INTRODUCTION: Complex fractionated atrial electrograms (CFAE) may identify critical sites for perpetuation of atrial fibrillation (AF) and provide useful targets for ablation. Current assessment of CFAE is subjective; automated detection algorithms may improve reproducibility, but their utility in guiding ablation has not been tested. METHODS AND RESULTS: In 67 patients presenting for initial AF ablation (42 paroxysmal, 25 persistent), LA and CS mapping were performed during induced or spontaneous AF. CFAE were identified by an online automated computer algorithm and displayed on electroanatomical maps. A mean of 28 +/- 18 sites/patient were identified (20 +/- 13% of mapped sites), and were more frequent during persistent AF. CFAE occurred most commonly within the CS, on the atrial septum, and around the pulmonary veins. Ablation initially targeting CFAE terminated AF in 88% of paroxysmal AF, but only 20% of persistent AF (P < 0.001). Subsequently, additional ablation was performed in all patients (PV isolation for paroxysmal AF, PV isolation + mitral and roof lines for persistent AF). Minimum follow-up was 1 year. One-year freedom from recurrent atrial arrhythmias without antiarrhythmic drug therapy after a single procedure was 90% for paroxysmal AF, and 68% for persistent AF. CONCLUSIONS: Ablation guided by automated detection of CFAE proved feasible, and was associated with a high AF termination rate in paroxysmal, but not persistent AF. As an adjunct to conventional techniques, it was associated with excellent long-term single procedure outcomes in both groups. Criteria for identifying optimal CFAE sites for ablation, and selection of patients most likely to benefit, require additional study.