Christopher F. Liu

Complex fractionated electrogram distribution and temporal stability in patients undergoing atrial fibrillation ablation.

Background: Targeting of complex fractionated electrograms (CFEs) has been described as an approach for catheter ablation of atrial fibrillation (AF); however, the distribution and temporal stability of CFE regions remain poorly defined.

Temporal Associations Between Thoracic Volume Overload and Malignant Ventricular Arrhythmias: A Study of Intrathoracic Impedance

Volume Overload and Ventricular Arrhythmias. Background: Acute exacerbations of heart failure (HF) are believed to trigger malignant ventricular arrhythmias, but the temporal association between fluid accumulation and ventricular arrhythmias has not been evaluated in an objective manner. We hypothesized that increased intrathoracic fluid accumulation in patients with HF, as measured by an index of intrathoracic impedance, is associated with an increased risk of ventricular arrhythmias.

Ubiquitous myocardial extensions into the pulmonary artery demonstrated by integrated intracardiac echocardiography and electroanatomic mapping: changing the paradigm of idiopathic right ventricular outflow tract arrhythmias.

Background— Idiopathic ventricular arrhythmias of left bundle branch block inferior axis morphology are usually localized to the right ventricular outflow tract (RVOT), presumably below the pulmonic valve (PV). However, the PV location is usually not confirmed by direct visualization. Methods and Results— Intracardiac echocardiography was used to visualize and tag the PV annulus, which was then integrated with 3-dimensional voltage maps of the RVOT. Distances were measured from the furthest extent of myocardial signal (bipolar voltage ≥1.5 mV) to the PV annulus. This was performed in 24 control patients and 24 prospective patients with RVOT arrhythmias. Myocardial signal beyond the PV was found in 92% of controls and 88% of RVOT arrhythmia patients ( P =1.000). Average myocardial extension was further on the septal side than on the free wall side for control patients (5.6 mm; interquartile range [IQR], 3.6–7.7, versus 1.7 mm; IQR (−)0.1 to (+)4.0; P =0.002) and RVOT arrhythmia patients (5.7 mm; IQR, 2.7–7.7, versus 1.4 mm; IQR, (−)0.8 to (+)4.8; P =0.004). Eleven (46%) RVOT arrhythmia foci were localized beyond the valve in the pulmonary artery (median 8.2 mm above PV; IQR, 6.6–10.3 mm); these locations were confirmed as supravalvular by direct intracardiac echocardiography visualization. Conclusions— Myocardial voltage extension into the pulmonary artery in humans is ubiquitous and can be demonstrated in vivo using 3-dimensional integrated intracardiac echocardiography to localize the PV. These extensions frequently serve as origins of presumed RVOT arrhythmias; intracardiac echocardiography localization of the PV allows reclassification of these as pulmonary arterial arrhythmias.Background—Idiopathic ventricular arrhythmias of left bundle branch block inferior axis morphology are usually localized to the right ventricular outflow tract (RVOT), presumably below the pulmonic valve (PV). However, the PV location is usually not confirmed by direct visualization. Methods and Results—Intracardiac echocardiography was used to visualize and tag the PV annulus, which was then integrated with 3-dimensional voltage maps of the RVOT. Distances were measured from the furthest extent of myocardial signal (bipolar voltage ≥1.5 mV) to the PV annulus. This was performed in 24 control patients and 24 prospective patients with RVOT arrhythmias. Myocardial signal beyond the PV was found in 92% of controls and 88% of RVOT arrhythmia patients (P=1.000). Average myocardial extension was further on the septal side than on the free wall side for control patients (5.6 mm; interquartile range [IQR], 3.6–7.7, versus 1.7 mm; IQR (−)0.1 to (+)4.0; P=0.002) and RVOT arrhythmia patients (5.7 mm; IQR, 2.7–7.7, versus 1.4 mm; IQR, (−)0.8 to (+)4.8; P=0.004). Eleven (46%) RVOT arrhythmia foci were localized beyond the valve in the pulmonary artery (median 8.2 mm above PV; IQR, 6.6–10.3 mm); these locations were confirmed as supravalvular by direct intracardiac echocardiography visualization. Conclusions—Myocardial voltage extension into the pulmonary artery in humans is ubiquitous and can be demonstrated in vivo using 3-dimensional integrated intracardiac echocardiography to localize the PV. These extensions frequently serve as origins of presumed RVOT arrhythmias; intracardiac echocardiography localization of the PV allows reclassification of these as pulmonary arterial arrhythmias.

Differentiation of Papillary Muscle From Fascicular and Mitral Annular Ventricular Arrhythmias in Patients With and Without Structural Heart Disease

Background—Idiopathic left ventricular arrhythmias (VAs) and those caused by structural heart disease can originate from the papillary muscles, fascicles, and mitral annulus. Differentiation of these arrhythmias can be challenging because they present with a right bundle branch block morphology by electrocardiography. We sought to identify clinical, electrocardiographic, and electrophysiological features that distinguish these left VAs in patients with and without structural heart disease. Method and Results—Patients undergoing catheter ablation for papillary muscle, fascicular, or mitral annular VAs were studied. Demographic data and electrocardiographic and electrophysiological findings were analyzed. Fifty-two VAs in 51 patients (32 [63%] male; mean age 61±15 years) with papillary muscle (n=18), fascicular (n=15), and mitral annular (n=19) origins were studied. Patients with papillary muscle VAs were older and had higher prevalence of left ventricular dysfunction (67% versus 13% of fascicular VA patients [P=0.009]) and coronary artery disease (78% versus 37% of mitral annular VA patients [P=0.036]). Papillary muscle VAs were distinguished electrocardiographically from fascicular VAs by longer QRS durations and lower prevalence of r<R′ V1 QRS morphology, and from mitral annular VAs by lower prevalence of positive precordial lead concordance. Using a stepwise electrocardiographic algorithm, the accuracy rates for the diagnosis of papillary muscle VAs, fascicular VAs, and mitral annular VAs were 83%, 87%, and 89%, respectively. Conclusions—Specific electrocardiographic characteristics, including QRS morphology and precordial lead morphology, can help distinguish between papillary muscle, fascicular, and mitral annular VAs.

Reappraisal of Cardiac Magnetic Resonance Imaging in Idiopathic Outflow Tract Arrhythmias

Because of prognostic and therapeutic implications, the distinction between idiopathic right ventricular (RV) outflow tract (iRVOT) and arrhythmogenic RV cardiomyopathy (ARVC) is clinically important. Over the last 2 decades multiple reports have identified RV abnormalities using CMR in patients with idiopathic VT, suggesting a link between these arrhythmias and ARVC. The purpose of this study was to assess for structural abnormalities in patients with iRVOT tachycardia using contemporary cardiac magnetic resonance (CMR) imaging.

Newly detected atrial high rate episodes predict long-term mortality outcomes in patients with permanent pacemakers

BACKGROUND Subclinical atrial high rate episodes (AHREs) detected by implanted devices in patients with no history of atrial fibrillation (AF) have been associated with an increased risk of stroke and systemic embolism. Data regarding the long-term survival of patients with permanent pacemakers and newly detected AHREs are limited. OBJECTIVE This study aimed to assess whether newly detected AHREs in pacemaker patients predict mortality outcomes. METHODS We evaluated 224 patients (mean age 74 ± 12 years; 118 men [53%]) with no history of AF who underwent dual-chamber pacemaker implantation from 2002 through 2004. During follow-up, patients with AHREs of ≥5-minute duration were identified. Mortality data were obtained from the National Death Index. RESULTS Thirty-nine patients (17%) had AHREs of ≥5-minute duration within 6 months of pacemaker implantation. Over a mean follow-up period of 6.6 ± 2.0 years, the rate of all-cause mortality was 29%. In multivariate analysis adjusted for age, sex, and cardiovascular diseases, AHREs were associated with a significant increase in cardiovascular mortality (hazard ratio [HR] 2.80; 95% confidence interval [CI] 1.24-6.31; P = .013) and stroke mortality (HR 9.65; 95% CI 1.56-59.9; P = .015), with a trend toward increased all-cause mortality (HR 1.79; 95% CI 0.98-3.26; P = .059). The subgroup of patients with AHREs of ≥5-minute but <1-day duration still had a significantly increased cardiovascular mortality (HR 3.24; 95% CI 1.37-7.66; P = .007). CONCLUSION AHREs are commonly encountered in pacemaker patients with no history of AF and are independent predictors of cardiovascular mortality.

Mechanisms, predictors, and trends of electrical failure of Riata leads

BACKGROUND Riata and Riata ST implantable cardioverter-defibrillator leads have been shown to be prone to structural and electrical failure. OBJECTIVE To determine predictors, mechanisms, and temporal patterns of Riata/ST lead electrical failure. METHODS All 314 patients who underwent Riata/ST lead implantation at our institution with greater than or equal to 90 days of follow-up were studied. The Kaplan-Meier analysis of lead survival was performed. Results from the returned product analysis of explanted leads with electrical lead failure were recorded. RESULTS During a median follow-up of 4.1 years, the Riata lead electrical failure rate was 6.6%. The rate of externalized conductors among failed leads was 57%. The engineering analysis of 10 explanted leads revealed 5 (50%) leads with electrical failure owing to breach of ethylene tetrafluoroethylene conductor coating. Female gender (hazard ratio 2.7; 95% confidence interval 1.1-6.7; P = .04) and age (hazard ratio 0.95; 95% confidence interval 0.92-0.97; P < .001) were multivariate predictors of lead failure. By using log-log analysis, we noted that the rate of Riata lead failure initially increased exponentially with a power of 2.1 but leads surviving past 4 years had a linear pattern of lead failure with a power of 1.0. CONCLUSIONS Younger age and female gender are independent predictors of Riata lead failure. Loss of integrity of conductor cables with ethylene tetrafluoroethylene coating is an important mode of electrical failure of the Riata lead. Further study of Riata lead failure trends is warranted to guide lead management.

Time course of adenosine-induced pulmonary vein reconnection after isolation: implications for mechanism of dormant conduction.

Background: Adenosine (ADO) has been proposed to reconnect isolated pulmonary veins (PVs) postablation through hyperpolarization of damaged myocytes in an animal model. However, PV reconnection can occur via ADO‐mediated sympathetic activation. We sought to determine the mechanism of ADO‐induced PV reconnection in the clinical setting by characterizing its time course and location in patients undergoing PV isolation.

Differential Effects of Adenosine on Pulmonary Vein Ectopy After Pulmonary Vein Isolation Implications for Arrhythmogenesis

Background— The mechanism of pulmonary vein (PV) triggers of atrial fibrillation remains unclear. We performed adenosine (ADO) testing after PV isolation to characterize spontaneous dissociated PV rhythm and ADO-induced PV ectopy. Methods and Results— Seventy-four patients (61 men; age, 61±10 years) undergoing PV isolation for atrial fibrillation were studied. For each isolated PV, dissociated ectopy was recorded and ADO was administered. After isolation of 270 PVs, 50 PVs with dissociated ectopy were identified. In 42 PVs exhibiting PV rhythm, ADO resulted in PV rhythm suppression in 35 (83%) PVs, with all occurring during ADO-induced bradycardia, and in PV rhythm acceleration in 13 (31%) PVs, with all occurring after resolution of ADO-induced bradycardia. In 11 PVs, both ADO-induced PV rhythm acceleration and suppression were seen. Among 220 electrically silent PVs, ADO induced PV ectopy in 28 (13%) veins. The timing of ADO-induced PV ectopy with respect to ADO effects on heart rate varied. ADO induced PV ectopy during the early phase of ADO effect only in 12 PVs, during the late phase of ADO effect only in 8 PVs, and during both early and late phases of ADO effect in 8 PVs. Conclusions— The mechanism of spontaneous PV rhythm after isolation is likely automaticity, given the close association of ADO effects on PV rhythm with its chronotropic and dromotropic effects. However, ADO can induce PV ectopy in electrically silent PVs in a manner not closely tied to its effects on heart rate and may be because of the activation of autonomic triggers.

Mechanistic Heterogeneity of Junctional Ectopic Tachycardia in Adults

Spontaneous junctional ectopic tachycardia (JET) in adults is rare, and the electrophysiologic mechanism has not been definitively established. Two patients who presented with JET, not associated with cardiac surgery, were evaluated and studied in the electrophysiology laboratory, and electrophysiologic and pharmacologic maneuvers were performed to assess the mechanisms of tachycardia. The junctional tachycardia in Patient 1 manifested characteristics consistent with a triggered mechanism, and was sensitive to adenosine. The junctional tachycardia in Patient 2 manifested characteristics consistent with abnormal automaticity, and was insensitive to adenosine. This is a rare clinical example of abnormal automaticity. These two cases demonstrate that JET may be due to multiple mechanisms, with data consistent with triggered activity and abnormal automaticity.