Brian P. Betensky

The V2 Transition Ratio: A New Electrocardiographic Criterion for Distinguishing Left From Right Ventricular Outflow Tract Tachycardia Origin

2011;57;2255-2262 J. Am. Coll. Cardiol. David Lin, Michael P. Riley, and Edward P. Gerstenfeld Fermin C. Garcia, Sanjay Dixit, David J. Callans, Joshua M. Cooper, Rupa Bala, Brian P. Betensky, Robert E. Park, Francis E. Marchlinski, Matthew D. Hutchinson, Origin Distinguishing Left From Right Ventricular Outflow Tract Tachycardia Transition Ratio: A New Electrocardiographic Criterion for 2 The V This information is current as of May 29, 2011 http://content.onlinejacc.org/cgi/content/full/57/22/2255 located on the World Wide Web at: The online version of this article, along with updated information and services, isOBJECTIVES We sought to develop electrocardiography (ECG) criteria for distinguishing left ventricular outflow tract (LVOT) from right ventricular outflow tract (RVOT) origin in patients with idiopathic outflow tract ventricular tachycardia (OTVT) and lead V(3) R/S transition. BACKGROUND Several ECG criteria have been proposed for differentiating left from right OTVT origin; ventricular tachycardias (VTs) with left bundle branch block and V(3) transition remain a challenge. METHODS We analyzed the surface ECG pattern of patients with OTVT with a precordial transition in lead V(3) who underwent successful catheter ablation. Sinus and VT QRS morphologies were measured in limb and precordial leads with electronic calipers. The V(2) and V(3) transition ratios were calculated by computing the percentage R-wave during VT (R/R+S)(VT) divided by the percentage R-wave in sinus rhythm (R/R+S)(SR). RESULTS We retrospectively analyzed ECGs from 40 patients (mean age 44 ± 14 years, 21 female) with outflow tract premature ventricular contractions (PVCs)/VT. Patients with structural heart disease, paced rhythms, and bundle branch block during sinus rhythm were excluded. The V(2) transition ratio was significantly greater for LVOT PVCs compared with RVOT PVCs (1.27 ± 0.60 vs. 0.23 ± 0.16; p < 0.001) and was the only independent predictor of LVOT origin. In 21 prospective cases, a V(2) transition ratio ≥0.60 predicted an LVOT origin with 91% accuracy. A PVC precordial transition occurring later than the sinus rhythm transition excluded an LVOT origin with 100% accuracy. CONCLUSIONS The V(2) transition ratio is a novel electrocardiographic measure that reliably distinguishes LVOT from RVOT origin in patients with lead V(3) precordial transition. This measure might be useful for counseling patients and planning an ablation strategy.

Clinical ResearchHeart Rhythm DisorderThe V2 Transition Ratio: A New Electrocardiographic Criterion for Distinguishing Left From Right Ventricular Outflow Tract Tachycardia Origin

2011;57;2255-2262 J. Am. Coll. Cardiol. David Lin, Michael P. Riley, and Edward P. Gerstenfeld Fermin C. Garcia, Sanjay Dixit, David J. Callans, Joshua M. Cooper, Rupa Bala, Brian P. Betensky, Robert E. Park, Francis E. Marchlinski, Matthew D. Hutchinson, Origin Distinguishing Left From Right Ventricular Outflow Tract Tachycardia Transition Ratio: A New Electrocardiographic Criterion for 2 The V This information is current as of May 29, 2011 http://content.onlinejacc.org/cgi/content/full/57/22/2255 located on the World Wide Web at: The online version of this article, along with updated information and services, isOBJECTIVES We sought to develop electrocardiography (ECG) criteria for distinguishing left ventricular outflow tract (LVOT) from right ventricular outflow tract (RVOT) origin in patients with idiopathic outflow tract ventricular tachycardia (OTVT) and lead V(3) R/S transition. BACKGROUND Several ECG criteria have been proposed for differentiating left from right OTVT origin; ventricular tachycardias (VTs) with left bundle branch block and V(3) transition remain a challenge. METHODS We analyzed the surface ECG pattern of patients with OTVT with a precordial transition in lead V(3) who underwent successful catheter ablation. Sinus and VT QRS morphologies were measured in limb and precordial leads with electronic calipers. The V(2) and V(3) transition ratios were calculated by computing the percentage R-wave during VT (R/R+S)(VT) divided by the percentage R-wave in sinus rhythm (R/R+S)(SR). RESULTS We retrospectively analyzed ECGs from 40 patients (mean age 44 ± 14 years, 21 female) with outflow tract premature ventricular contractions (PVCs)/VT. Patients with structural heart disease, paced rhythms, and bundle branch block during sinus rhythm were excluded. The V(2) transition ratio was significantly greater for LVOT PVCs compared with RVOT PVCs (1.27 ± 0.60 vs. 0.23 ± 0.16; p < 0.001) and was the only independent predictor of LVOT origin. In 21 prospective cases, a V(2) transition ratio ≥0.60 predicted an LVOT origin with 91% accuracy. A PVC precordial transition occurring later than the sinus rhythm transition excluded an LVOT origin with 100% accuracy. CONCLUSIONS The V(2) transition ratio is a novel electrocardiographic measure that reliably distinguishes LVOT from RVOT origin in patients with lead V(3) precordial transition. This measure might be useful for counseling patients and planning an ablation strategy.

Mecanismos de las arritmias cardiacas

Cardiac arrhythmias are prevalent among humans across all age ranges and may occur in the setting of underlying heart disease as well as in structurally normal hearts. While arrhythmias are widely varied in their clinical presentations, they possess shared electrophysiologic properties at the cellular level. The 3 main mechanisms responsible for cardiac arrhythmias are automaticity, triggered activity, and reentry. Although identifying the specific mechanism may at times be challenging for the clinician and require invasive electrophysiologic study, differentiating and understanding the underlying mechanism may be critical to the development of an appropriate diagnosis and treatment strategy.

Layered activation of epicardial scar in arrhythmogenic right ventricular dysplasia: possible substrate for confined epicardial circuits.

Background— Ventricular tachycardia ablation in arrhythmogenic right ventricular dysplasia (ARVD) is more successful when including epicardial ablation. Scarring may cause independent, layered epicardial activation and promote epicardially confined ventricular tachycardia circuits. We aimed to characterize transmural right ventricular activation in ARVD patients and to compare this with reference patients without structural heart disease. Methods and Results— Eighteen ARVD patients underwent detailed endocardial and epicardial sinus rhythm electroanatomic mapping. Bipolar activation was annotated at the sharpest intrinsic deflection including late potentials and compared with 6 patients with normal hearts. Total scar area was larger on the epicardium (97±78 cm2) than the endocardium (57±44 cm2; P =0.04), with significantly more isolated potentials. Total epicardial activation time was longer than endocardial (172±54 versus 99±27 ms; P <0.01), and both were longer than in reference patients. Earliest endocardial site was the right ventricular anteroseptum in 17 of 18 ARVD patients versus 5 of 6 controls ( P =0.446), and latest endocardial site was in the outflow tract in 13 of 18 ARVD patients versus 4 of 6 controls and tricuspid annulus in 5 of 18 ARVD patients versus 2 of 6 controls ( P =1.00). In reference patients, epicardial activation directly opposite endocardial sites occurred in 5.2±1.9 ms, suggesting direct transmural activation. In contrast, ARVD patients had major activation delay to the epicardium with laminar central scar activation from the scar border, not by direct transmural spread from the endocardium. Conclusions— Transmural right ventricular activation is modified by ARVD scarring with a delayed epicardial activation sequence suggestive of independent rather than direct transmural activation. This may predispose ventricular tachycardia circuits contained entirely within the epicardium in ARVD and explains observations on the need for direct epicardial ablation to eliminate ventricular tachycardia.Background— Ventricular tachycardia ablation in arrhythmogenic right ventricular dysplasia (ARVD) is more successful when including epicardial ablation. Scarring may cause independent, layered epicardial activation and promote epicardially confined ventricular tachycardia circuits. We aimed to characterize transmural right ventricular activation in ARVD patients and to compare this with reference patients without structural heart disease. Methods and Results— Eighteen ARVD patients underwent detailed endocardial and epicardial sinus rhythm electroanatomic mapping. Bipolar activation was annotated at the sharpest intrinsic deflection including late potentials and compared with 6 patients with normal hearts. Total scar area was larger on the epicardium (97±78 cm2) than the endocardium (57±44 cm2; P=0.04), with significantly more isolated potentials. Total epicardial activation time was longer than endocardial (172±54 versus 99±27 ms; P<0.01), and both were longer than in reference patients. Earliest endocardial site was the right ventricular anteroseptum in 17 of 18 ARVD patients versus 5 of 6 controls (P=0.446), and latest endocardial site was in the outflow tract in 13 of 18 ARVD patients versus 4 of 6 controls and tricuspid annulus in 5 of 18 ARVD patients versus 2 of 6 controls (P=1.00). In reference patients, epicardial activation directly opposite endocardial sites occurred in 5.2±1.9 ms, suggesting direct transmural activation. In contrast, ARVD patients had major activation delay to the epicardium with laminar central scar activation from the scar border, not by direct transmural spread from the endocardium. Conclusions— Transmural right ventricular activation is modified by ARVD scarring with a delayed epicardial activation sequence suggestive of independent rather than direct transmural activation. This may predispose ventricular tachycardia circuits contained entirely within the epicardium in ARVD and explains observations on the need for direct epicardial ablation to eliminate ventricular tachycardia.

Characterization of Trans-septal Activation During Septal Pacing Criteria for Identification of Intramural Ventricular Tachycardia Substrate in Nonischemic Cardiomyopathy

Background— Identification of intramural basal-septal ventricular tachycardia (VT) substrate is challenging in nonischemic cardiomyopathy. We sought to (1) characterize normal/abnormal trans-septal right ventricular (RV) to left ventricular activation; (2) assess the effect of opposite RV pacing on left ventricular septal bipolar electrograms (EGMs); and (3) establish criteria for the identification of intramural septal VT substrate. Methods and Results— Endocardial activation mapping and local EGM assessment of the left interventricular septum was performed during RV basal septal pacing in 40 patients undergoing VT ablation with no evidence of septal scar (group 1, n=14) and with septal scar (group 2, n=26) defined by low septal unipolar voltage ( 40 ms (sensitivity 60%, specificity 100%; P 95 ms during pacing (sensitivity 22%, specificity 91%; P <0.001) identified septal scar (13/26 pts). Conclusions— In patients with nonischemic cardiomyopathy, VT and septal scar, delayed transmural conduction time (>40 ms) and fractionated, late, split, and wide (>95 ms) bipolar EGMs during RV basal pacing identify intramural VT substrate. In select cases, the basal septum appears compartmentalized as the stimulated wavefront is rerouted to the scar border.Background—Identification of intramural basal-septal ventricular tachycardia (VT) substrate is challenging in nonischemic cardiomyopathy. We sought to (1) characterize normal/abnormal trans-septal right ventricular (RV) to left ventricular activation; (2) assess the effect of opposite RV pacing on left ventricular septal bipolar electrograms (EGMs); and (3) establish criteria for the identification of intramural septal VT substrate. Methods and Results—Endocardial activation mapping and local EGM assessment of the left interventricular septum was performed during RV basal septal pacing in 40 patients undergoing VT ablation with no evidence of septal scar (group 1, n=14) and with septal scar (group 2, n=26) defined by low septal unipolar voltage (<8.3 mV) and delayed enhancement on cardiac MRI with/without abnormal bipolar voltage (<1.5 mV) in sinus rhythm. Left ventricular trans-septal activation time was prolonged in Group 2 compared with Group 1 (55.3±33.0 versus 25.7±8.8 ms; P=0.003). In 6 group 2 patients, left ventricular septal breakthrough was displaced to the scar border. During RV pacing, group 2 had fractionated (8.8%), late (2.8%), and split (5.7%) EGMs not seen in group 1. Trans-septal activation >40 ms (sensitivity 60%, specificity 100%; P<0.001) and EGM duration >95 ms during pacing (sensitivity 22%, specificity 91%; P<0.001) identified septal scar (13/26 pts). Conclusions—In patients with nonischemic cardiomyopathy, VT and septal scar, delayed transmural conduction time (>40 ms) and fractionated, late, split, and wide (>95 ms) bipolar EGMs during RV basal pacing identify intramural VT substrate. In select cases, the basal septum appears compartmentalized as the stimulated wavefront is rerouted to the scar border.

Use of a Novel Endoscopic Catheter for Direct Visualization and Ablation in an Ovine Model of Chronic Myocardial Infarction

Background— Defining the arrhythmogenic substrate is essential for successful ablation of scar-related ventricular tachycardia. The visual characteristics of endocardial ischemic scar have not been described in vivo. The goal of this study was (1) to quantify the visual characteristics of normal tissue, scar border zone, and dense scar in vivo with the use of a novel endoscopic catheter that allows direct endocardial visualization and (2) to correlate visual attributes of myocardial scar with bipolar voltage. Methods and Results— Percutaneous transient balloon occlusion (150 minutes) of the mid left anterior descending coronary artery was performed in an ovine model. Animals survived for 41.5±0.7 days. Detailed bipolar voltage maps of the left ventricle were acquired with the use of NavX. Video snapshots of the endocardium were acquired at sites distributed throughout the left ventricle. Visual tissue characteristics of normal (>1.5 mV), border (0.5–1.5 mV), and dense scar (<0.5 mV) were quantified with the use of image processing. Radiofrequency lesions (10–20 W, 30 seconds) were delivered under direct visualization. Mean white-threshold pixel area was lowest in normal tissue (189 969±41 478 pixels2), intermediate in scar border zone (255 979±36 016 pixels2), and highest in dense scar (324 452±30 152 pixels2; P<0.0001 for all pairwise comparisons). Tissue whiteness, characteristic of scar, was inversely correlated with bipolar voltage (P<0.0001). During radiofrequency lesions, there was a significant increase in white-thresholded pixel area of the visual field after ablation (average increase, 85 381±52 618 pixels2; P<0.001). Conclusions— Visual characteristics of chronic infarct scar in vivo observed with the use of a novel endoscopic catheter correlate with bipolar electrogram voltage. Irrigated radiofrequency lesions in normal endocardial tissue and postinfarction zone can be visualized and quantified with the use of image processing. This technology shows promise for visually based delivery of radiofrequency lesions for the treatment of scar-based ventricular tachycardia.

Sudden cardiac death in patients with nonischemic cardiomyopathy.

Sudden cardiac death (SCD) is an important cause of mortality worldwide. Although SCD is most often associated with coronary heart disease, the risk of SCD in patients without ischemic heart disease is well-established. Nonischemic cardiomyopathies, including idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy represent three unique disease entities that have been shown to be highly associated with SCD and ventricular arrhythmias. A variety of risk stratification tools have been investigated, although the optimal strategy remains unknown. Identification of the arrhythmogenic substrate and treatment of ventricular arrhythmias in these subgroups can be challenging. Herein, we aim to discuss the current understanding of the anatomic and electrophysiologic substrate underlying ventricular arrhythmias and highlight features that may be associated with a higher risk of SCD in these 3 conditions.

Unequal Blood Pressures: A Manifestation of Subclavian Steal

A 75-year-old African American man with a history of renal cell carcinoma, atrial flutter status post-radiofrequency catheter ablation, abdominal aortic aneurysm, hyperlipidemia, hypertension, and tobacco dependence presented for routine care. The patient reported frequent episodes of lightheadedness lasting several seconds, associated with blurry vision, shortness of breath, and nausea. Symptoms initially began several years ago with 2 episodes of true syncope, although he denied loss of consciousness with the current events. His symptoms were provoked by driving with his left arm and exacerbated by neck extension. He denied arm pain or weakness. Medications included a statin, an angiotensin-receptor blocker, a beta-blocker, and an aspirin. Physical examination was notable for a blood pressure of 146/90 mm Hg in the right arm and unmeasurable blood pressure in the left arm. The left arm examination was remarkable for cool temperature and nonpalpable axillary, brachial, or radial pulses. Pulse examination on the right was normal. A 12-lead electrocardiogram demonstrated normal sinus rhythm with anteroseptal Q waves, unchanged from prior studies. His complete blood count and comprehensive metabolic panel were within normal limits. His cholesterol panel showed total cholesterol 180 mg/dL, triglycerides 179 mg/dL, low-density lipoprotein 114 mg/dL, and high-density lipoprotein 30 mg/dL. Arterial duplex ultrasound of the upper extremities revealed a patent distal left subclavian artery, with monophasic waveform and a velocity of 15 cm/s, suggestive of proximal left subclavian artery stenosis. The right subclavian artery was patent with triphasic waveforms and antegrade flow. Sagittal T1-weighted images on magnetic resonance imaging of the head and neck revealed moderate to severe stenosis of the left internal carotid artery and nonvisualization of the left vertebral artery on 2-dimensional time of flight imaging (Figure 1A). Angiography was diagnostic for subclavian steal, evidenced by total occlusion of the proximal left subclavian artery with

Long-term outcome of surgical cryoablation for refractory ventricular tachycardia in patients with non-ischemic cardiomyopathy

Aims Limited data exist on the long-term outcome of patients (pts) with non-ischemic cardiomyopathy (NICM) and ventricular tachycardia (VT) refractory to conventional therapies undergoing surgical ablation (SA). We aimed to investigate the long-term survival and VT recurrence in NICM pts with VT refractory to radiofrequency catheter ablation (RFCA) who underwent SA. Methods and results Consecutive pts with NICM and VT refractory to RFCA who underwent SA were included. VT substrate was characterized in the electrophysiology lab and targeted by RFCA. During SA, previous RFCA lesions/scars were identified and targeted with cryoablation (CA; 3 min/lesion; target -150 °C). Follow-up comprised office visits, ICD interrogations and the social security death index. Twenty consecutive patients with NICM who underwent SA (age 53 ± 16 years, 18 males, LVEF 41 ± 20%; dilated CM = 9, arrhythmogenic right ventricular CM = 3, hypertrophic CM = 2, valvular CM = 4, and mixed CM = 2) were studied. Percutaneous mapping/ablation in the electrophysiology lab was performed in 18 and 2 pts had primary SA. During surgery, 4.9 ± 4.0 CA lesions/pt were delivered to the endocardium (2) and epicardium (11) or both (7). VT-free survival was 72.5% at 1 year and over 43 ± 31 months (mos) (range 1-83mos), there was only one arrhythmia-related death. There was a significant reduction in ICD shocks in the 3-mos preceding SA vs. the entire follow-up period (6.6 ± 4.9 vs. 2.3 ± 4.3 shocks/pt, P = 0.001). Conclusion In select pts with NICM and VT refractory to RFCA, SA guided by pre-operative electrophysiological mapping and ablation may be a therapeutic option.

Distinct Electrocardiographic Form of Idiopathic Ventricular Arrhythmia Originating From the Left Bundle Branch.

Most premature ventricular contractions (PVCs) arise from the right or left ventricular outflow tract. Some VPCs originate near the His‐bundle region. However, there remains a paucity of information on PVCs originating directly from the cardiac conduction system. We describe 2 cases with idiopathic frequent PVCs that were mapped directly to the left bundle branch itself. We also provide an anatomic‐based mapping and ablation approach for management of these uncommon and challenging arrhythmias. In both cases we were able to either eliminate or significantly suppress the ectopic source by applying radiofrequency at this location without causing any significant impairment of the atrioventricular conduction.