Edward P. Gerstenfeld
University of California, San Francisco
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Edward P. Gerstenfeld.
Circulation | 2004
Sorin Lazar; Sanjay Dixit; Francis E. Marchlinski; David J. Callans; Edward P. Gerstenfeld
Background—Recent studies have demonstrated spatiotemporal organization in atrial fibrillation (AF), with a left-to-right atrial frequency gradient during AF in isolated sheep hearts. We hypothesized that human AF would also manifest a left-to-right atrial frequency gradient. Methods and Results—Thirty-one patients aged 56.7±10.5 years with a history of paroxysmal or persistent (>1 month) AF were included. Recordings were made at each pulmonary vein (PV) ostium and simultaneously from the coronary sinus (CS) and posterior right atrium (RA) during AF. Sequential fast Fourier transforms (FFTs) were performed. FFT profiles were analyzed to determine the dominant frequency (DF). There were 18 patients with paroxysmal AF and 13 with persistent AF. In the paroxysmal group, there was a significant left-to-right atrial DF gradient, with DF highest at the PV/left atrial (LA) junction, intermediate at the CS, and lowest in the RA (6.2±0.8, 5.5±0.7, and 5.1±0.6 Hz, respectively; P<0.001). There were no patients in whom DF was greater at the RA than the PV/LA junction. In the persistent group, there was no significant difference between DF recorded from the LA/PV junction, CS, and RA (6.1±0.7, 5.8±0.6, and 5.8±0.6 Hz, respectively; P=NS). Conclusions—In humans with paroxysmal AF, DFs are highest at the PV/LA junction, intermediate in the CS, and slowest in the posterior RA. These findings agree with animal models that suggest that the posterior LA may play an important role in maintaining paroxysmal AF. The role of the posterior LA in persistent AF requires further study.
Journal of the American College of Cardiology | 2009
Oscar Cano; Mathew D. Hutchinson; David Lin; Fermin C. Garcia; Erica S. Zado; Rupa Bala; Michael P. Riley; Joshua M. Cooper; Sanjay Dixit; Edward P. Gerstenfeld; David J. Callans; Francis E. Marchlinski
OBJECTIVES The aim of the study was to define the epicardial substrate and ablation outcome in patients with left ventricular nonischemic cardiomyopathy (NICM) and suspected epicardial ventricular tachycardia (VT). BACKGROUND Ventricular tachycardia in NICM often originates from the epicardium. METHODS Twenty-two patients with NICM underwent detailed endocardial and epicardial bipolar voltage maps and VT ablation for suspected epicardial VT. Eight patients with normal hearts and idiopathic VT served to define normal epicardial electrograms. Low-voltage regions were also assessed for wide (>80 ms), split, or late electrograms. RESULTS Normal epicardial bipolar voltage was identified as >1.0 mV on the basis of the reference population. Confluent low-voltage areas were present in 18 epicardial (82%) and 12 endocardial (54%) maps and were typically over basal lateral LV. In the 18 patients with epicardial VT on the basis of activation/pacemapping, the mean epicardial area was greater than the endocardial low-voltage area (55.3 +/- 33.5 cm(2) vs. 22.9 +/- 32.4 cm(2), p < 0.01). Epicardial low-voltage areas showed 49.7% wide (>80 ms), split, and/or late electrograms rarely seen in the reference patients (2.3%). During follow-up of 18 +/- 7 months, ablation resulted in VT elimination in 15 of 21 patients (71%) including 14 of 18 patients (78%) with epicardial VT. CONCLUSIONS In patients with NICM and VT of epicardial origin, the substrate is characterized by areas of basal LV epicardial > endocardial bipolar low voltage. The electrograms in these areas are not only small (<1.0 mV) but wide (>80 ms), split, and/or late, and help identify the substrate targeted for successful ablation.
Circulation | 2004
Edward P. Gerstenfeld; David J. Callans; Sanjay Dixit; Andrea M. Russo; Hemal M. Nayak; David Lin; Ward Pulliam; Sultan Siddique; Francis E. Marchlinski
Background—A proarrhythmic consequence of pulmonary vein (PV) isolation can be a recurrent organized left atrial (LA) tachycardia after ablation. This arrhythmia is frequently referred to as “left atrial flutter,” but the mechanism and best ablation strategy have not been determined. Methods and Results—Isolation of arrhythmogenic PVs was initially performed by segmental ostial PV ablation guided by a circular mapping catheter in 341 patients. Patients whose predominant recurrent arrhythmia was a persistent organized tachycardia returned for mapping and ablation. Recurrent organized LA tachycardias (cycle length 253±33 ms, range 213 to 328 ms) occurred in 10 (2.9%) of 341 patients (age 59±9 years, 1 woman). Mapping was consistent with a focal origin in 8 patients and with macroreentry in 1 patient and was unclear in 1 patient owing to degeneration to atrial fibrillation. Focal tachycardias originated from reconnected segments of prior isolated PVs (6 patients), the posterior LA (1 patient), or the superior septum (1 patient). Focal atrial tachycardias were ablated with point lesions that targeted the earliest activation. All reconnected PVs were also reisolated. Reentrant LA flutter occurred around the left PVs in 1 patient. After 6.7±2.3 months of follow-up, 9 (90%) of 10 patients were arrhythmia free (4 of whom were taking antiarrhythmic drug therapy), and one was having recurrent atrial fibrillation. Conclusions—Recurrent organized LA tachycardia after PV isolation is uncommon and typically has a focal origin from reconnected PV ostia. Reisolation of the PV and ablation of non-PV foci are sufficient to treat this proarrhythmia. Linear lesions are only required when a macroreentrant mechanism is present.
Journal of Cardiovascular Electrophysiology | 2003
Sanjay Dixit; Edward P. Gerstenfeld; David J. Callans; Francis E. Marchlinski
ECG Patterns of RVOT Tachycardias. Introduction: The superior right ventricular outflow tract (RVOT) septum and free wall are common locations of origin for outflow tract ventricular tachycardias (VT). We hypothesized that (1) unique ECG morphologies of pace maps from septal and free‐wall sites in the superior RVOT could be identified using magnetic electroanatomic mapping for accurate anatomical localization; and (2) this ECG information could help facilitate pace mapping and accurate VT localization.
Circulation | 2004
Francis E. Marchlinski; Erica S. Zado; Sanjay Dixit; Edward P. Gerstenfeld; David J. Callans; Henry H. Hsia; David Lin; Hemal M. Nayak; Andrea M. Russo; Ward Pulliam
Background—To gain insight into the pathogenesis of right ventricular (RV) cardiomyopathy and ventricular tachycardia (VT), we determined the clinical and electroanatomic characteristics and outcome of ablative therapy in consecutive patients with (1) RV dilatation, (2) multiple left bundle-branch block (LBBB)–type VTs, and (3) an abnormal endocardial substrate defined by contiguous electrogram abnormalities. Methods and Results—All 21 patients had detailed RV bipolar electrogram voltage mapping. Eighteen patients had simultaneous left ventricular (LV) mapping, including all 4 patients with right bundle-branch block (RBBB) VT. VT was ablated in 19 patients by use of focal and/or linear lesions with irrigated-tip catheters in 10 of 19 patients. Eighteen patients were men, age 47±18 years, and none had a family history of RV dysplasia. RV volume was 223±89 cm3. Electrogram abnormalities extended from perivalvular tricuspid valves (5 patients), pulmonic valves (6 patients), or both valves (10 patients). Electrogram abnormalities always involved free wall, spared the apex, and included the septum in 15 patients (71%). The area of abnormality was 55±37 cm2 (range, 12 to 130 cm2) and represented 34±19% of the RV. In 52 of 66 LBBB VTs, the origin was from the RV perivalvular region. LV perivalvular low-voltage areas noted in 5 patients were associated with a RBBB VT origin. No VT recurred after ablation in 17 patients (89%) during 27±22 months. Conclusions—In patients with RV cardiomyopathy and VT, (1) perivalvular electrogram abnormalities represent the commonly identified substrate and source of most VT, (2) LV perivalvular endocardial electrogram abnormalities and VT can occasionally be identified, and (3) aggressive ablative therapy provides long-term VT control.
Journal of Cardiovascular Electrophysiology | 2005
Jian-Fang Ren; Francis E. Marchlinski; David J. Callans; Edward P. Gerstenfeld; Sanjay Dixit; David Lin; Hemal M. Nayak; Henry H. Hsia
Introducton:A 10% incidence of left atrial (LA) thrombus formation has been detected using intracardiac echocardiography (ICE) imaging monitoring during LA ablation for atrial fibrillation (AF). The aim of this study was to determine if the intensity of anticoagulation reduces LA thrombus formation during pulmonary vein isolation procedure in patients with AF and spontaneous echo contrast (SEC).
Journal of Cardiovascular Electrophysiology | 2004
David J. Callans; Edward P. Gerstenfeld; Sanjay Dixit; Erica S. Zado; Mark Vanderhoff; Jian-Fang Ren; Francis E. Marchlinski
Introduction: Pulmonary vein (PV) isolation is effective in the treatment of most patients with atrial fibrillation (AF). Some advocate the addition of linear ablation techniques to improve efficacy; however, previous studies suggest recurrent PV conduction is responsible for AF recurrence. The aim of this study was to determine the effectiveness of repeat PV isolation in patients with recurrent AF after an initial ablation procedure and to determine if any patient characteristics predict failure of repeat PV isolation procedures.
Journal of Cardiovascular Electrophysiology | 2001
Edward P. Gerstenfeld; Peter Guerra; Paul B. Sparks; Kyoko Hattori; Michael D. Lesh
Ablation of Focal Atrial Fibrillation. Introduction: Ablative therapy for atrial fibrillation (AF) by targeting initiating triggers, usually in or around the pulmonary veins, has been reported by several centers. Evidence for an overall improvement in quality of life (QOL) and amelioration of symptoms is lacking.
Circulation-arrhythmia and Electrophysiology | 2011
Mathew D. Hutchinson; Edward P. Gerstenfeld; Benoit Desjardins; Rupa Bala; Michael P. Riley; Fermin C. Garcia; Sanjay Dixit; David Lin; Wendy S. Tzou; Joshua M. Cooper; Ralph J. Verdino; David J. Callans; Francis E. Marchlinski
Background—Patients with nonischemic left ventricular cardiomyopathy (LVCM) and ventricular tachycardia (VT) have complex 3-dimensional substrate with variable involvement of the endocardium (ENDO) and epicardium (EPI). The purpose of this study was to determine whether ENDO unipolar (UNI) mapping with a larger electric field of view could identify EPI low bipolar (BIP) voltage regions in patients with LVCM undergoing VT ablation. Methods and Results—The reference value for normal ENDO unipolar voltage was determined from 6 patients without structural heart disease. Consecutive patients undergoing VT ablation over an 8-year period with detailed (>100 points) LV ENDO and EPI mapping and normal LV ENDO BIP voltage were identified. From this cohort, we compared patients with structurally normal hearts and normal EPI BIP voltage (EPI−, group 1) with patients with LVCM and low LV EPI BIP voltage regions present (EPI+, group 2). Confluent regions of ENDO UNI and EPI BIP low voltage (>2 cm2) were measured. The normal signal amplitude was >8.27 mV for LV ENDO UNI electrograms. Detailed LV ENDO-EPI maps in 5 EPI− patients were compared with 11 EPI+ patients. Confluent ENDO UNI low-voltage regions were seen in 9 of 11 (82%) of the EPI+ (group 2) patients compared with none of 5 EPI− (group 1) patients (P<0.001). In all 9 patients with ENDO UNI low voltage, the ENDO UNI low-voltage regions were directly opposite to an area of EPI BIP low voltage (61% ENDO UNI-EPI BIP low-voltage area overlap). Conclusions—EPI arrhythmia substrate can be reliably identified in most patients with LVCM using ENDO UNI voltage mapping in the absence of ENDO BIP abnormalities.
Journal of Cardiovascular Electrophysiology | 2003
Edward P. Gerstenfeld; David J. Callans; Sanjay Dixit; Erica S. Zado; Francis E. Marchlinski
Introduction: The etiology of atrial fibrillation (AF) recurrences after pulmonary vein (PV) isolation is not well described. The aim of this study was to examine the reason for recurrent AF in patients undergoing a repeat attempt at AF trigger ablation.