Stuart Beldner
North Shore University Hospital
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Featured researches published by Stuart Beldner.
Heart Rhythm | 2008
David Lin; Leonard Ilkhanoff; Edward P. Gerstenfeld; Sanjay Dixit; Stuart Beldner; Rupa Bala; Fermin C. Garcia; David J. Callans; Francis E. Marchlinski
BACKGROUND The most common site of origin of idiopathic ventricular tachycardia (VT) is the right ventricular outflow tract. Idiopathic VT also can arise from the left ventricular outflow tract and the surrounding structures. Morphologic descriptions of 12-lead ECG characteristics of the aortic cusp region are limited. OBJECTIVE The purpose of this study was to define unique ECG characteristics of the aortic cusp region by performing a systematic analysis of pacemapping of this region in patients with structurally normal hearts. METHODS A combination of electroanatomic mapping, intracardiac echocardiography, and fluoroscopic guidance was used to study a total of 30 patients with structurally normal hearts undergoing left-sided ablation procedures. Each of the aortic valve cusps and the aortomitral continuity were paced at threshold and analyzed offline to determine unique ECG characteristics. RESULTS Pacing from the left coronary cusp typically produced a multiphasic QRS morphology consistent with an M or W pattern in lead V(1) with a precordial transition (R>S) no later than V(2). Pacing from the right coronary cusp typically resulted in a left bundle-type pattern with a broad small R wave in V(2) and a precordial transition generally at V(3). Pacing from the aortomitral continuity resulted in a qR pattern that was not observed anywhere else in the left ventricular outflow tract. When comparing the right coronary cusp and left coronary cusp, the precordial transition was earlier in the left coronary cusp than in the right coronary cusp. Pacing the noncoronary cusp uniformly resulted in atrial capture. CONCLUSION When considering ablation of idiopathic VT, the aortic cusps and aortomitral continuity must be considered as possible foci. The 12-lead ECG, a readily and easily obtainable source of information, has useful characteristics for differentiating VTs arising from the cusp region.
Journal of Cardiovascular Electrophysiology | 2005
Francis E. Marchlinski; Fermin C. Garcia; Amir Siadatan; William H. Sauer; Stuart Beldner; Erica S. Zado; Henry H. Hsia; David Lin; Joshua M. Cooper; Ralph J. Verdino; Edward P. Gerstenfeld; Sanjay Dixit; Andrea M. Russo; David J. Callans
Recurrent ventricular tachycardia (VT) in the setting of coronary artery disease is frequently a life‐threatening electrophysiologic emergency. Even in patients with an implantable defibrillator, recurrent VT is frequently accompanied by repeated and disabling shock therapy. Catheter ablative therapy offers the ability to provide immediate control of recurrent VT. Long‐term elimination of VT should be anticipated in most patients. This article reviews the strategies, tools, techniques, and expected outcome for catheter ablation of stable and unstable ventricular arrhythmias in the setting ischemic heart disease.
Pacing and Clinical Electrophysiology | 1999
Daniel Lee; Stuart Beldner; Frank Pollaro; Ram Jadonath; Paul Maccaro; Bruce Goldner
The patient is a 65-year-old man referred for evaluation of recurrent episodes of syncope, each preceded by coughing. His past medical history is significant for coronary artery disease. His only medications were aspirin and metoprolol (25 mg three times a day). ECG showed normal sinus rhythm with left bundle branch hlock. Echocardiogram demonstrated normal left ventricular function and mild mitral regurgitation. The patient was asked to cough voluntarily while a rhythm strip was recorded, during v̂ ĥich 7 seconds of transient complete heart hlock was recorded [Fig. 1) and the patient lost consciousness. On electrophysiology study, the AH interval was 85 ms and the HV was 80 ms at a sinus cycle length of 620 ms. Atrioventricular (AV) nodal Wenkebach occurred at 340 ms. A DDDR pacemaker was implanted and subsequently cough did not provoke syncope. The
Pacing and Clinical Electrophysiology | 2013
Joonhyuk Kim; Shalin Desai; Ram Jadonath; Stuart Beldner
The definition of a successful ablation of atrial fibrillation can vary among electrophysiologists. A commonly described endpoint is bidirectional block of the four pulmonary veins. A case is described in which entrance block into a pulmonary vein was achieved early during pulmonary vein isolation. However, triggers from the pulmonary vein continued to conduct into the atrium, revealing the block was only unidirectional. Further ablation resulted in true electrical isolation and highlights the importance of achieving bidirectional block. (PACE 2013; 36:e143–e145)
Pacing and Clinical Electrophysiology | 2011
Joonhyuk Kim; Stuart Beldner; Ram Jadonath; Erik Altman
Clinical Case A 41-year-old obese woman underwent elective gastric banding and had syncope on postoperative day 1. Vitals signs were notable for bradycardia (38 beats per minute [bpm]) and hypotension (73/45). Telemetry monitoring revealed high-grade atrioventricular (AV) block and dopamine was started, with improvement of symptoms and vital signs. On interview, the patient recalled a camping trip in Long Island, New York, one month prior to admission. There had been ensuing arthralgia, but she did not recall an insect bite. Physical exam was unremarkable. She was admitted to the cardiac care unit (CCU) and started on ceftriaxone for suspicion of Lyme disease. Attempts at weaning the dopamine resulted in a 10-second ventricular pause and a temporary pacing wire (TPW) was placed via the right internal jugular vein. Subsequently, the Lyme IgG/IgM titers returned at 4.59 IU (normal < 0.9 IU, unequivocal 0.91–1.09 IU, positive > 1.1 IU). It was explained to the patient that the TPW would be required to maintain a safe heart rate until AV conduction resumed or a stable junctional escape rhythm developed. She expressed concern about the possibility of a lengthy hospitalization, since she has two small children at home without proper supervision. Four days later, she was still noted to have thirddegree AV block without a stable escape rhythm, but she was adamant about being discharged. As a result of patient pressure, a permanent pacemaker (PPM) with a single-pass VDD lead was implanted. She was observed overnight and was discharged the next day.
Pacing and Clinical Electrophysiology | 2008
Marshal Fox; Trevor Verga; Ram Jadonath; Stuart Beldner
In this report we describe a case of atrial flutter degenerating into ventricular fibrillation after carotid sinus pressure. Carotid sinus massage is an extremely valuable and widely used diagnostic and therapeutic modality. Although generally considered a rather benign maneuver, it is not without potential risk.
The Journal of Innovations in Cardiac Rhythm Management | 2018
Joseph Donnelly; Apoor Patel; Stuart Beldner
The discovery, characterization, and ablation of the papillary muscles have evolved rapidly since the initial description in 2008. New innovations in pacemapping, intracardiac imaging, ablation catheters, and ablation methodologies have dramatically impacted the approach to the treatment of papillary muscle ventricular arrhythmias. This review provides an up-to-date summary of these methods, as well as guidance on how to integrate them into clinical practice.
Pacing and Clinical Electrophysiology | 2018
James Gabriels; Joseph Donnelly; Jonathan Willner; Stuart Beldner; Apoor Patel; Brian Lima; Laurence M. Epstein
Subcutaneous implantable cardioverter-defibrillators (S-ICDs) are currently approved for use in the primary prevention of sudden cardiac death. The single S-ICD lead is tunneled in subcutaneous tissue in closeproximity to the sternum.Whenapatientwith aS-ICDundergoes a subsequent surgery that requires amedian sternotomy there arises a possibility of damage to the lead intraoperatively and contact between the lead and the sternotomy wires in the postoperative period. This may result in S-ICD malfunction. The optimal way to manage the lead during a surgery involving a median sternotomy in a patient with a S-ICD is not well defined. Implantation of a left ventricular assist device (LVAD) in a patient with an existing S-ICD raises another level of complexity given the potential for electromagnetic interference (EMI) from the LVAD, which may lead to inappropriate sensing and defibrillation.
Current Treatment Options in Cardiovascular Medicine | 2018
Joseph Donnelly; James Gabriels; Andrew Galmer; Jonathan Willner; Stuart Beldner; Laurence M. Epstein; Apoor Patel
Purpose of reviewA variety of complex vascular pathologies arise following the implantation of electronic cardiac devices. Pacemaker and defibrillator lead insertion may cause proximal venous obstruction, resulting in symptomatic venous congestion and the compromise of potential future access sites for cardiac rhythm lead management.Recent findingsVarious innovative techniques to recanalize the vein and establish alternate venous access have been pioneered over the past few years.SummaryA collaborative team of electrophysiologists and vascular specialists strategically integrate the patient’s vascular disease into the planning of electrophysiology procedures. When vascular complications occur after device implantation, the same team effectively manages both the resulting vascular sequelae and related cardiac rhythm device challenges. This review will outline the various vascular challenges related to device therapy and offer an effective strategy for their management.
Pacing and Clinical Electrophysiology | 2017
James Gabriels; Mohammad Khan; Jonah Zeitlin; Ram Jadonath; Apoor Patel; Stuart Beldner
Our patient is a 65-year-old man status post primary prevention implantable cardioverter defibrillator (ICD) for congestive heart failure in the setting of severe left ventricular systolic dysfunction due to a remote myocardial infarction. His β-blocker dose had been decreased secondary to symptomatic sinus node dysfunction and the decision was made to implant a dual-chamber device for atrial pacing support. Shortly after implant, he presented with an ICD discharge (Figure 1). The arrhythmia was not captured on a 12-lead electrocardiogram. Based on Figure 1, what is the chamber of origin of the arrhythmia? Does the addition of the atrial electrogram assist in the diagnosis? Are there any diagnostic maneuvers that could be used to confirm the diagnosis?