Research Summary:
Development and function of the cardiac conduction system; molecular regulation of cardiac pacemaker cells; mechanisms of cardiac arrhythmias Our lab is focused on cardiac pacemaker cells, specialized cardiomyocytes whose autonomous electrical activity allows the sinoatrial node to serve as the heart’s natural pacemaker. Specific questions include: How are pacemaker cells different from regular heart cells at the level of gene expression and regulation? How does their unique gene expression signature confer their distinctive electrophysiological properties? How have selection pressures generated functional differences in pacemaker cells among different vertebrate species? What are the molecular mechanisms that guide pacemaker cells to integrate electrically with the rest of the heart to form a node? How do pacemaker cell biology and function change in response to physiological and pathological stress? What is the mechanistic link between sinus node dysfunction and atrial fibrillation? Our approaches include mouse genetics, whole-animal and ex-vivo electrophysiology, cellular and molecular electrophysiology, gene expression analysis, and bioinformatics. Ultimately, we hope to design novel treatments for patients suffering from heart rhythm disorders, including sinus node dysfunction and atrial fibrillation.
Publications
ALPK3 Heterozygous Truncating Variants Cause Late-Onset Hypertrophic Cardiomyopathy With Frequent Apical Involvement and Apical Aneurysm.
Flecainide for the Treatment of Andersen-Tawil Syndrome.
RACE COMPARISONS FROM THE CARDIAC SARCOIDOSIS CONSORTIUM: BLACK CARDIAC SARCOIDOSIS PATIENTS HAVE HIGHER RATES OF COMORBIDITIES.
RISK OF ADVERSE OUTCOMES ASSOCIATED WITH INITIAL CLINICAL PRESENTATION OF CARDIAC SARCOIDOSIS.
ALPK3 heterozygous truncating variants cause late-onset hypertrophic cardiomyopathy with frequent apical involvement and apical aneurysm.
MP-470554-001 THE VALUE OF FUNCTIONAL FACSICULAR BLOCK IN PATIENTS WITH ATRIOVENTRICULAR REENTRANT TACHYCARDIA.
SEX DIFFERENCES IN CARDIAC SARCOIDOSIS TREATMENT AND OUTCOMES: FINDINGS FROM THE CARDIAC SARCOIDOSIS CONSORTIUM.
Acute alcohol exposure and electrocardiographic changes: Finding from the HOLIDAY trial.
Cholecystokinin-A signaling regulates automaticity of pacemaker cardiomyocytes.
Reply: Association of Adverse Events With the Different Diagnostic Schemes of Cardiac Sarcoidosis.
Single Cell Multi-Omics of an iPSC Model of Human Sinoatrial Node Development Reveals Genetic Determinants of Heart Rate and Arrhythmia Susceptibility.
Cholecystokinin-A Signaling Regulates Automaticity of Pacemaker Cardiomyocytes.
A very wide complex tachycardia.
Risk of Adverse Outcomes Associated With Cardiac Sarcoidosis Diagnostic Schemes.
ACUTE ALCOHOL EXPOSURE AND ELECTROCARDIOGRAPHIC CHANGES: FINDING FROM THE HOLIDAY (HOW ALCOHOL INDUCES ATRIAL TACHYARRHYTHMIAS) TRIAL.
A Randomized Trial of High vs Standard Power Radiofrequency Ablation for Pulmonary Vein Isolation: SHORT-AF.
Premature Atrial Contraction Location and Atrial Fibrillation Inducibility.
Randomized Comparison of a Radiofrequency Wire Versus a Radiofrequency Needle System for Transseptal Puncture.
The Value of Programmed Ventricular Extrastimuli From the Right Ventricular Basal Septum During Supraventricular Tachycardia.
Arrhythmia Monitoring and Outcomes in Patients With Cardiac Sarcoidosis: Insights From the Cardiac Sarcoidosis Consortium.
CARDIAC SARCOIDOSIS PATIENTS WHO MEET THE 1993 AND 2006 JAPANESE DIAGNOSTIC CRITERIA ARE MORE LIKELY TO HAVE ADVERSE OUTCOMES.
TRADITIONAL RISK FACTORS INCREASE THE RISK OF POOR OUTCOMES IN PATIENTS WITH CARDIAC SARCOIDOSIS.
Outcomes Associated With Catheter Ablation of Ventricular Tachycardia in Patients With Cardiac Sarcoidosis.
Acute Consumption of Alcohol and Discrete Atrial Fibrillation Events.
Transcriptional and Epigenetic Landscape of Cardiac Pacemaker Cells: Insights Into Cellular Specialization in the Sinoatrial Node.
Predictors of long-term success after catheter ablation of premature ventricular complexes.
The Role of the Left Septal Fascicle in Fascicular Arrhythmias: Clinical Presentation and Laboratory Evaluation.
Heart Failure, Atrioventricular Block, and Ventricular Tachycardia in Sarcoidosis.
A Randomized, Double-Blind, Placebo-Controlled Trial of Intravenous Alcohol to Assess Changes in Atrial Electrophysiology.
Abstract 12935: Predictors of Long-term Success After Catheter Ablation of Premature Ventricular Complexes.
Electrophysiologic approach to diagnosis and ablation of patients with permanent junctional reciprocating tachycardia associated with complex anatomy and/or physiology.
ATAC-Seq Reveals an Isl1 Enhancer That Regulates Sinoatrial Node Development and Function.
Predictors of adverse outcome in patients with frequent premature ventricular complexes: The ABC-VT risk score.
Long-Term Corticosteroid-Sparing Immunosuppression for Cardiac Sarcoidosis.
Ischemia with marked ST elevation or J-wave syndrome?
Premature MicroRNA-1 Expression Causes Hypoplasia of the Cardiac Ventricular Conduction System.
Surface ECG and intracardiac spectral measures predict atrial fibrillation recurrence after catheter ablation.
Use of Programmed Ventricular Extrastimulus During Supraventricular Tachycardia to Differentiate Atrioventricular Nodal Re-Entrant Tachycardia From Atrioventricular Re-Entrant Tachycardia.
Trends in Hospitalizations for Cardiac Sarcoidosis in the United States, 2005-2011.
Cover Image, Volume 28, Issue 7.
Atrial fibrillation patients with isolated pulmonary veins: Is sinus rhythm achievable?
Familial inappropriate sinus tachycardia: a new chapter in the story of HCN4 channelopathies.
Bundle Branch Re-Entrant Ventricular Tachycardia: Novel Genetic Mechanisms in a Life-Threatening Arrhythmia.
The QT Interval as a Noninvasive Marker of Atrial Refractoriness.
Clinical and Electrophysiological Characteristics of Incessant Atrioventricular Nodal Re-Entrant Tachycardia.
POST-SHOCK ELECTROMECHANICAL DISSOCIATION DURING DEFIBRILLATION THRESHOLD TESTING.
New Approaches to Biological Pacemakers: Links to Sinoatrial Node Development.
Response to letter regarding article, "variable clinical features and ablation of manifest nodofascicular/ventricular pathways".
The Effect of Direct Current Stimulation versus T-Wave Shock on Defibrillation Threshold Testing.
RNA sequencing of mouse sinoatrial node reveals an upstream regulatory role for Islet-1 in cardiac pacemaker cells.
Atrial Fibrillation.
Variable clinical features and ablation of manifest nodofascicular/ventricular pathways.
Idiopathic ventricular arrhythmia originating from the cardiac crux or inferior septum: epicardial idiopathic ventricular arrhythmia.
Specification of the mouse cardiac conduction system in the absence of Endothelin signaling.
Coupling interval dispersion and body mass index are independent predictors of idiopathic premature ventricular complex-induced cardiomyopathy.
Safety of new oral anticoagulants for patients undergoing atrial fibrillation ablation.
Randomized trial of conventional transseptal needle versus radiofrequency energy needle puncture for left atrial access (the TRAVERSE-LA study).
Unexpected potential following ablation of a right atriofascicular accessory pathway.
Narrow QRS Tachycardia with Ventriculoatrial Block.
Spatiotemporal regulation of an Hcn4 enhancer defines a role for Mef2c and HDACs in cardiac electrical patterning.
Ivabradine: a ray of hope for inappropriate sinus tachycardia.
Alcohol and vagal tone as triggers for paroxysmal atrial fibrillation.
Predictors of fluoroscopy time and procedural failure during biventricular device implantation.
PREDICTORS OF PROCEDURAL DIFFICULTY DURING BIVENTRICULAR DEVICE IMPLANTATION: A UNIVERSITY HOSPITAL EXPERIENCE.
Chapter 33 Current Indications for Temporary and Permanent Cardiac Pacing.
Abstract 10466: In Vivo Reprogramming of Murine Cardiac Fibroblasts into Induced Cardiomyocytes.
Changing QRS Morphology in a Patient with Wolff-Parkinson-White Syndrome.
Rapid and slow voltage-dependent conformational changes in segment IVS6 of voltage-gated Na(+) channels.
The position of the fast-inactivation gate during lidocaine block of voltage-gated Na+ channels.
Slow inactivation does not affect movement of the fast inactivation gate in voltage-gated Na+ channels.
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