- Queens College, CUNY
- SUNY - Upstate Medical Center
Awards & Honors
- 1996–1998: President, International Cardiac Electrophysiology Society
- 1998–Present: Secretary/Treasurer, International Cardiac Electrophysiology Society
- 2002: Distinguished Scientist Award, North American Society of Pacing and Electrophysiology (NASPE, currently Heart Rhythm Society)
- 2003: Excellence in Cardiovascular Science Award, NE Affiliate American Heart Association
- 2007: Carl J. Wiggers Award, American Physiological Society
- 2011: Distinguished Scientist Award, American College of Cardiology
- 2015: Distinguished Service Award, Cardiac Electrophysiology Society, Boston, Mass.
Cardiac arrhythmias or irregular heart rhythms claim more lives than any other mechanism of heart disease. Cardiac arrhythmias can be due to congenital defects in ion channels that generate the electrical impulse that sets the heart into motion or they may arise as a consequence of injury to the heart secondary to a heart attack or trauma. Electrical instability of the heart that develops under these conditions can lead to rapid and irregular rhythms of the heart, which can lead to sudden cardiac death. A principal focus of the Cardiovascular Research Program at the Lankenau Institute for Medical Research LIMR) is to understand how and why these arrhythmias develop, to identify those individuals who may be at risk for sudden cardiac death or sudden infant death syndrome (SIDS), and to develop treatments and cures.
Our work is focused in part on identifying defects in genes associated with these syndromes and by so doing, identifying the root cause of the disease. This will allow us to develop customized solutions for families afflicted with these syndromes. Genetic and genomic research is quickly transitioning us from a society in which treatment is empiric one-fits-all approach to one in which therapy is based on the specific cause of the disease and tailored to the individual patient. This knowledge is ushering in a new era that is changing the face of medicine as we know it today.
Atrial fibrillation (AF) is the most common arrhythmia encountered in the clinic. AF afflicts nearly one in 10 individuals 80 years of age and older and is increasing in prevalence as the longevity of Americans increases. Effective pharmacological treatment of AF is one of the greatest unmet medical needs facing our society today. Most available drugs have low efficacy and those with high efficacy, have high toxicity. Another critical focus of our team’s effort will be to develop drugs that are both safe and effective. Working with Biotechnology companies we are developing drugs that target the upper chambers of the heart (atria), but not the ventricles, where most of the adverse effects arise.
Heart failure affects close to five million Americans. Each year close to 500,000 new cases are diagnosed. Heart failure is the leading cause of hospitalization in people over the age of 65 and it is often associated with atrial fibrillation, which worsens the prognosis and quality of life of patients with heart failure. Many of the medications employed to treat AF in individuals without heart failure are contra-indicated in individuals with heart failure. An important part of our efforts will therefore be directed to development of drugs capable of safely and effectively suppressing AF in the setting of heart failure.
Investigators in our cardiovascular research program are also pursuing studies designed to help us understand why there is such a dramatic increase in the prevalence of AF with age. Despite intensive research in this field, the mechanisms responsible are not known and animal models to study this phenomenon have not been readily available. We have recently identified and animal model that develops AF in old age and are using this unique model to investigate the mechanisms underlying the pathogenesis of AF with advancing age.
Over 3,000 American with heart failure die every year waiting for a donor heart. There is a dire need for alternative solutions. Our scientists have undertaken an exciting challenge to build new hearts using stem cells donated by the intended recipient of the transplanted heart. This approach involves the use of cadaver hearts from which all cells are removed using detergents. What is left is almost a pure white image of a heart made out of collagen. This is referred to as a “ghost heart”. Using cells form the intended recipients skin or bone marrow, we will develop stem cells or progenitor cells that could be used to repopulate the heart with new heart cells. This high risk approach, if successful, will fill a sizable void and provide hearts to patients in end-stage heart failure that will hopefully not be rejected, thus avoiding anti-rejection medication.
Our cardiovascular research team is also pursuing a project designed to advance our understanding of mechanisms underlying Sudden Unexplained Death in Epilepsy (SUDEP). Epilepsy is one of the most common neurological diseases, affecting nearly one percent of the population. One of the more catastrophic yet enigmatic complication of epilepsy is a syndrome known as SUDEP. Individuals with epilepsy have up to a 24 times higher sudden death rate than the general population. We are pursuing the hypothesis that there is a genetic and pathophysiological link between electrical disturbances in the brain responsible for epilepsy and electrical disturbances in the heart responsible for cardiac arrhythmias, leading to sudden death. We are working with colleagues in Israel, Turkey and Taiwan to collect cases and genetically screen patients with epilepsy and inherited cardiac arrhythmia syndromes. Our goal is to find a common link between these two syndromes. Our pilot studies have identified several gene candidates and mutations in a variety of ion channels common to the brain and the heart.
Inherited syndromes that affect the electrical activity of the heart play a critical role in causing syndromes such as long QT, short QT and Brugada syndromes, taking the lives of infants, children and young adults, often with little or no warning. Using molecular genetic techniques, our scientists will conduct research aimed at unraveling the basis for a number of inherited diseases including the Long QT, Short QT, Brugada and early Repolarization syndromes. Using next generation and exome and genome wide screening techniques we seek to uncover new genes and mutations responsible for these syndromes. Using molecular biology and patch clamp technology will perform functional expression studies to help establish causality. These methodologies also permit us to look for drugs that can reverse the effect of the genetic defect and thus provide an effective treatment for the patient. These approaches will also be used to probe the genetic basis of why some patients develop life-threatening arrhythmias after a heart attack and others suffering with the same ischemic damage do not.
Our research team is also keen on understanding the basis for the very strong male predominance in the manifestation of the Brugada syndrome. This work is focused on demonstrating the effect of testosterone on the expression of the transient outward current, a cardiac potassium current at the heart of this syndrome.
On the atrial fibrillation front, we are pursuing studies aimed at development of drugs that exert atrial-selective inhibition of sodium channel current and thus of excitability in the atria. This field was pioneered by our team of investigators in 2007. We plan to expand on our recent discovery that rapidly dissociating sodium channel blockers when combined with agents that prolong action potential duration, via inhibition of IKr, IKur or IK-ACh, act synergistically to suppress and prevent the development of AF. We will also further explore our discovery that a combination of ranolazine and dronedarone act synergistically to provide safe and effective management of AF. Two heart failure models (ventricular tachypacing- and ischemia-induced injury) will be developed to study the effects of these drugs in the setting of heart failure. Our work focused on understanding the mechanisms underlying the marked increase in the prevalence of AF with advancing age is pointing us in the direction of intracellular calcium mishandling as an important contributing factor, which we are pursuing in earnest.
Our organ bioengineering program is a high-risk project with potentially great rewards. The first step in creating a cloned heart requires that they be decellularized using sodium dodecyl sulfate (SDS). Over the course of 48–72 hours, this detergent breaks down all cellular and genetic material from the donor heart leaving the collagen framework unharmed. The organ is termed a “ghost heart” because of its opaque white appearance. Progenitor cells generated from the patient’s own fibroblasts, bone marrow or other sources will then be used in an attempt to repopulate the organ and thus form a fully functioning human heart. We envision that if successful it will be 15–20 years before this approach becomes a practical alternative to heart transplantation.
In more recent years, our team has focused on development of pluripotent stem cell-derived cardiomyocytes for 1) creation of human models of inherited cardiac arrhythmia diseases; 2) regenerative therapy to improve function of injured hearts; and 3) safety pharmacology. In this program, we develop human models of disease by reprogramming somatic cells from blood or skin into induced pluripotent stem cells from patients with a wide variety of inherited cardiac arrhythmia syndromes and then direct the differentiation of these cells into cardiomyocytes. This approach allows our team to delve further into the pathophysiology of disease and to develop patient-specific therapies.
We also are working to advance understanding of how genetic defects in ion channels that are common to both brain and heart may be responsible for development of epilepsy as well as life-threatening arrhythmias of the heart and thus contribute to sudden unexpected death in epilepsy and have identified ion channelopathies common to both syndromes.
These programs complement each other, enabling our team to evaluate and validate genetic, molecular and electrophysiologic findings and ultimately translate them into an understanding of human disease. These projects also provide us a platform to accelerate drug discovery and its implementation in the clinic.
- Recent advances in the treatment of Brugada syndrome. Antzelevitch C, Argenziano M. Expert Rev Cardiovascular Ther. 2018 Jun;16(6):387-404.
- Tpeak-Tend as a predictor of ventricular arrhythmogenesis. Antzelevitch C, Di Diego JM, Argenziano M. Int J Cardiol. 2017 Dec 15;249:75-76.
- Should theophylline be added to the J wave syndrome therapeutic armamentarium? Antzelevitch C, Viskin S. Pacing Clin Electrophysiol. 2017 Nov 16. doi: 10.1111/pace.13237.
- Theophylline: The forgotten antiarrhythmic drug…. now for malignant early repolarization. Viskin S, Havakuk O, Antzelevitch C, Rosso R. Pacing ClinElectrophysiol. 2017 Nov 16. doi: 10.1111/pace.13239.
- Brugada Syndrome. In: Encyclopedia of Cardiovascular Research and Medicine. Cardiac Electrophysiology, Arrhythmias and Sudden Death Section, Vasan Ramachandran and Douglas Sawyer, Editors-in-Chief. Antzelevitch C. And In: Elsevier Biomedical Sciences Reference Modules, 2017
- Mechanisms Underlying Arrhythmogenesis in the J Wave Syndromes. Savio-Galimberti E, Argenziano M, Antzelevitch C. In: Cardiac Mapping 5 th Edition. Mohammad Shenasa, Gerhard Hindricks, David Callans, John M. Miller, Mark E. Josephson, eds, 2017.
- Cardiac Arrhythmias Related to Sodium Channel Dysfunction. Savio-Galimberti E, Argenziano M, Antzelevitch C. Handb Exp Pharmacol. 2017 Oct 1. doi: 10.1007/164_2017_43.
- Mechanisms of cardiac arrhythmias and conduction disturbances. Chen PS, Antzelevitch C. In: Hurst’s The Heart 14th ed. Fuster V, O’Rourke R, Walsh R, Poole-Wilson P, eds. McGraw Hill, New York, NY, Chapter 79, 2017.
- Ajmaline-Induced Slowing of Conduction in the Right Ventricular Outflow Tract Cannot Account for ST Elevation in Patients With Type I Brugada ECG. Antzelevitch C, Patocskai B. Circ Arrhythm Electrophysiol. 2017 Oct;10(10). doi:10.1161/CIRCEP.117.005775.
- Mechanisms Underlying Epicardial Radiofrequency Ablation to Suppress Arrhythmogenesis in Experimental Models of Brugada Syndrome. Patocskai B, Yoon N,Antzelevitch C. JACC Clin Electrophysiol. 2017 Apr;3(4):353-363.
- J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge. Antzelevitch C., Yan GX, Ackerman MJ, et al. Europace. 2017 Apr 1;19(4):665-694.
- Effectiveness of Late INa Versus Peak INa Block in the Setting of Ventricular Fibrillation. Burashnikov A, Antzelevitch C. Circ Arrhythm Electrophysiol. 2017 Mar;10(3).
- Andersen-Tawil syndrome: Clinical presentation and predictors of symptomatic arrhythmias - Possible role of polymorphisms K897T in KCNH2 and H558R in SCN5A gene. Krych M, Biernacka EK, Ponińska J, Kukla P, Filipecki A, Gajda R, Hasdemir C, Antzelevitch et al. J Cardiol. 2017 Mar 20.
- Ranolazine for Congenital Long-QT Syndrome Type III: Experimental and Long-Term Clinical Data. Chorin E, Hu D, Antzelevitch C, Hochstadt A, Belardinelli L, et al. Circ Arrhythm Electrophysiol. 2016 Oct;9(10).
- Further Insights in the Most Common SCN5A Mutation Causing Overlapping Phenotype of Long QT Syndrome, Brugada Syndrome, and Conduction Defect. Veltmann C, Barajas-Martinez H, Wolpert C, ...Antzelevitch C. J Am Heart Assoc. 2016 Jul 5;5(7). doi: 10.1161/JAHA.116.003379.
- J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge: Endorsed by the Asia Pacific Heart Rhythm Society (APHRS), the European Heart Rhythm Association (EHRA), the Heart Rhythm Society (HRS), and the Latin American Society of Cardiac Pacing and Electrophysiology (Sociedad Latinoamericana de Estimulación Cardíaca y Electrofisiología [SOLAECE]). Antzelevitch C, Yan GX, et al. Heart Rhythm. 2016 Jul 11. doi:10.1016/j.hrthm.2016.05.024.
- Atrial fibrillation in inherited cardiac channelopathies: From mechanisms to management. Enriquez A, Antzelevitch C, Bismah V, Baranchuk A. Heart Rhythm. 2016 Jun 9. pii: S1547-5271(16)30408-8.
- Prognostic significance of fever-induced Brugada syndrome. Mizusawa Y, Morita H, Adler A, ... Antzelevitch C. Heart Rhythm. 2016 Mar 23. pii: S1547-5271(16)30088-1.
- Programmed Ventricular Stimulation for Risk Stratification in the Brugada Syndrome: A Pooled Analysis. Sroubek J, Probst V, Mazzanti A, Delise P, ... Antzelevitch C. Circulation. 2016 Feb 16;133(7):622-30.
- Cellular and Ionic Mechanisms Underlying Effects of Cilostazol, Milrinone and Isoproterenol to Suppress Arrhythmogenesis in an Experimental Model of Early Repolarization Syndrome. Patocskai B, Barajas-Martinez H, Hu D, Gurabi Z, Koncz I, Antzelevitch C. Heart Rhythm. 2016 Jan 25. pii: S1547-5271(16)00124-7. doi:10.1016/j.hrthm.2016.01.024.
- Mechanisms underlying atrial-selective block of sodium channels by Wenxin Keli: Experimental and theoretical analysis. Hu D, Barajas-Martínez H, Burashnikov A, Panama BK, Cordeiro JM, Antzelevitch C. Int J Cardiol. 2016 Jan 7;207:326-334. doi:10.1016/j.ijcard.2016.01.016.
- Novel Timothy syndrome mutation leading to increase in CACNA1C window current. Boczek N, Miller EM, Ye D, Nesterenko V, Tester DJ, Antzelevitch C, Czosek RJ, Ackerman MJ, Ware SM. Heart Rhythm 12(1):211-9, 2015. PMID:25260352
- Management of ventricular arrhythmias in suspected channelopathies. Obeyesekere MN, Antzelevitch C, Krahn AD. Circ Arrhythm Electrophysiol. 8:221-31, 2015. PMID: 25691556
- Inhibition of IKr potentiates development of atrial-selective INa block leading to effective suppression of atrial fibrillation. Burashnikov A, Belardinelli L, Antzelevitch C. Heart Rhythm, 12:836-44, 2015. PMID: 25546810
- Usefulness of exercise test in the diagnosis of short QT syndrome. Giustetto C, Scrocco C, Schimpf R, ... Antzelevitch C. Europace. 2015 Apr;17(4):628-34. doi: 10.1093/europace/euu351. PMID: 25833882
- J Wave syndromes: Brugada and Early Repolarization Syndromes. Antzelevitch C, Yan GX. Heart Rhythm. 2015. Apr 10. pii: S1547-5271(15)00427-0. doi: 10.1016/j.hrthm.2015.04.014. PMID: 25869754
- Novel Therapeutic Strategies for the Management of Ventricular Arrhythmias Associated with the Brugada Syndrome. Patocskai B and Antzelevitch C. Expert Opinion on Orphan Drugs 3:1-19, 2015.
- High prevalence of concealed Brugada syndrome in patients with atrioventricular nodal reentrant tachycardia. Hasdemir C, Payzin S, Kocabas U, ... Antzelevitch C. Heart Rhythm. 2015 May 14. pii: S1547-5271(15)00272-6. doi: 10.1016/j.hrthm.2015.03.015. [Epub ahead of print] PMID: 25998140
- Calcium Channel Mutations in Cardiac Arrhythmia Syndromes. Betzenhauser MJ, Pitt GS, Antzelevitch C. Curr Mol Pharmacol. 2015 May 18. [Epub ahead of print] PMID: 25981977
- Risk stratification in Brugada syndrome: Clinical characteristics, electrocardiographic parameters, and auxiliary testing. Adler A, Rosso R, Chorin E, Havakuk O, Antzelevitch C, Viskin S. Heart Rhythm. 2016 Jan;13(1):299-310. doi: 10.1016/j.hrthm.2015.08.038.
- Malignant early repolarization: It's the T-wave, stupid…. Viskin S, Havakuk O, Antzelevitch C, Rosso R. Heart Rhythm. 2015 Dec 9. pii: S1547-5271(15)01532-5. doi: 10.1016/j.hrthm.2015.12.017. [Epub ahead of print] No abstract available
- Bases genéticas y moleculares del síndrome de Brugada mediado por canales de sodio. [Genetic and molecular basis for sodium channel-mediated Brugada syndrome.] Barajas-Martínez H, Hu D, Antzelevitch C. Arch Cardiol Mex, 83:295-302, 2013.
- ABCC9 is a novel Brugada and early repolarization syndrome susceptibility gene. Hu D, Barajas-Martínez H, Terzic A, ... Antzelevitch C. Int J Cardiol, 171:431-442, 2014. PMCID3947869
- A temporal window of vulnerability for development of atrial fibrillation with advancing heart failure. Burashnikov A, Di Diego JM, Sicouri S, ... Antzelevitch C. Eur J Heart Fail, 16:271-280, 2014. NIHMS63161
- Mechanisms underlying the development of the electrocardiographic and arrhythmic manifestations of early repolarization syndrome. Koncz I, Gurabi Z, Patocskai B, Panama BK, Szél T, Hu D, Barajas-Martínez H, Antzelevitch C. J Mol Cell Cardiol, 68:20-28, 2014. PMCID3943882.
- Cellular mechanism underlying hypothermia-induced ventricular tachycardia/ventricular fibrillation in the setting of early repolarization and the protective effect of quinidine, cilostazol and milrinone. Gurabai Z, Koncz I, Patocskai B, Nesterenko VV, Antzelevitch C. Circ Arrhythm Electrophysiol, 7:134-142, 2014. PMCID3951442
- Abnormal repolarization as the basis for late potentials and fractionated electrograms recorded from epicardium in experimental models of Brugada syndrome. Szél T, Antzelevitch C. J Am Col Cardiol, 63:2037-2045, 2014. PMCID4024366
- PQ segment depression in short QT syndrome patients: a novel marker for diagnosing short QT syndrome? Tülümen E, Giustetto C, Wolpert C, ... Antzelevitch C. Heart Rhythm, 11:1024-1030, 2014. PMCID4108989
- Acute myocardial ischemia: cellular mechanisms underlying ST segment elevation. Di Diego JM, Antzelevitch C. J Electrocardiol, 47:486-490, 2014. PMCID4116460
- The role of late INa in development of cardiac arrhythmias. Antzelevitch C, Nesterenko V, Shyrock JC, Rajamani S, Song Y, Belardinelli L. Handb Exp Pharmacol. 2014; 221:137-168. PMCID4076160
- Ranolazine effectively suppresses atrial fibrillation in the setting of heart failure. Burashnikov A, Di Diego J, Barajas-Martínez H... Antzelevitch C. Circ Heart Fail, 7:627-633, 2014. PMCID4102661
- Mutations in SCN10A responsible for a large fraction of cases of Brugada syndrome. Hu D, Barajas-Martínez H, Pfeiffer R, Dezi F, ... Antzelevitch C. J Am Coll Cardiol 64:66-79, 2014. PMCID4116276
- A CACNA1C variant associated with reduced voltage-dependent inactivation, increased CaV1.2 channel window current, and arrhythmogenesis. Hennessey JA, Boczek NJ, Jiang YH,... Antzelevitch C. PloS One, 9:e106982, 2014. PMCID4153713
- Optical and electrical recordings from isolated coronary-perfused ventricular wedge preparations. Di Diego JM, Sicouri S, Myles RC, Burton FL, Smith GL, Antzelevitch C. J Mol Cell Cardiol, 54:53-64, 2013. PMCID3535682
- Role of late sodium channel current block in the management of atrial fibrillation. Burashnikov A, Antzelevitch C. Cardiovasc Drugs Ther, 27:79-89, 2013. PMCID3557765
- Mechanisms of cardiac arrhythmia. In: Electrical Diseases of the Heart. Vol. 1: Basic Foundations and Primary Electrical Diseases. 2nd ed. Antzelevitch C, Burashnikov A, Gussak I, Antzelevitch C, eds. New York, NY: Springer; 93-128, 2013.
- Mechanisms of action of antiarrhythmic drugs in for atrial fibrillation. In: Electrical Diseases of the Heart. Vol. 1: Basic Foundations and Primary Electrical Diseases. 2nd ed. Gussak I, Antzelevitch C, eds. Burashnikov A, Antzelevitch C. New York, NY:Springer; 141-156, 2013.
- Brugada Syndrome: Cellular mechanisms and approaches to therapy. In: Electrical Diseases of the Heart. Vol. 1: Basic Foundations and Primary Electrical Diseases. 2nd ed. Antzelevitch C, Viskin S. Gussak I, Antzelevitch C, eds. New York, NY: Springer; 497-536, 2013.
- Cardiomyocyte calcium cycling in a naturally occurring German shepherd dog model of inherited ventricular arrhythmia and sudden cardiac death. Jesty SA, Jung SW, Cordeiro JM, Gunn TM, Di Diego JM, Hemsley S, Kornreich BG, Hooker G, Antzelevitch C, Moïse NS. J Vet Cardiol 15:5-14, 2013. NIHMSID510226
- Early repolarization syndrome: a decade of progress. Gussak I, Antzelevitch C. J Electrocardio 46:110-113, 2013. PMCID3832739
- Extending the conditions of application of an inversion of the Hodgkin-Huxley gating model. Raba AE, Cordeiro JM, Antzelevitch C, Beaumont J. Bull Math Biol, 75:752-773, 2013. PMCID3855235
- Identification and characterization of a transient outward K+ current in human induced pluripotent stem cell-derived cardiomyocytes. Cordeiro JM, Nesterenko VV, Sicouri S, Goodrow RJ Jr., Treat JA, Wu Y, Doss MX, Antzelevitch C, Di Diego JM. J Mol Cell Cardiol, 60:36-46, 2013. PMCID3779808
- Antiarrhythmic effects of the highly selective late sodium channel current blocker GS-458967. Sicouri S, Belardinelli L, Antzelevitch C. Heart Rhythm, 10:1036-1043, 2013. PMCID3836836
- Identification of a novel de novo mutation associated with PRKAG2 cardiac syndrome and early onset of heart failure. Liu Y, Bai R, Wang L, Zhang C, ... Antzelevitch C. Plos One, 8:e64603, 2013. PMCID3669303
- Tissue-specific effects of acetylcholine in the canine heart. Calløe K, Goodrow R, Olesen SP, Antzelevitch C, Cordeiro JM. Am J Physiol Heart Circ Physiol, 305:H66-H75, 2013. PMCID3727104
- Ventricular fibrillation associated with complete right bundle branch block. Aizawa Y, Takatsuki S, Kimura T, ... Antzelevitch C. Heart Rhythm, 10:1028-1035, 2013. PMCID3770839
- Common variants at the SCN5A/SCN10A and HEY2 loci are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac death. Bezzina CR, Barc J, Mizusawa Y, Antzelevitch C, et al. Nat Genet, 1044-1049, 2013. PMCID3869788
- Cellular mechanisms underlying the effects of milrinone and cilostazol to suppress arrhythmogenesis associated with Brugada syndrome. Szél T, Koncz I, Antzelevitch C. Heart Rhythm, 10:1720-1727, 2013. PMCID3825770
- J wave syndromes: molecular and cellular mechanisms. Antzelevitch C. J Electrocardiol, 46:510-518, 2013. PMCID3825797
- The arrhythmogenic consequences of increasing late INa in the cardiomyocyte. Shryock JC, Song Y, Rajamani S, Antzelevitch C, Belardinelli L. Cardiovasc Res, 99:600-611, 2013. PMCID3841414
- Fever-induced Brugada pattern: how common is it and what does it mean? Adler A, Topaz G, Heller K, Zeltser D, Ohayon T, Rozovski U, Halkin A, Rosso R, Ben-Shachar S, Antzelevitch C, Viskin S. Heart Rhythm, 10:1375-1382, 2013.PMCID3832740
- Developmental changes in expression and biophysics of ion channels in the canine ventricle. Cordeiro JM, Panama BP, Goodrow RJ, Zygmunt AC, White C, Treat JA, Zeina T, Nesterenko VV, Di Diego JM, Burashnikov A, Antzelevitch C. J Mol Cell Cardiol, 64:79-89, 2013. PMCID3837711
- Electrophysiologic characteristics and pharmacologic response of human cardiomyocytes isolated from a patient with hypertrophic cardiomyopathy. Barajas-Martinez H, Hu D, Goodrow Jr RJ, Joyce F, Antzelevitch C. Pacing Clin Electrophysiol, 36:1512-1515, 2013. PMCID3855624