Charles Antzelevitch: Difference between revisions

Add links
From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
AnomieBOT (talk | contribs)
Bots
6,297,796 edits
m Dating maintenance tags: {{When?}}
Dloyle (talk | contribs)
172 edits
m Answering Wiki editors' questions in text
Line 45: Line 45:
In the realm of acquired arrhythmias, Antzelevitch's research team was the first to recognize that the antianginal drug ranolazine blocks the electrical pathway in the heart known as the late sodium channel, an atrial-selective action that has potential benefit in the treatment of AF.<ref>{{cite journal|url=http://circ.ahajournals.org/content/110/8/904.short |title=Electrophysiological Effects of Ranolazine, a Novel Antianginal Agent With Antiarrhythmic Properties |website=Circ.ahajournals.org |date=2004-08-09 |accessdate=2016-04-14}}</ref> With cardiac electrophysiologist Alexander Burashnikov, PhD, Antzelevitch subsequently hypothesized and then demonstrated that combining ranolazine with dronedarone, a drug with a similar action but different mechanism, can significantly suppress the occurrence of AF.<ref name="AF" /><ref>{{cite web|url=http://content.onlinejacc.org/article.aspx?articleID=1143752 |title=Synergistic Effect of the Combination of Ranolazine and Dronedarone to Suppress Atrial Fibrillation |website=Content.onlinejacc.org |accessdate=2016-04-14}}</ref>
In the realm of acquired arrhythmias, Antzelevitch's research team was the first to recognize that the antianginal drug ranolazine blocks the electrical pathway in the heart known as the late sodium channel, an atrial-selective action that has potential benefit in the treatment of AF.<ref>{{cite journal|url=http://circ.ahajournals.org/content/110/8/904.short |title=Electrophysiological Effects of Ranolazine, a Novel Antianginal Agent With Antiarrhythmic Properties |website=Circ.ahajournals.org |date=2004-08-09 |accessdate=2016-04-14}}</ref> With cardiac electrophysiologist Alexander Burashnikov, PhD, Antzelevitch subsequently hypothesized and then demonstrated that combining ranolazine with dronedarone, a drug with a similar action but different mechanism, can significantly suppress the occurrence of AF.<ref name="AF" /><ref>{{cite web|url=http://content.onlinejacc.org/article.aspx?articleID=1143752 |title=Synergistic Effect of the Combination of Ranolazine and Dronedarone to Suppress Atrial Fibrillation |website=Content.onlinejacc.org |accessdate=2016-04-14}}</ref>


In more recent years,{{when?|date=December 2017}} Antzelevitch is 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, he develops 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 directs the differentiation of these cells into cardiomyocytes. This approach allows him to delve further into the pathophysiology of disease and to develop patient-specific therapies.
Since 2010, Antzelevitch is 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, he develops 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 directs the differentiation of these cells into cardiomyocytes. This approach allows him to delve further into the pathophysiology of disease and to develop patient-specific therapies.


Additionally, his team is working to advance understanding of how genetic defects in ion channels that are common to both brain and heart may be responsible for induced epilepsy as well as life-threatening arrhythmias of the heart and thus contribute to Sudden Unexpected Death in Epilepsy.
Additionally, his team is working to advance understanding of how genetic defects in ion channels that are common to both brain and heart may be responsible for induced epilepsy as well as life-threatening arrhythmias of the heart and thus contribute to Sudden Unexpected Death in Epilepsy.


==Publications==
==Publications==

Revision as of 18:24, 27 December 2017

Charles Antzelevitch
Alma materUpstate Medical Center, SUNY at Syracuse (PhD)
Queens College, City University of New York (BA)
AwardsNorth American Society of Pacing and Electrophysiology (currently Heart Rhythm Society) Distinguished Scientist Award (2002)
American Heart Association Northeast Affiliate (currently Founders Affiliate[55]) Excellence in Cardiovascular Science Award (2003)
American Physiological Society Carl J. Wiggers Award (2007)
American College of Cardiology Distinguished Scientist Award (2011)
Cardiac Electrophysiology Society Distinguished Service Award (2015)
Scientific career
FieldsCardiology, Electrophysiology, Pharmacology, Genetics
InstitutionsLankenau Institute for Medical Research
Masonic Medical Research Laboratory

Charles Antzelevitch is an American cardiovascular research scientist internationally known for his work in cardiac electrophysiology and arrhythmia syndromes. Currently, he is professor and executive director of cardiovascular research at Lankenau Institute for Medical Research (LIMR), a biomedical research facility in Wynnewood, Pennsylvania, and director of research at Lankenau Heart Institute, both part of Main Line Health.[1]

Antzelevitch was president of the Cardiac Electrophysiology Society from 1996 to 1998[2] and has served as secretary/treasurer since 1998.[3] He is an associate editor of Heart Rhythm,[4] the official journal of the Heart Rhythm Society[5] and the Cardiac Electrophysiology Society,[6] and serves on the editorial board of several other peer-reviewed medical publications, including Journal of Electrocardiology[7] and Journal of the American College of Cardiology.[8]

Education and career

Antzelevitch graduated from Queens College, City University of New York with a BA in biology. He earned a PhD in pharmacology from State University of New York (SUNY) Upstate Medical University in 1978.[1] From 1977 to 1980, he held a postdoctoral fellowship in the department of experimental cardiology at the Masonic Medical Research Laboratory (MMRL) in Utica, New York.[9][10] After his fellowship, he joined the staff at MMRL as a research scientist, where he continued his scientific work until 2015.[11] While at MMRL, Antzelevitch was named executive director and director of research (1984)[10] and became Gordon K. Moe Scholar, an endowed chair in experimental cardiology (1987).[9]

He was a member of the faculty at SUNY Health Science Center in Syracuse, New York, from 1980 until 2015. In 1980, he received an appointment as assistant professor in the department of pharmacology. He was later promoted to associate professor (1983), research professor (1986), and professor (1995) of pharmacology.[9][10][12]

In 2015, Antzelevitch became professor and executive director of cardiovascular research at LIMR and director of research at Lankenau Heart Institute.[11] In June 2017, he was appointed Professor of Medicine and Pharmacology and Experimental Therapeutics at the Sidney Kimmel College of Medicine at Thomas Jefferson University.

Research

Antzelevitch wrote his doctoral thesis in 1977 on the cardiac actions of quinidine.[13] After joining MMRL, he began investigating and publishing scholarly articles on the mechanisms underlying ventricular arrhythmias, including parasystole and reentry.[14][15][16] Later, his interests expanded to include the genetic origins of inherited arrhythmia syndromes such as long QT,[17][18] short QT,[19] Brugada,[20][21] and early repolarization syndromes,[22][23] as well as the development of potential new treatments for atrial fibrillation (AF).[24][25][26] These investigations continue to be a focus of his current research at LIMR.[11]

In the 2010s, Antzelevitch began an ongoing investigation into genetic risk factors linked with the occurrence of life-threatening arrhythmias following myocardial infarction.[27] Additionally, with cardiac researcher Jose Di Diego, MD, Antzelevitch is exploring the heart-related therapeutic applications of human induced pluripotent stem cells and progenitor cells, including a possible role in the engineering of bioartificial hearts suitable for heart transplantation.[28][29] The first step in the organ bioengineering process is decellularization of cadaver hearts using detergents such as sodium dodecyl sulfate, leaving a collagen framework.[30] This bioartificial organ platform is termed a "ghost heart" because of its opaque white appearance. Induced pluripotent stem cells or progenitor cells generated from a patient's skin, blood, bone marrow or other sources will then be used in an attempt to repopulate the organ and to form a fully functioning human heart without risk of rejection.

Scientific achievements

Scientific discoveries

Antzelevitch's body of research has expanded scientific understanding of the heart's electrical system in a number of ways. His work has been instrumental in identifying the cellular and ionic basis for the various waves that make up the electrocardiogram (ECG), including the J wave, T wave and U wave.[31][32][33] He and his research team helped to identify reflected reentry, late phase 3 early afterdepolarizations, and phase 2 reentry (electrical dysfunctions that promote extra heart beats) as potential trigger mechanisms for dangerous tachycardia and fibrillation.[14][25][34]

His research team pioneered work demonstrating electrical heterogeneity within ventricular myocardium, showing that cells in the epicardium and endocardium differ with respect to electrical properties and response to pharmacologic agents.[35][36] In 1990, his team at MMRL, including Serge Sicouri, MD, discovered the M cell, a unique type of heart cell in the deep layers of the ventricular myocardium. The researchers observed that the M cell has different electrical properties from other heart cells, responds differently to drugs that affect the heart, and may be associated with potentially dangerous wave formations on ECGs.[37][38]

In 2000, Antzelevitch and colleagues reported experimental findings challenging the belief that early repolarization (an ECG variant often seen in athletes) is always a benign condition by demonstrating that early repolarization is linked to the development of arrhythmias leading to sudden cardiac death in experimental models.[39][40] Validation of this hypothesis came 8 years later in clinical studies from leading centers around the world.[41][42][43][44]

With cardiac researcher Gan-Xin Yan, MD, PhD, Antzelevitch used coronary-perfused wedge preparation technology[45] to develop a research model that helped pinpoint the cellular, ionic and genetic mechanisms underlying inherited arrhythmia syndromes such as long QT,[17] short QT,[19] Brugada,[20][46] and early repolarization[22][23] syndromes. With his research team, Antzelevitch has discovered 10 of the 19 genes found to be associated with Brugada syndrome, 5 of the 7 genes associated with early repolarization syndrome, and 4 of the 6 genes associated with short QT syndrome. In 2000, his research team, along with international colleagues, described a possible genetic link between long QT syndrome and sudden infant death syndrome.[47]

Contributions to clinical practice

Antzelevitch's research has helped to establish diagnostic criteria and treatment approaches for both inherited and acquired arrhythmia syndromes. With his colleagues, he demonstrated that quinidine could be used to treat ventricular tachycardia in experimental models of Brugada syndrome.[38][48] In 2000, Antzelevitch participated in the first Brugada syndrome consensus conference, which culminated in the report of diagnostic criteria for the inherited syndrome.[49] In 2005, he organized and was the lead co-author of the second Brugada syndrome consensus conference report, which elaborated on diagnostic criteria and addressed risk stratification and treatment approaches.[50] "In April 2015, Antzelevitch and LIMR colleague Yan convened a consensus conference to update the scientific and clinical communities on the mechanisms, diagnosis, prognosis, risk stratification, and treatment of Brugada syndrome and early repolarization syndrome, collectively known as J wave syndromes. In 2016, the report of the J-Wave Expert Consensus Conference was published simultaneously in Journal of Arrythmia,[51] Europace,[52] and Heart Rhythm.[53] Additionally, Antzelevitch and Yan edited J Wave Syndromes: Brugada and Early Repolarization Syndromes, a medical textbook containing further material to help clinicians identify and manage patients with these conditions.[54]

In the realm of acquired arrhythmias, Antzelevitch's research team was the first to recognize that the antianginal drug ranolazine blocks the electrical pathway in the heart known as the late sodium channel, an atrial-selective action that has potential benefit in the treatment of AF.[55] With cardiac electrophysiologist Alexander Burashnikov, PhD, Antzelevitch subsequently hypothesized and then demonstrated that combining ranolazine with dronedarone, a drug with a similar action but different mechanism, can significantly suppress the occurrence of AF.[26][56]

Since 2010, Antzelevitch is 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, he develops 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 directs the differentiation of these cells into cardiomyocytes. This approach allows him to delve further into the pathophysiology of disease and to develop patient-specific therapies.

Additionally, his team is working to advance understanding of how genetic defects in ion channels that are common to both brain and heart may be responsible for induced epilepsy as well as life-threatening arrhythmias of the heart and thus contribute to Sudden Unexpected Death in Epilepsy.

Publications

Antzelevitch has published 6 reference texts, more than 500 original peer-reviewed journal articles and book chapters, and over 370 abstracts.[11]

Selected peer-reviewed publications

Below are the top 20 most-cited journal articles authored or co-authored by Antzelevitch, according to Google Scholar:[57]

  • Maron, BJ; Towbin, JA; Thiene, G; Antzelevitch, C; Corrado, D; Arnett, D; Moss, AJ; Seidman, CE; Young, BJ (2006). "Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention". Circulation. 113 (14): 1807–1816. doi:10.1161/circulationaha.106.174287. PMID 16567565.
  • Antzelevitch, C; Brugada, P; Borggrefe, M; Brugada, J; Brugada, R; Corrado, D; Gussak, I; LeMarec, H; Nademanee, K; Perez Riera, AR; Shimizu, W; Schulze-Bahr, E; Tan, H; Wilde, A (2005). "Brugada syndrome: report of the second consensus conference. Endorsed by the Heart Rhythm Society and the European Heart Rhythm Association". Circulation. 111 (5): 659–670. doi:10.1161/01.cir.0000152479.54298.51. PMID 15655131.
  • Chen, Q; Kirsch, GE; Zhang, D; Brugada, R; Brugada, J; Brugada, P; Potenza, D; Moya, A; Borggrefe, M; Breithardt, G; Ortiz-Lopez, R; Wang, Z; Antzelevitch, C; O'Brien, RE; Schulze-Bahr, E; Keating, MT; Towbin, JA; Wang, Q (1998). "Genetic basis and molecular mechanism for idiopathic ventricular fibrillation". Nature. 392 (6673): 293–296. doi:10.1038/32675. PMID 9521325.
  • Yan, GX; Antzelevitch, C (1999). "Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation". Circulation. 100 (15): 1660–1666. doi:10.1161/01.cir.100.15.1660. PMID 10517739.
  • Yan, GX; Antzelevitch, C (1998). "Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome". Circulation. 98 (18): 1928–1936. doi:10.1161/01.cir.98.18.1928. PMID 9799215.
  • Yan, GX; Antzelevitch, C (1996). "Cellular basis for the electrocardiographic J wave". Circulation. 93 (2): 372–379. doi:10.1161/01.cir.93.2.372. PMID 8548912.
  • Antzelevitch, C; Sicouri, S; Litovsky, SH; Lukas, A; Krishnan, SC; Di Diego, JM; Gintant, GA; Liu, DW (1991). "Heterogeneity within the ventricular wall. Electrophysiology and pharmacology of epicardial, endocardial, and M cells". Circ Res. 69 (6): 1427–1449. doi:10.1161/01.res.69.6.1427. PMID 1659499.
  • Wilde, AA; Antzelevitch, C; Borggrefe, M; Brugada, J; Brugada, R; Brugada, P; Corrado, D; Hauer, RN; Kass, RS; Nademanee, K; Priori, SG; Towbin, JA (2002). "Proposed diagnostic criteria for the Brugada syndrome: consensus report". Circulation. 106 (19): 2514–2519. doi:10.1161/01.cir.0000034169.45752.4a. PMID 12417552.
  • Brugada, R; Brugada, J; Antzelevitch, C; Kirsch, GE; Potenza, D; Towbin, JA; Brugada, P (2000). "Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts". Circulation. 101 (5): 510–515. doi:10.1161/01.cir.101.5.510. PMID 10662748.
  • Brugada, R; Hong, K; Dumaine, R; Cordeiro, J; Gaita, F; Borggrefe, M; Menendez, TM; Brugada, J; Pollevick, GD; Wolpert, C; Burashnikov, E; Matsuo, K; Wu, YS; Guerchicoff, A; Bianchi, F; Giustetto, C; Schimpf, R; Brugada, P; Antzelevitch, C (2004). "Sudden death associated with short-QT syndrome linked to mutations in HERG". Circulation. 109 (1): 30–35. doi:10.1161/01.cir.0000109482.92774.3a. PMID 14676148.
  • Haverkamp, W; Breithardt, G; Camm, AJ; Janse, MJ; Rosen, MR; Antzelevitch, C; Escande, D; Franz, M; Malik, M; Moss, A; Shah, R (2000). "The potential for QT prolongation and pro-arrhythmia by non–anti-arrhythmic drugs: clinical and regulatory implications. Report on a Policy Conference of the European Society of Cardiology". Cardiovasc Res. 47 (2): 219–233. doi:10.1016/s0008-6363(00)00119-x. PMID 10947683.
  • Brugada, J; Brugada, R; Antzelevitch, C; Towbin, J; Nademanee, K; Brugada, P (2002). "Long-term follow-up of individuals with the electrocardiographic pattern of right bundle-branch block and ST-segment elevation in precordial leads V1 to V3". Circulation. 105 (1): 73–78. doi:10.1161/hc0102.101354. PMID 11772879.
  • Antzelevitch, C; Pollevick, GD; Cordeiro, JM; Casis, O; Sanguinetti, MC; Aizawa, Y; Guerchicoff, A; Pfeiffer, R; Oliva, A; Wollnik, B; Gelber, P; Bonaros, EP Jr; Burashnikov, E; Wu, Y; Sargent, JD; Schickel, S; Oberheiden, R; Bhatia, A; Hsu, LF; Haissaguerre, M; Schimpf, R; Borggrefe, M; Wolpert, C (2007). "Loss-of-function mutations in the cardiac calcium channel underlie a new clinical entity characterized by ST-segment elevation, short QT intervals, and sudden cardiac death". Circulation. 115 (4): 442–449. doi:10.1161/CIRCULATIONAHA.106.668392. PMC 1952683. PMID 17224476.
  • Liu, DW; Antzelevitch, C (1995). "Characteristics of the delayed rectifier current (IKr and IKs) in canine ventricular epicardial, midmyocardial, and endocardial myocytes. A weaker IKs contributes to the longer action potential of the M cell". Circ Res. 76 (3): 351–365. doi:10.1161/01.res.76.3.351. PMID 7859382.
  • Gussak, I; Antzelevitch, C; Bjerregaard, P; Towbin, JA; Chaitman, BR (1999). "The Brugada syndrome: clinical, electrophysiologic and genetic aspects". J Am Coll Cardiol. 33 (1): 5–15. doi:10.1016/s0735-1097(98)00528-2. PMID 9935001.
  • Sicouri, S; Antzelevitch, C (1991). "A subpopulation of cells with unique electrophysiological properties in the deep subepicardium of the canine ventricle. The M cell". Circ Res. 68 (6): 1729–1741. doi:10.1161/01.res.68.6.1729. PMID 2036721.
  • Antzelevitch, C; Belardinelli, L; Zygmunt, AC; Burashnikov, A; Di Diego, JM; Fish, JM; Cordeiro, JM; Thomas, G (2004). "Electrophysiological effects of ranolazine, a novel antianginal agent with antiarrhythmic properties". Circulation. 110 (8): 904–910. doi:10.1161/01.CIR.0000139333.83620.5D. PMC 1513623. PMID 15302796.
  • Antzelevitch, C; Shimizu, W; Yan, GX; Sicouri, S; Weissenburger, J; Nesterenko, VV; Burashnikov, A; Di Diego, J; Saffitz, J; Thomas, GP (1999). "The M Cell: its contribution to the ECG and to normal and abnormal electrical function of the heart". J Cardiovasc Electrophysiol. 10 (8): 1124–1152. doi:10.1111/j.1540-8167.1999.tb00287.x. PMID 10466495.
  • Antzelevitch, C; Sicouri, S (1994). "Clinical relevance of cardiac arrhythmias generated by afterdepolarizations. Role of M cells in the generation of U waves, triggered activity and torsade de pointes". J Am Coll Cardiol. 23 (1): 259–277. doi:10.1016/0735-1097(94)90529-0. PMID 8277090.
  • Dumaine, R; Towbin, JA; Brugada, P; Vatta, M; Nesterenko, DV; Nesterenko, VV; Brugada, J; Brugada, R; Antzelevitch, C (1999). "Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent". Circ Res. 85 (9): 803–809. doi:10.1161/01.res.85.9.803. PMID 10532948.

Reference texts

  • Antzelevitch C, Brugada P, Brugada J, Brugada R, Nademanee K, Towbin J (1999). The Brugada Syndrome. Armonk (NY): Futura. (Camm AJ, editor. Clinical approaches to tachyarrhythmias; vol. 10). ISBN 0879934344.
  • Gussak I, Antzelevitch C, editors (2003). Cardiac Repolarization: Bridging Basic and Clinical Science. Totowa (NJ): Humana. (Contemporary cardiology). ISBN 1588290697.
  • Antzelevitch C, editor (2005). The Brugada Syndrome: From Bench to Bedside. Malden (MA): Blackwell Futura. ISBN 1405127783.
  • Gussak I, Antzelevitch C, editors (2008). Electrical Diseases of the Heart: Genetics, Mechanisms, Treatment, Prevention. London: Springer. ISBN 1846288533.
  • Antzelevitch C, guest editor (2011). Basic Science for the Clinical Electrophysiologist. Philadelphia: Saunders. (Cardiac electrophysiology clinics; vol. 3, no 1). ISBN 1455704237.
  • Gussak I, Antzelevitch C, editors (2013). Electrical Diseases of the Heart. 2nd ed. London: Springer. 2 vol. ISBN 9781447148807 (vol. 1); 9781447149774 (vol. 2).
  • Antzelevitch C, Yan G-X, editors. J Wave Syndromes. Springer International Publishing AG, Switzerland, 2016. DOI: 10.1007/978-3-319-31578-2

Honors

  • 1996 – President, International Cardiac Electrophysiology Society
  • 1998 – Secretary/Treasurer, International Cardiac Electrophysiology Society
  • 2002 – Distinguished Scientist Award, North American Society of Pacing and Electrophysiology (currently Heart Rhythm Society)
  • 2003 – Excellence in Cardiovascular Science Award, American Heart Association Northeast Affiliate (currently Founders Affiliate)[58]
  • 2007 – Carl J. Wiggers Award, American Physiological Society
  • 2011 – Distinguished Scientist Award, American College of Cardiology
  • 2015 – Associate Editor, Heart Rhythm journal
  • 2015 – Distinguished Service Award, Cardiac Electrophysiology Society, Boston, Massachusetts
  • 2016 – Douglas P. Zipes Lecture Award, Heart Rhythm Society, San Francisco, CA

References

  1. ^ a b "Charles Antzelevitch, PhD, FACC, FAHA, FHR - LIMR - Researcher Profile". Limr.org. Retrieved 2016-04-14.[permanent dead link]
  2. ^ "CES Past Presidents — Cardiac Electrophysiology Society". Cardiaceps.org. Retrieved 2016-04-14.
  3. ^ "About CardiacEPS — Cardiac Electrophysiology Society". Cardiaceps.org. Retrieved 2016-04-14.
  4. ^ [1] [dead link]
  5. ^ "Heart Rhythm Society". Hrsonline.org. Retrieved 2016-04-14.
  6. ^ "Cardiac Electrophysiology Society". Cardiaceps.org. Retrieved 2016-04-14.
  7. ^ [2] [dead link]
  8. ^ "JACC : Editorial Board and Staff". Content.onlinejacc.org. Retrieved 2016-04-14.
  9. ^ a b c Amy Neff Roth (2010-10-16). "Charles Antzelevitch's profile - News - Uticaod - Utica, NY". Uticaod.com. Retrieved 2016-04-14.
  10. ^ a b c "History". Mmrl.edu. Retrieved 2016-04-14.
  11. ^ a b c d "Prominent Cardiac Researcher, Charles Antzelevitch, PhD, Joins Lankenau Institute for Medical Research and Lankenau Heart Institute: Main Line Health, Philadelphia, Pennsylvania". Mainlinehealth.org. 2015-07-22. Retrieved 2016-04-14.
  12. ^ "New Westminster College, British Columbia, Canada – Professor Dr. Charles Antzelevitch, B.A., Ph.D". Newwestminstercollege.ca. 2014-03-19. Retrieved 2016-04-14.
  13. ^ Antzelevitch C (1977). Cardiac Actions of Quinidine (Thesis). Syracuse (NY): State University of New York Upstate Medical Center
  14. ^ a b "Characteristics of reflection as a mechanism of reentrant arrhythmias and its relationship to parasystole". Circ.ahajournals.org. 1980-01-01. Retrieved 2016-04-14.
  15. ^ "The Case for Modulated Parasystole". Pacing and Clinical Electrophysiology. 5: 911–926. 2015-03-31. doi:10.1111/j.1540-8159.1982.tb00030.x. Retrieved 2016-04-14.
  16. ^ "The Effects of Milrinone on Action Potential Characteristics... : Journal of Cardiovascular Pharmacology". Journals.lww.com. 2015-09-01. Retrieved 2016-04-14.
  17. ^ a b Gan-Xin Yan, MD; Charles Antzelevitch. "Cellular Basis for the Normal T Wave and the Electrocardiographic Manifestations of the Long-QT Syndrome". Circ.ahajournals.org. Retrieved 2016-04-14.
  18. ^ Shimizu, W; Antzelevitch, C (2015-09-28). "Differential effects of beta-adrenergic agonists and antagonists in LQT1, LQT2 and LQT3 models of the long QT syndrome". J. Am. Coll. Cardiol. 35: 778–86. PMID 10716483.
  19. ^ a b Patel, C; Antzelevitch, C (2015-09-28). "Cellular basis for arrhythmogenesis in an experimental model of the SQT1 form of the short QT syndrome". Heart Rhythm. 5: 585–90. doi:10.1016/j.hrthm.2008.01.022. PMC 2361425. PMID 18362027.
  20. ^ a b "The Brugada Syndrome". Journal of Cardiovascular Electrophysiology. 9: 513–516. doi:10.1111/j.1540-8167.1998.tb01844.x. Retrieved 2016-04-14.
  21. ^ [3] [dead link]
  22. ^ a b [4] [dead link]
  23. ^ a b [5] [dead link]
  24. ^ Alexander Burashnikov, PhD; Charles Antzelevitch, PhD (2003-04-14). "Reinduction of Atrial Fibrillation Immediately After Termination of the Arrhythmia Is Mediated by Late Phase 3 Early Afterdepolarization–Induced Triggered Activity". Circ.ahajournals.org. Retrieved 2016-04-14.
  25. ^ a b "Late-Phase 3 EAD. A Unique Mechanism Contributing to Initiation of Atrial Fibrillation". Pacing and Clinical Electrophysiology. 29: 290–295. doi:10.1111/j.1540-8159.2006.00336.x. Retrieved 2016-04-14.
  26. ^ a b Burashnikov, A; Di Diego, JM; Zygmunt, AC; Belardinelli, L; Antzelevitch, C (2008-03-19). "Atrial-Selective Sodium Channel Block as a Strategy for Suppression of Atrial Fibrillation". Annals of the New York Academy of Sciences. 1123: 105–112. doi:10.1196/annals.1420.012. PMC 2366169. PMID 18375582. Retrieved 2016-04-14.
  27. ^ [6] [dead link]
  28. ^ "Maximum Diastolic Potential of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes Depends Critically on IKr". PLoS ONE. 7: e40288. 2012-07-05. doi:10.1371/journal.pone.0040288. Retrieved 2016-04-14.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  29. ^ [7] [dead link]
  30. ^ Ott, HC; Matthiesen, TS; Goh, SK; Black, LD; Kren, SM; Netoff, TI; Taylor, DA. "Perfusion-decellularized matrix: using nature's platform to engineer a bioartificial heart". Nature Medicine. 14: 213–221. doi:10.1038/nm1684. PMID 18193059. Retrieved 2016-04-14.
  31. ^ "Cardiovascular Research". Cardiovascres.oxfordjournals.org. Retrieved 2016-04-14.
  32. ^ Antzelevitch C (2004). "Cellular basis for the repolarization waves of the ECG." In: Malik M, Camm AJ, editors. Dynamic Electrocardiography. Elmsford (NY): Blackwell Futura. p. 291–300. ISBN 1405119608
  33. ^ Antzelevitch C (2002). "Cellular basis for J, T and U waves of the ECG". In: Ovsyshcher IE, editor. New Developments in Cardiac Pacing and Electrophysiology. Armonk (NY): Futura, p. 1–8. ISBN 0879937068
  34. ^ "Cardiovascular Research". Cardiovascres.oxfordjournals.org. Retrieved 2016-04-14.
  35. ^ Litovsky, SH; Antzelevitch, C (2015-09-28). "Transient outward current prominent in canine ventricular epicardium but not endocardium". Circ. Res. 62: 116–26. doi:10.1161/01.res.62.1.116. PMID 2826039.
  36. ^ "Heterogeneity within the ventricular wall. Electrophysiology and pharmacology of epicardial, endocardial, and M cells". Circres.ahajournals.org. 1991-12-01. Retrieved 2016-04-14.
  37. ^ S Sicouri; C Antzelevitch (2016-04-01). "A subpopulation of cells with unique electrophysiological properties in the deep subepicardium of the canine ventricle. The M cell". Circres.ahajournals.org. Retrieved 2016-04-14.
  38. ^ a b Antzelevitch, C; Shimizu, W; Yan, GX; Sicouri, S; Weissenburger, J; Nesterenko, VV; Burashnikov, A; Di Diego, J; Saffitz, J; Thomas, GP (1999). "The M cell: its contribution to the ECG and to normal and abnormal electrical function of the heart". J. Cardiovasc. Electrophysiol. 10: 1124–52. doi:10.1111/j.1540-8167.1999.tb00287.x. PMID 10466495. Retrieved 2016-04-14.
  39. ^ Gussak, I; Antzelevitch, C (2015-09-28). "Early repolarization syndrome: clinical characteristics and possible cellular and ionic mechanisms". J Electrocardiol. 33: 299–309. PMID 11099355.
  40. ^ "Augmentation of J Waves and Electrical Storms in Patients with Early Repolarization". New England Journal of Medicine. 358: 2078–2079. doi:10.1056/NEJMc0708182. Retrieved 2016-04-14.
  41. ^ Rosso, R; Kogan, E; Belhassen, B; Rozovski, U; Scheinman, MM; Zeltser, D; Halkin, A; Steinvil, A; Heller, K; Glikson, M; Katz, A; Viskin, S (2015-09-28). "J-point elevation in survivors of primary ventricular fibrillation and matched control subjects: incidence and clinical significance. -". J. Am. Coll. Cardiol. 52: 1231–8. doi:10.1016/j.jacc.2008.07.010. PMID 18926326.
  42. ^ "Sudden Cardiac Arrest Associated with Early Repolarization". New England Journal of Medicine. 358: 2016–2023. doi:10.1056/NEJMoa071968. Retrieved 2016-04-14.
  43. ^ "Long-Term Outcome Associated with Early Repolarization on Electrocardiography". New England Journal of Medicine. 361: 2529–2537. doi:10.1056/NEJMoa0907589. Retrieved 2016-04-14.
  44. ^ "The early repolarization pattern in the general population: clinical correlates and heritability". Pubfacts.com. Retrieved 2016-04-14.
  45. ^ "Characteristics and Distribution of M Cells in Arterially Perfused Canine Left Ventricular Wedge Preparations". Circ.ahajournals.org. Retrieved 2016-04-14.
  46. ^ Gan-Xin Yan, MD; Charles Antzelevitch, PhD. "Cellular Basis for the Brugada Syndrome and Other Mechanisms of Arrhythmogenesis Associated With ST-Segment Elevation". Circ.ahajournals.org. Retrieved 2016-04-14.
  47. ^ "Molecular Link between the Sudden Infant Death Syndrome and the Long-QT Syndrome". Nejm.org. 343: 262–267. doi:10.1056/NEJM200007273430405. Retrieved 2016-04-14.
  48. ^ Antzelevitch C, Brugada P, Brugada J, Brugada R, Nademanee K, Towbin JA. The Brugada Syndrome. Armonk (NY): Futura Publishing; 1999. (Camm AJ, editor. Clinical approaches to tachyarrhythmias; vol. 10). ISBN 0879934344.
  49. ^ "Proposed Diagnostic Criteria for the Brugada Syndrome". Circ.ahajournals.org. 2000-09-01. Retrieved 2016-04-14.
  50. ^ "Brugada Syndrome: Report of the Second Consensus Conference". Circ.ahajournals.org. 2005-01-17. Retrieved 2016-04-14.
  51. ^ Antzelevitch, C; Yan, GX; Ackerman, MJ; Borggrefe, M; Corrado, D; Guo, J; Gussak, I; Hasdemir, C; Horie, M; Huikuri, H; Ma, C; Morita, H; Nam, GB; Sacher, F; Shimizu, W; Viskin, S; Wilde, AA (2016). "J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge". J Arrhythm. 32 (5): 315–339. doi:10.1016/j.joa.2016.07.002. PMC 5063270. PMID 27761155.
  52. ^ Antzelevitch, C; Yan, GX; Ackerman, MJ; Borggrefe, M; Corrado, D; Guo, J; Gussak, I; Hasdemir, C; Horie, M; Huikuri, H; Ma, C; Morita, H; Nam, GB; Sacher, F; Shimizu, W; Viskin, S; Wilde, AA (2016). "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 Estimulacifin Cardiaca y Electrofisiologia [SOLAECE])". Europace: euw235. doi:10.1093/europace/euw235. PMID 27411360.
  53. ^ Antzelevitch, C; Yan, GX; Ackerman, MJ; Borggrefe, M; Corrado, D; Guo, J; Gussak, I; Hasdemir, C; Horie, M; Huikuri, H; Ma, C; Morita, H; Nam, GB; Sacher, F; Shimizu, W; Viskin, S; Wilde, AA (2016). "J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge". Heart Rhythm. 13 (10): e295–324. doi:10.1016/j.hrthm.2016.05.024. PMC 5035208. PMID 27423412.
  54. ^ Antzelevitch C, Yan GX, editors (2016). J Wave Syndromes: Brugada and Early Repolarization Syndromes. Cham (Switzerland): Springer. ISBN 3319315765.
  55. ^ "Electrophysiological Effects of Ranolazine, a Novel Antianginal Agent With Antiarrhythmic Properties". Circ.ahajournals.org. 2004-08-09. Retrieved 2016-04-14.
  56. ^ "Synergistic Effect of the Combination of Ranolazine and Dronedarone to Suppress Atrial Fibrillation". Content.onlinejacc.org. Retrieved 2016-04-14.
  57. ^ "Charles Antzelevitch - Google Scholar Citations". Scholar.google.com. Retrieved 2016-04-14.
  58. ^ "Affiliate List by States". Professional.heart.org. Retrieved 2016-04-14.

External links

Retrieved from "https://en.wikipedia.org/w/index.php?title=Charles_Antzelevitch&oldid=817332374"