Ionic and cellular basis for the predominance of the Brugada syndrome phenotype in males

Circulation

Volumn 106, Issue 15, 2002, Pages 2004-2011

  Di Diego, José M ^a   Cordeiro, Jonathan M ^a   Goodrow, Robert J ^a   Fish, Jeffrey M ^a   Zygmunt, Andrew C ^a   Pérez, Guillermo J ^a   Scornik, Fabiana S ^a   Antzelevitch, Charles ^a  

^a MASONIC MEDICAL RESEARCH LABORATORY   (United States)

Author keywords

Epicardium; Ion channels; Pinacidil; Sex

Indexed keywords

ION CHANNEL; PINACIDIL; TERFENADINE;

ACTION POTENTIAL; ANIMAL CELL; ANIMAL TISSUE; ARTICLE; AUTOSOMAL DOMINANT DISORDER; BRUGADA SYNDROME; CONTROLLED STUDY; DISEASE TRANSMISSION; DNA POLYMORPHISM; DOG; ELECTRIC POTENTIAL; EPICARDIUM; FEMALE; HEART REPOLARIZATION; HEART VENTRICLE FIBRILLATION; HEART VENTRICLE TACHYCARDIA; MALE; NONHUMAN; PENETRANCE; PHENOTYPE; PREVALENCE; PRIORITY JOURNAL; REENTRY ARRHYTHMIA; SEX DIFFERENCE; TISSUE SLICE;

ACTION POTENTIALS; ANIMALS; ARRHYTHMIA; CELLS, CULTURED; CULTURE TECHNIQUES; DOGS; FEMALE; HEART; KINETICS; MALE; PERICARDIUM; PHENOTYPE; PINACIDIL; SEX FACTORS; SYNDROME; TERFENADINE;

EID: 0037044399     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.CIR.0000032002.22105.7A     Document Type: Article

References (30)

1. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome: a multicenter report. J Am Coll Cardiol. 1992;20:1391-1396.
2. Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation. 1996;93:372-379.
3. Miyazaki T, Mitamura H, Miyoshi S, et al. Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome. J Am Coll Cardiol. 1996;27:1061-1070.
4. Chen Q, Kirsch GE, Zhang D, et al. Genetic basis and molecular mechanisms for idiopathic ventricular fibrillation. Nature. 1998;392:293-296.
5. Dumaine R, Towbin JA, Brugada P, et al. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ Res. 1999;85:803-809.
6. Antzelevitch C, Dumaine R. Electrical heterogeneity in the heart: physiological, pharmacological and clinical implications. In: Page E, Fozzard HA, Solaro RJ, eds. Handbook of Physiology: The Heart. New York, NY: Oxford University Press; 2002.
7. Antzelevitch C. The Brugada syndrome: ionic basis and arrhythmia mechanisms. J Cardiovasc Electrophysiol. 2001;12:268-272.
8. Balser JR. The cardiac sodium channel: gating function and molecular pharmacology. J Mol Cell Cardiol. 2001;33:599-613.
9. Bezzina CR, Rook MB, Wilde AA. Cardiac sodium channel and inherited arrhythmia syndromes. Cardiovasc Res. 2001;49:257-271.
10. Priori SG, Napolitano C, Grillo M. Concealed arrhythmogenic syndromes: the hidden substrate of idiopathic ventricular fibrillation? Cardiovasc Res. 2001;50:218-223.
11. Weiss R, Barmada MM, Nguyen T, et al. Clinical and molecular heterogeneity in the Brugada syndrome: a novel gene locus on chromosome 3. Circulation. 2002;105:707-713.
12. Antzelevitch C, Brugada P, Brugada, J, et al. The Brugada Syndrome. Armonk, NY: Futura Publishing Co; 1999.
13. Yan GX, Antzelevitch C. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST segment elevation. Circulation. 1999;100:1660-1666.
14. Lukas A, Antzelevitch C. Phase 2 reentry as a mechanism of initiation of circus movement reentry in canine epicardium exposed to simulated ischemia: the antiarrhythmic effects of 4-aminopyridine. Cardiovasc Res. 1996;32:593-603.
15. Antzelevitch C. The Brugada syndrome: ionic basis and arrhythmia mechanisms. J Cardiovasc Electrophysiol. 2001;12:268-272.
16. to and action potential notch are smaller in left vs. right canine ventricular epicardium. Am J Physiol. 1996;271:H548-H561.
17. Yan GX. Shimizu W, Amzelevitch C. Characteristics and distribution of M cells in arterially perfused canine left ventricular wedge preparations. Circulation. 1998;98:1921-1927.
18. Shimizu W, Antzelevitch C. Cellular basis for the electrocardiographic features of the LQT1 form of the long QT syndrome: effects of β-adrenergic agonists, antagonists, and sodium channel blockers on transmural dispersion of repolarization and torsade de pointes. Circulation. 1998;98:2314-2322.
19. Yan GX. Antzelevitch C. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long QT syndrome. Circulation. 1998;98:1928-1936.
20. Ks contributes to the longer action potential of the M cell. Circ Res. 1995;76:351-365.
21. Liu DW, Gintant GA, Antzelevitch C. Ionic bases for electrophysiological distinctions among epicardial, midmyocardial, and endocardial myocytes from the free wall of the canine left ventricle. Circ Res. 1993;72:671-687.
22. Brugada R, Brugada J, Kirsch GE, et al. Sodium channel blockers identify risk for sudden death in patients with ST segment elevation and RBBB but structurally normal hearts. Circulation. 2000;8:510-515.
23. Antzelevitch C. The Brugada syndrome. J Cardiovasc Electrophysiol. 1998;9:513-516.
24. 3. Circulation. 2002;105:73-78.
25. Nademanee K, Veerakul G, Nimmannit S. et al. Arrhythmogenic marker for the sudden unexplained death syndrome in Thai men. Circulation. 1997;96:2595-2600.
26. Priori SG. Long QT and Brugada syndromes: from genetics to clinical management. J Cardiovasc Electrophysiol. 2000;11:1174-1178.
27. Krishnan SC, Antzelevitch C. Flecainide-induced arrhythmia in canine ventricular epicardium: phase 2 reentry? Circulation. 1993;87:562-572.
28. 2+]-induced electrical heterogeneity and extrasystolic activity in isolated canine ventricular epicardium: phase 2 reentry. Circulation. 1994;89:1839-1850.
29. Antzelevitch C, Fish J. Electrical heterogeneity within the ventricular wall. Basic Res Cardiol. 2001;96:517-527.
30. Song M, Helguera G, Eghbali M, et al. Remodeling of Ky4.3 potassium channel gene expression under the control of sex hormones. J Biol Chem. 2001;276:31883-31890.