Screening for drug-induced (acquired) long QT syndrome: is it time to apply new methods?

mogenic marker for the sudden unexplained death syndrome in Thai men. Circulation 1997; 96: 2595–2600. [7] Priori SG, Napolitano C, Glordano U et al. Brugada syndrome and sudden cardiac death in children. Lancet 2000; 355: 808–9. [8] Corrado D, Buja G, Basso C et al. What is the Brugada syndrome? Cardiol Rev 1999; 7: 191–5. [9] Brugada R, Brugada J, Antzelevitch C et al. Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts. Circulation 2000; 101: 510–15. [10] Remme CA, Wever EFD, Wilde AAM, Derksen R, Hauer RNW. Diagnosis and long-term follow-up of Brugada syndrome in patients with idiopathic ventricular fibrillation. Eur Heart J 2001; 22: 400–409. [11] Viskin S, Fish R, Eldar M et al. Prevalence of the Brugada sign in idiopathic ventricular fibrillation and healthy controls [see comments]. Heart 2000; 84: 31–36. [12] Chen Q, Kirsch GE, Zhang D et al. Genetic basis and molecular mechanisms for idiopathic ventricular fibrillation. Nature 1998; 392: 293–6. [13] Yan GX, Antzelevitch C. Cellular basis for the Brugada Syndrome and other mechanisms of arrhythmogenesis associated with ST segment elevation. Circulation 1999; 100: 1660–6. [14] Rook MB, Alshinawi CB, Groenewegen WA et al. Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome. Cardiovasc Res 1999; 44: 507–17. [15] 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: 803–9. [16] Deschenes I, Baroudi G, Berthet M et al. Electrophysiological characterization of SCN5A mutations causing long QT (E1784K) and Brugada (R1512W and R1432G) syndromes [see comments]. Cardiovasc Res 2000; 46: 55–65. [17] Bezzina C, Veldkamp MW, van Den Berg MP et al. A single Na(+) channel mutation causing both long-QT and Brugada syndromes. Circ Res 1999; 85: 1206–13. [18] Alshinawi C, Mannens M, Wilde AAM. Mutations in the human cardiac sodium channel gene (SCN5A) in patients with Brugada syndrome (Abstr). Eur Heart J 1998; 19 (Abstr Suppl): 78. [19] Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996; 93: 372–9. [20] Gussak I, Antzelevitch C, Bjerregaard P et al. The Brugada syndrome: clinical, electrophysiological and genetic aspects. J Am Coll Cardiol 1999; 33: 5–15. [21] 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: 1061–70. [22] 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. [23] 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: Oxford University Press 2000:. [24] Antzelevitch C. Ion channels and ventricular arrhythmias. Cellular and ionic mechanisms underlying the Brugada syndrome. Curr Opin Cardiol 1999; 14: 274–9. [25] Tarin N, Farre J, Rubio JM et al. Brugada-like electrocardiographic pattern in a patient with a mediastinal tumor. PACE 1999; 22: 1264–66. [26] Carlsson J, Erdogan A, Schulte B et al. Possible role of left ventricular programmed stimulation in Brugada syndrome. PACE 2000; (In Press). [27] Litovsky SH, Antzelevitch C. Differences in the electrophysiological response of canine ventricular subendocardium and subepicardium to acetylcholine and isoproterenol. A direct effect of acetylcholine in ventricular myocardium. Circ Res 1990; 67: 615–27. [28] Krishnan SC, Antzelevitch C. Flecainide-induced arrhythmia in canine ventricular epicardium: Phase 2 Reentry? Circulation 1993; 87: 562–72. [29] Matsuo K, Shimizu W, Kurita T et al. Increased dispersion of repolarization time determined by monophasic action potentials in two patients with familial idiopathic ventricular fibrillation. J Cardiovasc Electrophysiol 1998; 9: 74–83. [30] Xiao YF, Wright SN, Wang GK et al. Coexpression with beta(1)-subunit modifies the kinetics and fatty acid block of hH1(alpha) Na(+) channels [In Process Citation]. Am J Physiol Heart Circ Physiol 2000; 279: H35–H46. [31] Kuryshev YA, Brittenham GM, Fujioka H et al. Decreased sodium and increased transient outward potassium currents in iron-loaded cardiac myocytes. Implications for the arrhythmogenesis of human siderotic heart disease. Circulation 1999; 100: 675–83. [32] Shimizu W, Matsuo K, Takagi M et al. Body surface distribution and response to drugs of ST segment elevation in Brugada syndrome: clinical implication of eighty-seven-lead body surface potential mapping and its application to twelvelead electrocardiograms. J Cardiovasc Electrophysiol 2000; 11: 396–404.