8-4-3 ⓔ文献

  1. Hayashi M, Shimizu W, et al: The spectrum of epidemiology underlying sudden cardiac death. Circ Res, 2015; 116: 1887–1906.

  2. Priori SG, Wilde AA, et al: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart rhythm, 2013; 10: 1932–1963.

  3. 遺伝性不整脈の診療に関するガイドライン (2017年改訂版).https://www.j-circ.or.jp/cms/wp-content/uploads/2020/02/JCS2017_aonuma_h.pdf

  4. Stiles MK, Wilde AAM, et al: 2020 APHRS/HRS expert consensus statement on the investigation of decedents with sudden unexplained death and patients with sudden cardiac arrest, and of their families. Heart Rhythm, 2020; S1547–5271 (20) 30953–X. doi: 10.1016/j.hrthm.2020.10.010.

  5. Schwartz PJ, Stramba–Badiale M, et al. Prevalence of the congenital long-QT syndrome. Circulation, 2009; 120: 1761–1767.

  6. Shimizu W, Noda T, et al: Epinephrine unmasks latent mutation carriers with LQT1 form of congenital long–QT syndrome. J Am Coll Cardiol, 2003; 41: 633–642.

  7. Shimizu W, Noda T, et al: Diagnostic value of epinephrine test for genotyping LQT1, LQT2, and LQT3 forms of congenital long QT syndrome. Heart Rhythm, 2004; 1: 276–283.

  8. Schwartz PJ, Priori SG, et al: Genotype–phenotype correlation in the long-QT syndrome: Gene–specific triggers for life-threatening arrhythmias. Circulation, 2001; 103: 89–95.

  9. Wilde AAM, Jongbloed RJE, et al: Auditory stimuli as a trigger for arrhythmic events differentiate HERG–related (LQT2) patients from KVLQT1–related patients (LQT1). J Am Coll Cardiol, 1999; 33: 327–332.

  10. Moss AJ, Shimizu W, et al: Clinical aspects of type–1 long–QT syndrome by location, coding type, and biophysical function of mutations involving the KCNQ1 gene. Circulation, 2007; 115: 2481–2489.

  11. Shimizu W, Moss AJ, et al: Genotype–phenotype aspects of type 2 long QT syndrome. J Am Coll Cardiol, 2009; 54: 2052–2062.

  12. Wilde AA, Moss AJ, et al: Clinical aspects of type 3 long–QT syndrome: An International Multicenter Study. Circulation, 2016; 134: 872–882.

  13. Vincent GM, Schwartz PJ, et al: High efficacy of beta–blockers in long–QT syndrome type 1: contribution of noncompliance and QT-prolonging drugs to the occurrence of beta–blocker treatment "failures". Circulation, 2009; 119: 215–221.

  14. Shimizu W, Horie M, et al: Mutation site–specific differences in arrhythmic risk and sensitivity to sympathetic stimulation in LQT1 form of congenital long QT syndrome–Multi–center study in Japan–. J Am Coll Cardiol, 2004; 44: 117-125.

  15. Etheridge SP, Compton SJ, et al: A new oral therapy for long QT syndrome: long–term oral potassium improves repolarization in patients with HERG mutations. J Am Coll Cardiol, 2003; 42: 1777–1782.

  16. Shimizu W, Antzelevitch C: Sodium channel block with mexiletine is effective in reducing dispersion of repolarization and preventing torsade de pointes in LQT2 and LQT3 models of the long–QT syndrome. Circulation, 1997; 96: 2038–2047.

  17. Funasako M, Aiba T, et al: Pronounced shortening of QT interval with mexiletine infusion test in patients with type 3 congenital long QT syndrome. Circ J, 2016; 80: 340–345.

  18. Mazzanti A, Maragna R, et al. Gene–Specific Therapy With Mexiletine Reduces Arrhythmic Events in Patients With Long QT Syndrome Type 3. J Am Coll Cardiol, 2016; 67: 1053–1058.

  19. 不整脈非薬物治療ガイドライン (2018年改訂版) (日本循環器学会/日本不整脈心電学会合同ガイドライン).https//www.j-circ.or.jp/cms/wp-content/uploads/2018/07/JCS2018_kurita_nogami.pdf

  20. 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.

  21. Shimizu W, Aiba T, et al: Mechanisms of disease: current understanding and future challenges in Brugada syndrome. Nat Clin Pract Cardiovasc Med, 2005; 2: 408–414.

  22. Antzelevitch C, Yan GX, et al: J–Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge. J Arrhythm, 2016; 32: 315–339.

  23. Yamagata K, Horie M, et al: Genotype–Phenotype correlation of SCN5A mutations for the clinical and electrocardiographic characteristics of probands with Brugada syndrome: A Japanese Multicenter Registry. Circulation, 2017; 135: 2255–2270.

  24. Matsuo K, Akahoshi M, et al: The prevalence, incidence and prognostic value of the Brugada–type electrocardiogram. A population-based study of four decades. J Am Coll Cardiol, 2001; 38: 765–770.

  25. Miyasaka Y, Tsuji H, et al: Prevalence and mortality of the Brugada–type electrocardiogram in one city in Japan. J Am Coll Cardiol, 2001; 38: 771–774.

  26. Atarashi H, Ogawa S, et al: Three–year follow–up of patients with right bundle branch block and ST segment elevation in the right precordial leads: Japanese registry of Brugada syndrome. Idiopathic ventricular fibrillation investigators. J Am Coll Cardiol, 2001; 37: 1916–1920.

  27. Furuhashi M, Uno K, et al: Prevalence of asymptomatic ST segment elevation in right precordial leads with right bundle branch block (Brugada–type ST shift) among the general Japanese population. Heart, 2001; 86: 161–166.

  28. Sakabe M, Fujiki A, et al: Proportion and prognosis of healthy people with coved or saddle–back type ST segment elevation in the right precordial leads during 10 years follow–up. Eur Heart J, 2003; 24: 1488–1493.

  29. Yamakawa Y, Ishikawa T, et al: Prevalence of the right bundle–branch block and right precordial ST–segment elevation (Brugada–type electrocardiogram) in Japanese children. Circ J, 2004; 68: 275–279.

  30. Yoshinaga M, Anan R, et al: Prevalence and time of appearance of Brugada electrocardiographic pattern in young male adolescents from a three–year follow–up study. Am J Cardiol, 2004; 94: 1186–1189.

  31. Oe H, Takagi M, et al: Prevalence and clinical course of the juveniles with Brugada–type ECG in Japanese population. Pacing Clin Electrophysiol, 2005; 28: 549–554.

  32. Aiba T, Shimizu W, et al: Cellular basis for trigger and maintenance of ventricular fibrillation in the Brugada syndrome model: High resolution optical mapping study. J Am Coll Cardiol, 2006; 47: 2074–2085.

  33. Nademanee K, Veerakul G, et al: Prevention of ventricular fibrillation episodes in brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium. Circulation, 2011; 123: 1270–1279.

  34. Kamakura S, Ohe T, et al: Long–term prognosis of probands with Brugada–pattern ST elevation om V1–V3 leads. Circ Arrhythmia and Electrophysiol, 2009; 2: 495–503.

  35. Takagi M, Aonuma K, et al: The prognostic value of early repolarization (J wave) and ST–segment morphology after J wave in Brugada syndrome: multicenter study in Japan. Heart Rhythm, 2013; 10: 533–539.

  36. Watanabe A, Fukushima Kusano K, et al: Low–dose isoproterenol for repetitive ventricular arrhythmia in patients with Brugada syndrome. Eur Heart J, 2006; 27: 1579–1583.

  37. Ohgo T, Okamura H, et al: Acute and chronic management in patients with Brugada syndrome associated with electrical storm of ventricular fibrillation. Heart Rhythm, 2007; 4: 695–700.

  38. Hermida JS, Denjoy I, et al: Hydroquinidine therapy in Brugada syndrome. J Am Coll Cardiol, 2004; 43: 1853–1860.

  39. Leenhardt A, Lucet V, et al: Catecholaminergic polymorphic ventricular tachycardia in children. A 7–year follow–up of 21 patients. Circulation, 1995; 91: 1512–1519.

  40. Inoue YY, Aiba T, et al: Different responses to exercise between Andersen-Tawil syndrome and catecholaminergic polymorphic ventricular tachycardia. Europace, 2018; 20: 1675–1682.

  41. Kawata H, Ohno S, et al: Catecholaminergic polymorphic ventricular tachycardia (CPVT) associated with ryanodine receptor (RyR2) gene mutations–Long–term prognosis after initiation of medical treatment. Circ J, 2016; 80: 1907–1915.

  42. Watanabe H, Chopra N, et al: Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans. Nat Med, 2009; 15: 380–383.

  43. van der Werf C, Kannankeril PJ, et al: Flecainide therapy reduces exercise-induced ventricular arrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia. J Am Coll Cardiol, 2011; 57: 2244–2254.

  44. Gussak I, Brugada P, et al: Idiopathic short QT interval: a new clinical syndrome? Cardiology, 2000; 94: 99–102.

  45. Gaita F, Giustetto C, et al: Short QT syndrome: a familial cause of sudden death. Circulation, 3003; 108: 965–970.

  46. Giustetto C, Di Monte F, et al: Short QT syndrome: clinical findings and diagnostic–therapeutic implications. Eur Heart J, 2006; 27: 2440–2447.

  47. Haïssaguerre M, Derval N, et al: Sudden cardiac arrest associated with early repolarization. N Engl J Med, 2008; 358: 2016–2023.

  48. Antzelevitch C, Yan GX: J wave syndromes. Heart Rhythm, 2010; 7: 549–558.

  49. Nademanee K, Haissaguerre M, et al: Mapping and ablation of ventricular fibrillation associated with early repolarization syndrome. Circulation, 2019; 140: 1477–1490.