Abstract
Ventricular fibrillation (VF) in the absence of structural heart disease is classified as ’idiopathic ventricular fibrillation’or ’primary electrical disease’. In those cases the arrhythmogenic substrate should in principle be looked for in the excitation and conduction properties of the heart. However, some minimal abnormalities are considered compatible with idiopathic VF (table 1) [1]. Moreover, it should be realized that even with all currently available highly sophisticated diagnostic techniques discrete structural abnormalities might be overlooked. Careful follow-up might indeed unmask structural heart disease in these patients.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Survivors of out-of-hospital cardiac arrest with apparently normal heart. Need for Definition and standardized clinical evaluation. Consensus Statement of the Joint Steering Committees of the Unexplained Cardiac Arrest Registry of Europe and of the Idiopathic Ventricular Fibrillation Registry in the United States. Circulation 1997; 95:265–72.
Wilde A.A.M., Jongbloed R.J.E., Doevendans P.A., et al. Auditory stimuli as a trigger for arrhythmic events differentiate HERG-related (LQTS2) patients from KVLQT,-related patients (LQTS,). J Am Coll Cardiol1999; 33:327–32.
Schwartz P.J, Priori S.G, Spazzolini C, et al. Genotype-phenotype correlation in the long-QT syndrome. Gene-specific triggers for life-threatening arrhythmias. Circulation 2001; 103:89–96.
Osher H.L., Wolff L.: Electrocardiographic pattern simulating acute myocardial injury. Am J Med Sci 1953; 226:541–45.
Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart disease: description of 6 cases. Am Heart J 1989; 118:1203–9.
Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol1992; 20:1391–6.
Alings M, Wilde A. “ Brugada” Syndrome. Clinical data and suggested pathophysiological mechanism. Circulation 1999; 99:666–73.
Remme C.A, Wever E.F.D., Wilde A.A.M. et al. Diagnosis and long-term follow-up of the Brugada syndrome in patients with idiopathic ventricular fibrillation. EuT. Heart J. 2001; 22:400–409.
Hermida J.S, Lemoine J.L, Bou Aoun F, et al. Prevalence of the Brugada syndrome in a apparently healthy population. Am J Cardiol2000; 86:91–4.
Miyasaka Y, Yamada K, Sugiura T, et al. Prevalence and mortality of right bundle branch block and right precordial ST-segment elevation (Brugada type ECG) in a general population. Circulation 2000; 102Supp II:676A.
Chen Q, Kirsch G.E, Zhang D, et al. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature 1998; 392:293–6.
Bezzina C.R, Rook M.B, Wilde A.A.M. The cardiac sodium channel and inherited arrhythmia syndromes. Cardiovasc Res 2001; 49:257–271.
Wilde A.A.M, Veldkamp M.W. What we can leam from individual resuscitated patients. Cardiovasc Res 2000; 46: 14–6.
Gasparini M, Priori S.G, Mantica M, et al. Provocative test in the Brugada Syndrome: do we have the right tools? Circulation 2000; 102SuppII:677A.
London B, Barmada M, Nguyen T, et al. Identifying a second Brugada Syndrome locus on chromosome 3. Circulation 2000; 102SuppII:280A.
Way Q, Shen J, Splawski I, et al. SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome. Cell1995; 80:805–11.
Schott J.J, Alshinawi C, Kyndt F, et al. Cardiac conduction defects associate with mutations in SCN5A. Nature Genet 1999; 23:20–1.
Bezzina C, Veldkamp M.W, van den Berg M.P, et al. A single Na+ channel mutation causing both long-QT and Brugada syndromes. Circ Res 1999; 1206–13.
Veldkamp M.W, Viswanathan P.C, Bezzina C, et al. Two distinct congenital arrhythmias evoked by a multidysfunctional Na+ channel. Circ Res 2000; 86:91–9.
Coumel P, Fidelle J, Lucet V, et al. Catecholamine-induced severe ventricular arrhythmias with Adam-Stokes syndrome in children: report of four cases. Br Heart J 1978; 40suppl:28–37.
Leenhardt A, Lucet V, Denjoy I, et al. Catecholaminergic polymorphic ventricular tachycardia in children. A 7-year follow-up of 21 patients. Circulation 1995; 91:1512–9.
Swan H, Piipo K, Viitasalo M, et al. Arrhythmie disorder mapped to ehromosome 1942-1943 causes malignant polymorphic ventricular taehyeardia in strueturally normal hearts. J Am Coll Cardiol 1999; 34:2035–42.
Rampazzo A, Nava A, Eme P, et al. A new loeus for Arrhythmogenic right ventricular cardiomyopathy (ARVD2) maps to ehromosome 1q42-q43. Hum Mol Genet 1995; 4:2151–54.
Nava A, Canciani B, Daliento L, et al. Juvenile sudden death and effort ventricular tachyeardias in a family with right ventricular cardiomyopathy. Int J Cardiol 1988; 21:111–25.
Priori S.G, Napolitano C, Tiso N, et al. Mutations in the cardiac ryanodine receptor gene (hRyR1) underlie catecholaminergic polymorphic ventricular tachycardia. Circulation 2000; 102:r49–53.
Laitinen P.J, Brown K.M, Piippo K, et al. Mutations of the cardiac ryanodine receptor (RyRI) gene in familial polymorphic ventricular tachycardia. Circulation 2001; 103:485–90.
Tiso N, Stephan D.A, Nava A, et al. Identification of mutations in the cardiac ryanodinge receptor gene in families affected with Arrhythmogenic right ventricular cardiomyopathy type 2 (ARVD2). Hum Mol Genet 2001; 10:189–94.
Leenhardt A, Glaser E, Burguera M, et al. Short-coupled variant ofTorsades de Pointes. A new electrocardiographic entity in the spectrum of idiopathic ventricular arrhythmias. Circulation 1994; 89:206–15.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2001 Springer Science+Business Media Dordrecht
About this chapter
Cite this chapter
Wilde, A.A. (2001). Idiopathic Ventricular Fibrillation. In: Doevendans, P.A., Wilde, A.A.M. (eds) Cardiovascular Genetics for Clinicians. Developments in Cardiovascular Medicine, vol 239. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-1019-1_14
Download citation
DOI: https://doi.org/10.1007/978-94-010-1019-1_14
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-010-3888-1
Online ISBN: 978-94-010-1019-1
eBook Packages: Springer Book Archive