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Polymorphic Catecholergic Ventricular Tachycardia

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Polymorphic Catecholergic Ventricular Tachycardia Polymorphic catecholergic ventricular tachycardia Author: Doctor Vincent Lucet1 Creation Date: March 2000 Update: August 2002 January 2004 Scientific Editor: Doctor Damien Bonnet 1pédiatrie générale, Château des Côtes, 78350 Les Loges En Josas, France. [email protected] Abstract Keywords Name of the disease and its synonyms Names of excluded diseases Diagnostic criteria/Definition Differential diagnosis Frequence Clinical description Management/treatment Etiology Biological diagnostic method Genetic counseling Unresolved questions and comments References Abstract Identified in 1978, catecholaminergic polymorphic ventricular tachycardia mainly occurs in children over 3 years old with apparently healthy hearts. It is a primary dysrhythmia usually discovered during the work-up conducted after syncope with or without seizure. Syncopes mainly occur during exertion or emotional experiences. The electrocardiogram is normal (particularly the QT interval). During exercise or acceleration of the sinus rhythm, stereotyped and repetitive ventricular extrasystoles appear: first isolated and monomorphic, they become polymorphic and occur in salvos, with bidirectional ventricular tachycardia. Ventricular arrhythmia may be very rapid and interspersed with bursts of supraventricular or junctional tachycardia. During the paroxysms, torsade en pointes and ventricular fibrillation may appear and sometimes revert spontaneously. The same arrhythmia can be induced by stress tests or injecting small doses of isoprenaline. Patients are treated with powerful beta-blockers with delayed action. The spontaneous outcome is poor: half of the untreated patients die before age of 20 years. The disorder, recently assigned to the group of rhythm channelopathies, is familial in 1/3 cases. Somes cases are associated with abnormal transmembrane calcium transport (a mutation of the cardiac ryanodine-receptor gene, RyR2, has been found in several families). Keywords Ventricular tachycardia, arrhythmia, sudden death, torsade de pointes, long QT syndrome, ventricular fibrillation, calcium channelopathy • Isolated cases or small series of patients have Name of the disease and its synonyms been described in the literature using the • Catecholaminergic polymorphic ventricular following terms: tachycardias (CPVT) • Syncopal paroxysmal tachycardia • Malignant paroxysmal polymorphic ventricular tachycardia Lucet, V. Polymorphic catecholergic ventricular tachycardia. Orphanet encyclopedia. January 2004. http://www.orpha.net/data/patho/GB/uk-tvpc.pdf 1 • Multifocal ventricular premature beats • Torsade de pointes with short coupling interval • Paroxysmal ventricular fibrillation (electrocardiogram aspect) • Bidirectional tachycardia • Long QT syndromes (genetic investigation). • Double tachycardia induced by But some borderline forms exist in which both catecholamines prolonged QT intervals and effort- or • Syncopal tachyarrhythmia isoprenaline chlorhydrate-induced • Familial polymorphic ventricular tachycardia reproducible CPTV are seen. • Catecholamine- or exercise-induced polymorphic ventricular tachycardia Frequency In our experience, CPTV is a rare rhythm Names of excluded diseases disorder, often misunderstood, that occurs about By definition, the following entities are excluded half as frequently as long QT syndromes. The from the differential diagnosis : rhythm disorder is not seen in newborns (in • Long QT syndromes: Jervell & Lange–Nielsen contrast to long QT syndromes). The effort- syndrome (autosomal recessive with induced ventricular extrasystoles and syncopes associated deafness), Romano–Ward can appear later during childhood (after 3 years). syndrome (autosomal dominant with no Clinical description deafness) Diagnosis is primarily derived from medical • Brugada syndrome history taking after the occurrence of syncopes, • Arrhythmogenic right ventricular dysplasia with or without seizures, triggered by physical • Torsade-de-pointes syndromes with short exertion or emotional upheavals. Loss of coupling interval consciousness can be long and accompanied by sphincter release (urinary and anal). Diagnostic criteria/Definition Neurological sequelae are possible after a more- CPVT is a primary arrhythmia seen in children or-less prolonged coma. Sudden death is the over 3 years old without evident cardiopathy; it natural outcome in the absence of adapted provokes prolonged syncopes, with or without therapy. Electrocardiogram anomalies can be seizures, often triggered repeatedly and seen after paroxysms and these children are reproducibly by physical exertion, emotional often treated for epilepsy for several months or upheavals or the injection of small doses of even years before the correct diagnosis is made. isoprenaline chlorhydrate. The standard electrocardiogram is normal, but sinus Management/treatment bradycardia is common at rest, as is the left As soon as diagnosis is made, it is imperative QRS axis for this age (1/2 patients). With that treatment with a beta-blocker be started. We physical exercise, for a sinus rhythm threshold > prefer nadolol because of its long half-life, 130/minute, ventricular extrasystoles appear: allowing a single dose per day (80–160 mg in first alone and monomorphic, then polymorphic teenagers). and in salvos. During these polymorphic Under treatment, sinus brachycardia is ventricular tachycardia attacks, interspersed sometimes more severe. Ventricular bidirectional ventricular tachycardia salvos, or extrasystoles persist, usually for sinus rhythms supraventricular or atrioventricular (nodal) and exceeding 130/minute. In contrast, the syncopes His–Purkinje system tachycardia bursts are disappear as long as the medication is taken seen. The arrhythmia can degenerate at any regularly. The beta-blocker is life-long therapy. time into torsade de pointes or ventricular Particularly severe forms can justify the fibrillation which can (but does not always) revert implantation of a cardioverter defibrillator. spontaneously. Etiology Differential diagnosis This primary rhythm disorder was recently By definition, the hearts of these children are assigned to the group of rhythm anatomically normal and the affected individuals channelopathies, along with long QT syndromes. are a priori free of any known metabolic disease. Indeed, several teams have demonstrated a Before advancing the diagnosis, the following calcium-channel abnormality in affected families must be eliminated: associated with a dominant mutation in the • Cardiomyopathy (echocardiography) cardiac ryanodine-receptor gene (RyR2) • Metabolic disease (biological work-up) localized to chromosome 1q42–43. More rarely, • Pheochromocytoma (catecholamine dosage) the disorder has been linked to a recessive • Arrhythmogenic right ventricular mutation on chromosome 1p13–21. dysplasia(angiography or scintigraphy) • Brugada syndrome (electrocardiogram, Biological diagnostic method provocation test) None exists. Lucet, V. Polymorphic catecholergic ventricular tachycardia. Orphanet encyclopedia. January 2004. http://www.orpha.net/data/patho/GB/uk-tvpc.pdf 2 Genetic counseling DE PAOLA AA, HOROWITZ LN, MARQUES FB The existence of familial forms for 1/3 patients et al. Control of multiform ventricular tachycardia justifies the undertaking of a complete familial by propanolol in a child with no identifiable investigation at the time of the first diagnosis. An cardiac disease and sudden death. Am Heart J autosomal dominant transmission has been 1990: 119: 1429–1432. established in some families bearing a mutation DUBNER SJ, GIMENO GM, ELENCWAJG B et on chromosome 1q42–43. Recessive inheritance al. Ventricular fibrillation with spontaneous of a mutation on chromosome 1p13–21 has also reversion on ambulatory ECG in the absence of been demonstrated in a Bedouin tribe. heart disease. Am Heart J 1983; 105: 691–693. HAISSAGUERRE M, WARIN JF, VEAUX P et Unresolved questions and comments al. Tachycardie ventriculaire catécholergique. À This severe primary rhythm disorder that occurs propos d’un cas avec anomalies associées de in children over 3 years old is probably more l’intervalle QT. Ann Cardiol Angéiol 1987; 36: misunderstood than rare. This misunderstanding 19–22. can lead to dramatic accidents during sporting LAHAT H, ELDAR M, LEVY-NISSENBAUM E et events, especially swimming. The beta-blocker al. Autosomal recessive catecholamine or treatment is prescribed for the patient’s entire life exercise-induced polymorphic ventricular without interruption. The progress made in tachycardia: clinical features and assignment of molecular genetics have provided a better the disease gene to chromosome 1p13–21. understanding of this arrhythmia, as well as the Circulation 2001; 103: 2822–2827. possible similarities (and differences) between LAITINEN PJ, BROWN KM, PIIPO K et al. CPTV and long QT syndromes or right Mutations of the cardiac ryanodine receptor ventricular dysplasia. Familial genetic analysis (RyR2) gene in familial polymorphic ventricular should include repeated monitoring of children a tachycardia. Circulation 2001; 103: 485–490. priori disease-free, because electrical signs can LEENHARDT A, LUCET V, DENJOY I et al. appear late in childhood or during young Catecholaminergic polymorphic ventricular adulthood. tachycardia in children. Circulation 1995; 91: 1512–1519. References LUCET V, GRAU F, DENJOY I et al. Devenir à BENSON DW Jr, GALLAGHER JJ, STERBA R long terme des tachycardies ventriculaires et al. Catecholamine induced double polymorphes catécholergiques de l’enfant. À tachycardia.
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