Europace Advance Access originally published online on August 3, 2006
Europace 2006 8(10):899-900; doi:10.1093/europace/eul087
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ELECTROPHYSIOLOGY
Negative flecainide test in Brugada syndrome patients with previous positive response
Laboratory of Clinical Cardiac Electrophysiology, Division of Cardiology, ‘La Paz’ University Hospital, Paseo de la Castellana, 261, 28046 Madrid, Spain
Manuscript submitted 20 December 2005. Accepted after revision 16 May 2006.
* Corresponding author. Tel: +34 91 727 75 64; fax: +34 91 727 75 64. E-mail address: jlmerino{at}secardiologia.es
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Abstract |
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 Top Abstract IntroductionPatient 1Patient 2DiscussionReferences |
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Class I antiarrhythmic drug infusion has been established as the standard test to unmask Brugada syndrome. This report presents two patients with Brugada syndrome with positive flecainide response which was not reproducible in a subsequent test.
Key Words: Flecainide, Brugada syndrome, Electrocardiogram
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Introduction |
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TopAbstractIntroductionPatient 1Patient 2DiscussionReferences |
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Many patients with Brugada syndrome (BS) show transient spontaneous ECG normalization.1
Flecainide administration is an accepted method to unmask the BS ECG abnormalities in patients who have a normal baseline ECG.2 The reproducibility of flecainide administration to unmask the BS ECG has been systematically assessed only in one study, which reported a concordant positive response of two tests performed on different days in all patients.3 This report presents two patients with BS and negative flecainide challenge following a previous positive response with the same drug. |
Patient 1 |
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TopAbstractIntroductionPatient 1Patient 2DiscussionReferences |
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A 16-year-old woman was referred for BS risk stratification. Her father and grandfather had died suddenly at 26 and 47 years of age, respectively. She had no history of palpitations, dizziness, syncope, or sudden death, and she was not receiving any drugs. Physical examination, blood count, biochemistry, and electrolytes were normal. Baseline ECG and transthoracic echocardiography were also normal. A 2 mg/kg flecainide infusion in another institution had led to coved ST-segment elevation in leads V1–V3 (Figure 1). No ventricular tachyarrhythmias were inducible at electrophysiological evaluation that was performed 3 days later in our institution. Normal ECG was demonstrated both at baseline and following a 2 mg/kg flecainide infusion during the procedure. The patient was discharged 24 h later without drugs or device therapies.
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Patient 2 |
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TopAbstractIntroductionPatient 1Patient 2DiscussionReferences |
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A 51-year-old man with no family history of syncope or sudden death was admitted to our centre. He had a previous history of a single syncopal episode documented previous to atrial fibrillation. At follow-up, asymptomatic atrial fibrillation episodes were documented and treated with daily administration of 200 mg flecainide. Coved-type ST-segment elevation from V1 to V3 was observed at follow-up, and he was referred for risk stratification. Physical and transthoracic echocardiography examinations were normal, and blood analysis showed no electrolytic disturbances. After flecainide had been discontinued for 6 days, a surface ECG showed only slight ST-segment elevation with non-diagnostic saddle-back configuration in leads V1–V3, and ventricular fibrillation was induced by ventricular programmed stimulation from the right ventricular outflow tract. No change in ECG was observed after 2 mg/kg flecainide infusion (Figure 2). An ICD was implanted, and the patient was discharged 5 days later.
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Discussion |
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TopAbstractIntroductionPatient 1Patient 2DiscussionReferences |
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Class I antiarrhythmic drug infusion has been established as the standard test to unmask BS.4
Initial reports found positive responses to this challenge in all patients and relatives with this inherited disease.2 Other authors have systematically studied the reproducibility of the response to flecainide infusion and reported concordant positive responses in two tests performed on different days in all subjects.3 These reports suggested that a negative response to flecainide challenge was sufficient to rule out BS. However, Wolpert et al.5 demonstrated disparate responses of Brugada patients to flecainide and ajmaline, with a failure of flecainide in seven of 22 cases (32%). In addition, Priori et al.6 found a negative response to class I antiarrhythmic drug administration in six of 41 patients with previous ECG documentation of BS. Our report provides further evidence that a negative response to flecainide administration is not sufficient to rule out the syndrome and that negative responses can change to positive if the test is performed on another day. Whether the test should be repeated whenever a negative response is found in BS relatives or in patients with suspicion of BS warrants further investigation.
Finally, this report has important limitations. First, the position of the precordial electrodes could have been somewhat different in the two responses in each patient. Secondly, oral flecainide consumption was compared with an intravenous test in the second patient. However, it is important to stress that these limitations are characteristics of the current management in clinical practice. In addition, the present report does not provide any explanation for the negative flecainide challenge response found in some individuals with a previous positive result. Different factors, such as autonomic modulation and body temperature,7–11 which are known to interfere with BS ECG expression could be responsible for this.
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References |
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[1] Brugada J, Brugada P, Brugada R. The ajmaline challenge in Brugada syndrome: a useful tool or misleading information? Eur Heart J 2003; 24: 1085–6.
[2] 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: 510–5.
[3] Gasparini M, Priori SG, Mantica M, et al. Flecainide test in Brugada syndrome: a reproducible but risky tool. Pacing Clin Electrophysiol 2003; 26: 338–41.[CrossRef][Medline]
[4] Wilde AA, Antzelevitch C, Borggrefe M, et al. Proposed diagnostic criteria for the Brugada syndrome: consensus report. Circulation 2002; 106: 2514–9.
[5] Wolpert C, Echternach C, Veltmann C, et al. Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome. Heart Rhythm 2005; 2: 254–60.[CrossRef][Web of Science][Medline]
[6] Priori SG, Napolitano C, Gasparini M, et al. Clinical and genetic heterogeneity of right bundle branch block and ST-segment elevation syndrome: a prospective evaluation of 52 families. Circulation 2000; 102: 2509–15.
[7] Saura D, Garcia-Alberola A, Carrillo P, Pascual D, Martinez-Sanchez J, Valdes M. Brugada-like electrocardiographic pattern induced by fever. Pacing Clin Electrophysiol 2002; 25: 856–9.[CrossRef][Medline]
[8] Pastor A, Nunez A, Cantale C, Cosio FG. Asymptomatic Brugada syndrome case unmasked during dimenhydrinate infusion. J Cardiovasc Electrophysiol 2001; 12: 1192–4.[CrossRef][Web of Science][Medline]
[9] Rouleau F, Asfar P, Boulet S, et al. Transient ST segment elevation in right precordial leads induced by psychotropic drugs: relationship to the Brugada syndrome. J Cardiovasc Electrophysiol 2001; 12: 61–5.[CrossRef][Web of Science][Medline]
[10] Shimizu W. Gender difference and drug challenge in Brugada syndrome. J Cardiovasc Electrophysiol 2004; 15: 70–1.[Web of Science][Medline]
[11] Ahn J and Hurst JW. Worrisome thoughts about the diagnosis and treatment of patients with Brugada waves and the Brugada syndrome. Circulation 2004; 109: 1463–7.
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