Sodium Channel Blockers Identify Risk for Sudden Death in Patients With ST-Segment Elevation and Right Bundle Branch Block but Structurally Normal Hearts
Background —A mutation in the cardiac sodium channel gene (SCN5A) has been described in patients with the syndrome of right bundle branch block, ST-segment elevation in leads V1 to V3, and sudden death (Brugada syndrome). These electrocardiographic manifestations are transient in many patients with...
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| Published in | Circulation (New York, N.Y.) Vol. 101; no. 5; pp. 510 - 515 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
08.02.2000
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7322 1524-4539 1524-4539 |
| DOI | 10.1161/01.CIR.101.5.510 |
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| Abstract | Background
—A mutation in the cardiac sodium channel gene (SCN5A) has been described in patients with the syndrome of right bundle branch block, ST-segment elevation in leads V1 to V3, and sudden death (Brugada syndrome). These electrocardiographic manifestations are transient in many patients with the syndrome. The present study examined arrhythmic risk in patients with overt and concealed forms of the disease and the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk.
Methods and Results
—The effect of intravenous ajmaline (1 mg/kg), procainamide (10 mg/kg), or flecainide (2 mg/kg) on the ECG was studied in 34 patients with the syndrome and transient normalization of the ECG (group A), 11 members of 3 families in whom a SCN5A mutation was associated with the syndrome and 8 members in whom it was not (group B), and 53 control subjects (group C). Ajmaline, procainamide, or flecainide administration resulted in ST-segment elevation and right bundle branch block in all patients in group A and in all 11 patients with the mutation in group B. A similar pattern could not be elicited in the 8 patients in group B who lacked the mutation or in any person in group C. The follow-up period (37±33 months) revealed no differences in the incidence of arrhythmia between the 34 patients in whom the phenotypic manifestation of the syndrome was transient and the 24 patients in whom it was persistent (log-rank, 0.639).
Conclusions
—The data demonstrated a similar incidence of potentially lethal arrhythmias in patients displaying transient versus persistent ST-segment elevation and right bundle branch block, as well as the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk. |
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| AbstractList | Background
—A mutation in the cardiac sodium channel gene (SCN5A) has been described in patients with the syndrome of right bundle branch block, ST-segment elevation in leads V1 to V3, and sudden death (Brugada syndrome). These electrocardiographic manifestations are transient in many patients with the syndrome. The present study examined arrhythmic risk in patients with overt and concealed forms of the disease and the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk.
Methods and Results
—The effect of intravenous ajmaline (1 mg/kg), procainamide (10 mg/kg), or flecainide (2 mg/kg) on the ECG was studied in 34 patients with the syndrome and transient normalization of the ECG (group A), 11 members of 3 families in whom a SCN5A mutation was associated with the syndrome and 8 members in whom it was not (group B), and 53 control subjects (group C). Ajmaline, procainamide, or flecainide administration resulted in ST-segment elevation and right bundle branch block in all patients in group A and in all 11 patients with the mutation in group B. A similar pattern could not be elicited in the 8 patients in group B who lacked the mutation or in any person in group C. The follow-up period (37±33 months) revealed no differences in the incidence of arrhythmia between the 34 patients in whom the phenotypic manifestation of the syndrome was transient and the 24 patients in whom it was persistent (log-rank, 0.639).
Conclusions
—The data demonstrated a similar incidence of potentially lethal arrhythmias in patients displaying transient versus persistent ST-segment elevation and right bundle branch block, as well as the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk. A mutation in the cardiac sodium channel gene (SCN5A) has been described in patients with the syndrome of right bundle branch block, ST-segment elevation in leads V1 to V3, and sudden death (Brugada syndrome). These electrocardiographic manifestations are transient in many patients with the syndrome. The present study examined arrhythmic risk in patients with overt and concealed forms of the disease and the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk.BACKGROUNDA mutation in the cardiac sodium channel gene (SCN5A) has been described in patients with the syndrome of right bundle branch block, ST-segment elevation in leads V1 to V3, and sudden death (Brugada syndrome). These electrocardiographic manifestations are transient in many patients with the syndrome. The present study examined arrhythmic risk in patients with overt and concealed forms of the disease and the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk.The effect of intravenous ajmaline (1 mg/kg), procainamide (10 mg/kg), or flecainide (2 mg/kg) on the ECG was studied in 34 patients with the syndrome and transient normalization of the ECG (group A), 11 members of 3 families in whom a SCN5A mutation was associated with the syndrome and 8 members in whom it was not (group B), and 53 control subjects (group C). Ajmaline, procainamide, or flecainide administration resulted in ST-segment elevation and right bundle branch block in all patients in group A and in all 11 patients with the mutation in group B. A similar pattern could not be elicited in the 8 patients in group B who lacked the mutation or in any person in group C. The follow-up period (37+/-33 months) revealed no differences in the incidence of arrhythmia between the 34 patients in whom the phenotypic manifestation of the syndrome was transient and the 24 patients in whom it was persistent (log-rank, 0.639).METHODS AND RESULTSThe effect of intravenous ajmaline (1 mg/kg), procainamide (10 mg/kg), or flecainide (2 mg/kg) on the ECG was studied in 34 patients with the syndrome and transient normalization of the ECG (group A), 11 members of 3 families in whom a SCN5A mutation was associated with the syndrome and 8 members in whom it was not (group B), and 53 control subjects (group C). Ajmaline, procainamide, or flecainide administration resulted in ST-segment elevation and right bundle branch block in all patients in group A and in all 11 patients with the mutation in group B. A similar pattern could not be elicited in the 8 patients in group B who lacked the mutation or in any person in group C. The follow-up period (37+/-33 months) revealed no differences in the incidence of arrhythmia between the 34 patients in whom the phenotypic manifestation of the syndrome was transient and the 24 patients in whom it was persistent (log-rank, 0.639).The data demonstrated a similar incidence of potentially lethal arrhythmias in patients displaying transient versus persistent ST-segment elevation and right bundle branch block, as well as the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk.CONCLUSIONSThe data demonstrated a similar incidence of potentially lethal arrhythmias in patients displaying transient versus persistent ST-segment elevation and right bundle branch block, as well as the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk. A mutation in the cardiac sodium channel gene (SCN5A) has been described in patients with the syndrome of right bundle branch block, ST-segment elevation in leads V1 to V3, and sudden death (Brugada syndrome). These electrocardiographic manifestations are transient in many patients with the syndrome. The present study examined arrhythmic risk in patients with overt and concealed forms of the disease and the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk. The effect of intravenous ajmaline (1 mg/kg), procainamide (10 mg/kg), or flecainide (2 mg/kg) on the ECG was studied in 34 patients with the syndrome and transient normalization of the ECG (group A), 11 members of 3 families in whom a SCN5A mutation was associated with the syndrome and 8 members in whom it was not (group B), and 53 control subjects (group C). Ajmaline, procainamide, or flecainide administration resulted in ST-segment elevation and right bundle branch block in all patients in group A and in all 11 patients with the mutation in group B. A similar pattern could not be elicited in the 8 patients in group B who lacked the mutation or in any person in group C. The follow-up period (37+/-33 months) revealed no differences in the incidence of arrhythmia between the 34 patients in whom the phenotypic manifestation of the syndrome was transient and the 24 patients in whom it was persistent (log-rank, 0.639). The data demonstrated a similar incidence of potentially lethal arrhythmias in patients displaying transient versus persistent ST-segment elevation and right bundle branch block, as well as the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk. |
| Author | Kirsch, Glenn E. Potenza, Domenico Antzelevitch, Charles Towbin, Jeffrey A. Brugada, Ramon Brugada, Josep Brugada, Pedro |
| Author_xml | – sequence: 1 givenname: Ramon surname: Brugada fullname: Brugada, Ramon organization: From the Departments of Cardiology (R.B.) and Pediatrics (J.A.T.), Baylor College of Medicine, Houston, Texas; the Arrhythmia Unit, Cardiovascular Institute, Hospital Clínic, University of Barcelona, Barcelona, Spain (J.B.); the Masonic Medical Research Laboratory, Utica, New York (C.A.); the Rammelkamp Center for Research, MetroHealth Campus, Case Western Reserve University, Cleveland, Ohio (G.E.K); the Cardiology Department, Casa Sollievo della Sofferenza, S. Giovani Rotondo, Italy (D.P.); and – sequence: 2 givenname: Josep surname: Brugada fullname: Brugada, Josep organization: From the Departments of Cardiology (R.B.) and Pediatrics (J.A.T.), Baylor College of Medicine, Houston, Texas; the Arrhythmia Unit, Cardiovascular Institute, Hospital Clínic, University of Barcelona, Barcelona, Spain (J.B.); the Masonic Medical Research Laboratory, Utica, New York (C.A.); the Rammelkamp Center for Research, MetroHealth Campus, Case Western Reserve University, Cleveland, Ohio (G.E.K); the Cardiology Department, Casa Sollievo della Sofferenza, S. Giovani Rotondo, Italy (D.P.); and – sequence: 3 givenname: Charles surname: Antzelevitch fullname: Antzelevitch, Charles organization: From the Departments of Cardiology (R.B.) and Pediatrics (J.A.T.), Baylor College of Medicine, Houston, Texas; the Arrhythmia Unit, Cardiovascular Institute, Hospital Clínic, University of Barcelona, Barcelona, Spain (J.B.); the Masonic Medical Research Laboratory, Utica, New York (C.A.); the Rammelkamp Center for Research, MetroHealth Campus, Case Western Reserve University, Cleveland, Ohio (G.E.K); the Cardiology Department, Casa Sollievo della Sofferenza, S. Giovani Rotondo, Italy (D.P.); and – sequence: 4 givenname: Glenn E. surname: Kirsch fullname: Kirsch, Glenn E. organization: From the Departments of Cardiology (R.B.) and Pediatrics (J.A.T.), Baylor College of Medicine, Houston, Texas; the Arrhythmia Unit, Cardiovascular Institute, Hospital Clínic, University of Barcelona, Barcelona, Spain (J.B.); the Masonic Medical Research Laboratory, Utica, New York (C.A.); the Rammelkamp Center for Research, MetroHealth Campus, Case Western Reserve University, Cleveland, Ohio (G.E.K); the Cardiology Department, Casa Sollievo della Sofferenza, S. Giovani Rotondo, Italy (D.P.); and – sequence: 5 givenname: Domenico surname: Potenza fullname: Potenza, Domenico organization: From the Departments of Cardiology (R.B.) and Pediatrics (J.A.T.), Baylor College of Medicine, Houston, Texas; the Arrhythmia Unit, Cardiovascular Institute, Hospital Clínic, University of Barcelona, Barcelona, Spain (J.B.); the Masonic Medical Research Laboratory, Utica, New York (C.A.); the Rammelkamp Center for Research, MetroHealth Campus, Case Western Reserve University, Cleveland, Ohio (G.E.K); the Cardiology Department, Casa Sollievo della Sofferenza, S. Giovani Rotondo, Italy (D.P.); and – sequence: 6 givenname: Jeffrey A. surname: Towbin fullname: Towbin, Jeffrey A. organization: From the Departments of Cardiology (R.B.) and Pediatrics (J.A.T.), Baylor College of Medicine, Houston, Texas; the Arrhythmia Unit, Cardiovascular Institute, Hospital Clínic, University of Barcelona, Barcelona, Spain (J.B.); the Masonic Medical Research Laboratory, Utica, New York (C.A.); the Rammelkamp Center for Research, MetroHealth Campus, Case Western Reserve University, Cleveland, Ohio (G.E.K); the Cardiology Department, Casa Sollievo della Sofferenza, S. Giovani Rotondo, Italy (D.P.); and – sequence: 7 givenname: Pedro surname: Brugada fullname: Brugada, Pedro organization: From the Departments of Cardiology (R.B.) and Pediatrics (J.A.T.), Baylor College of Medicine, Houston, Texas; the Arrhythmia Unit, Cardiovascular Institute, Hospital Clínic, University of Barcelona, Barcelona, Spain (J.B.); the Masonic Medical Research Laboratory, Utica, New York (C.A.); the Rammelkamp Center for Research, MetroHealth Campus, Case Western Reserve University, Cleveland, Ohio (G.E.K); the Cardiology Department, Casa Sollievo della Sofferenza, S. Giovani Rotondo, Italy (D.P.); and |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1263405$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/10662748$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1161/circ.88.3.8353864 10.1111/j.1540-8167.1998.tb01844.x 10.1016/S0022-0736(97)80021-0 10.1016/0735-1097(92)90253-J 10.1016/S0735-1097(98)00528-2 10.1161/circ.96.8.2595 10.1016/0735-1097(95)00613-3 10.1038/32675 10.1056/NEJM199505043321809 10.1016/0002-8703(94)90070-1 10.1016/0002-8703(90)90025-S 10.1161/circ.97.5.457 10.1111/j.1540-8167.1997.tb00796.x 10.1016/0735-1097(95)00485-8 |
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| Keywords | Human Prognosis Arrhythmia Sudden death Right Cardiovascular disease Bundle branch block Ionic channel Antiarrhythmic agent Conduction disorder Excitability disorder Ventricular fibrillation ST elevation Alkaloid Chemotherapy Treatment Follow up study Heart block Heart disease Sodium ion Ajmaline Antagonist |
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—A mutation in the cardiac sodium channel gene (SCN5A) has been described in patients with the syndrome of right bundle branch block, ST-segment... A mutation in the cardiac sodium channel gene (SCN5A) has been described in patients with the syndrome of right bundle branch block, ST-segment elevation in... |
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| SubjectTerms | Adult Anti-Arrhythmia Agents - therapeutic use Antiarythmic agents Biological and medical sciences Bundle-Branch Block - complications Bundle-Branch Block - genetics Cardiovascular system Death, Sudden, Cardiac - etiology Electrocardiography - drug effects Female Follow-Up Studies Humans Male Medical sciences Middle Aged NAV1.5 Voltage-Gated Sodium Channel Pedigree Pharmacology. Drug treatments Risk Factors Sodium Channel Blockers Sodium Channels - genetics |
| Title | Sodium Channel Blockers Identify Risk for Sudden Death in Patients With ST-Segment Elevation and Right Bundle Branch Block but Structurally Normal Hearts |
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