Brugada syndrome: Difference between revisions

No edit summary
No edit summary
Line 24: Line 24:
*Type 2-Elevated ST segment (>1mm) descends toward baseline then rises again (saddleback) to upright T wave  
*Type 2-Elevated ST segment (>1mm) descends toward baseline then rises again (saddleback) to upright T wave  
*Type 3-Elevated ST segment (<1mm) descends toward baseline then rises again to upright T wave  
*Type 3-Elevated ST segment (<1mm) descends toward baseline then rises again to upright T wave  
====EKG monitoring====
*V1-v2 lead placement in 2nd or 3rd IC spaces (rather than conventional 4th IC space) increases chance of recording type I pattern<ref>Shimizu  W., Matsuo  K., Takagi  M.; Body surface distribution and response to drugs of ST segment elevation in Brugada syndrome: clinical implication of eighty-seven-lead body surface potential mapping and its application to twelve-lead electrocardiograms. J Cardiovasc Electrophysiol. 11 2000:396-404.</ref>
*Other factors that increase type I EKG tracings<ref>Ikeda  T., Abe  A., Yusu  S.; The full stomach test as a novel diagnostic technique for identifying patients at risk of Brugada syndrome. J Cardiovasc Electrophysiol. 17 2006:602-607.</ref><ref>Shimeno  K., Takagi  M., Maeda  K., Tatsumi  H., Doi  A., Yoshiyama  M.; Usefulness of multichannel Holter ECG recording in the third intercostal space for detecting type 1 Brugada ECG: comparison with repeated 12-lead ECGs. J Cardiovasc Electrophysiol. 20 2009:1026-1031.</ref><ref>Keller  D.I., Huang  H., Zhao  J.; A novel SCN5A mutation, F1344S, identified in a patient with Brugada syndrome and fever-induced ventricular fibrillation. Cardiovasc Res. 70 2006:521-529.</ref>:
**Fever
**Night time
**After heavy meals
[[File:Brugada.jpg]]
[[File:Brugada.jpg]]



Revision as of 19:50, 5 August 2016

Background

  • Consider as cause of syncope in patients with family history of sudden death
  • 80% of Brugada syndrome diagnosed only after a cardiac arrest[1]
  • Autosomal dominant Na-channelopathy which increases the risk of sudden cardiac death (~10%/yr)[2]
  • Much more common in men (up to 9x), particularly Southeast Asian males
  • ECG shows incomplete RBBB with ST elevation in V1-V3
    • In uncomplicated RBBB, usually there no ST change to slight ST depression
    • If presenting symptom is chest pain rather than syncope, consider strongly STEMI

Clinical Features

  • Typically asymptomatic
  • ECG findings can be more prominent during times of illness or fever
  • Patients may have Vfib arrest or sudden death
  • Diagnostic EKG findings transient and variable, with only 1/3 of serial EKGs diagnostic in confirmed spontaneous coved-type Brugada syndrome pts[3]

Differential Diagnosis

ST Elevation

Evaluation

ECG Criteria

Note - ECG findings can be transient

  • Type 1-Elevated ST segment (>2mm) descends with upward convexity to a TWI
  • Type 2-Elevated ST segment (>1mm) descends toward baseline then rises again (saddleback) to upright T wave
  • Type 3-Elevated ST segment (<1mm) descends toward baseline then rises again to upright T wave

EKG monitoring

  • V1-v2 lead placement in 2nd or 3rd IC spaces (rather than conventional 4th IC space) increases chance of recording type I pattern[4]
  • Other factors that increase type I EKG tracings[5][6][7]:
    • Fever
    • Night time
    • After heavy meals

Brugada.jpg

Management

  • Cardiology consultation

Disposition

  • Needs EP consult and VF-inducing electrophysiologic study (EPS), though EPS is controversial prognosticator[8]
  • Inpatient vs outpatient ICD placement
    • Prophylactic ICDs may have risks of complications greater than benefits conferred[9][10]
    • Mortality around 10% per year without ICD placement[citation needed]
    • Antidysrhythmics have no effect on prognosis

External Links

See Also

References

  1. Paul M., Gerss J., Schulze-Bahr E.; Role of programmed ventricular stimulation in patients with Brugada syndrome: a meta-analysis of worldwide published data. Eur Heart J. 28 2007:2126-2133.
  2. Cerrato N, Giustetto C, et al. Prevalence of Type 1 Brugada Electrocardiographic Pattern Evaluated by Twelve-Lead Twenty-Four-Hour Holter Monitoring. The American Journal of Cardiology.115(1). 2015. 52-56.
  3. Richter S., Sarkozy A., Veltmann C.; Variability of the diagnostic ECG pattern in an ICD patient population with Brugada syndrome. J Cardiovasc Electrophysiol. 20 2009:69-75.
  4. Shimizu W., Matsuo K., Takagi M.; Body surface distribution and response to drugs of ST segment elevation in Brugada syndrome: clinical implication of eighty-seven-lead body surface potential mapping and its application to twelve-lead electrocardiograms. J Cardiovasc Electrophysiol. 11 2000:396-404.
  5. Ikeda T., Abe A., Yusu S.; The full stomach test as a novel diagnostic technique for identifying patients at risk of Brugada syndrome. J Cardiovasc Electrophysiol. 17 2006:602-607.
  6. Shimeno K., Takagi M., Maeda K., Tatsumi H., Doi A., Yoshiyama M.; Usefulness of multichannel Holter ECG recording in the third intercostal space for detecting type 1 Brugada ECG: comparison with repeated 12-lead ECGs. J Cardiovasc Electrophysiol. 20 2009:1026-1031.
  7. Keller D.I., Huang H., Zhao J.; A novel SCN5A mutation, F1344S, identified in a patient with Brugada syndrome and fever-induced ventricular fibrillation. Cardiovasc Res. 70 2006:521-529.
  8. Viskin S and Rosso R. Risk of Sudden Death in Asymptomatic Brugada Syndrome: Not as High as We Thought and Not as Low as We Wished…But the Contrary. J Am Coll Cardiol. 2010;56(19):1585-1588.
  9. Sacher F., Probst V., Iesaka Y.; Outcome after implantation of a cardioverter-defibrillator in patients with Brugada syndrome: a multicenter study. Circulation. 114 2006:2317-2324.
  10. Rosso R., Glick A., Glikson M.; Outcome after implantation of cardioverter defibrillator in patients with Brugada syndrome: a multicenter Israeli study (ISRABRU). Isr Med Assoc J. 10 2008:435-439.