Brugada syndrome risk factors

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The EKG changes of Brugada syndrome can vary over time, depending on the autonomic balance and the administration of antiarrhythmic drugs. Adrenergic stimulation decreases the ST segment elevation, while vagal stimulation worsens it. During sleep, there is heightened vagal tone, and the pattern may be exacerbated at that time (as is the risk of sudden cardiac death at that time). The administration of class Ia, Ic and III drugs increases the ST segment elevation, as does fever. The impact of exercise depends upon when the EKG is obtained: during exercise the ST segment elevation may decrease but may increase later after exercise when the body temperature has risen. Similar to early repolarization variant, when the heart rate decreases, the ST segment elevation increases and when the heart rate increases the ST segment elevation decreases. While Brugada syndrome is often associated with polymorphic VT which may be self terminating, in the presence of autonomic imbalance, hypokalemia, fever or exacerbating drugs sustained ventricular fibrillation and sudden cardiac death may result.[1]

Risk Factors: Agents and Scenarios that Provoke the Brugada Syndrome Pattern

The electrocardiographic findings of Brugada syndrome are often concealed, but can be unmasked or modulated by a number of drugs and pathophysiological states including (in alphabetical order)[1]:

Risk Statification[33][34]

  • Patients with syncope and an abnormal Type 1 ECG are at higher risk
  • Asymptomatic patients at risk can be identified
    • Presence of spontaneous Type 1 ST-segment elevation
    • Characteristics of the S wave
    • Presence of late potentials
    • Inducibility of VT/VF using PES is controversial as a risk factor. Some groups have advocated that programmed electrical stimulation (PES) be performed to induce ventricular fibrillation for risk assessment in Brugada patients [35][36]

Other groups have not reproduced the predictive value of these tests,[33][37] so the value of programmed electrical stimulation (PES) and inducibility remains controversial.

References

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  26. Shimizu W, Antzelevitch C, Suyama K, Kurita T, Taguchi A, Aihara N; et al. (2000). "Effect of sodium channel blockers on ST segment, QRS duration, and corrected QT interval in patients with Brugada syndrome". J Cardiovasc Electrophysiol. 11 (12): 1320–9. PMID 11196553.
  27. 27.0 27.1 Bolognesi R, Tsialtas D, Vasini P, Conti M, Manca C (1997). "Abnormal ventricular repolarization mimicking myocardial infarction after heterocyclic antidepressant overdose". Am J Cardiol. 79 (2): 242–5. PMID 9193039.
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  36. Brugada P, Brugada R, Mont L, Rivero M, Geelen P, Brugada J (2003). "Natural history of Brugada syndrome: the prognostic value of programmed electrical stimulation of the heart". Journal of Cardiovascular Electrophysiology. 14 (5): 455–7. PMID 12776858. Retrieved 2012-10-13. Unknown parameter |month= ignored (help)
  37. Eckardt L, Probst V, Smits JP, Bahr ES, Wolpert C, Schimpf R, Wichter T, Boisseau P, Heinecke A, Breithardt G, Borggrefe M, LeMarec H, Böcker D, Wilde AA (2005). "Long-term prognosis of individuals with right precordial ST-segment-elevation Brugada syndrome". Circulation. 111 (3): 257–63. doi:10.1161/01.CIR.0000153267.21278.8D. PMID 15642768. Retrieved 2012-10-13. Unknown parameter |month= ignored (help)

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