Brugada syndrome risk factors: Difference between revisions
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*[[α-adrenergic agonists]] | *[[α-adrenergic agonists]] | ||
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*[[ | *[[Carotid sinus massage]] | ||
*[[Cocaine]] | *[[Cocaine]] | ||
*[[Fever]]. It is for this reason that [[antipyretic]] agents are recommended to aggressively treat a fever in the patient with Brugada syndrome. | *[[Fever]]. It is for this reason that [[antipyretic]] agents are recommended to aggressively treat a fever in the patient with Brugada syndrome. | ||
Revision as of 14:52, 14 October 2012
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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.
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]:
- A combination of glucose and insulin
- Ajmaline (a diagnostic test agent)
- α-adrenergic agonists
- β-adrenergic blockers
- Carotid sinus massage
- Cocaine
- Fever. It is for this reason that antipyretic agents are recommended to aggressively treat a fever in the patient with Brugada syndrome.
- Flecainide (a diagnostic test agent)
- Hypercalcemia
- Hyperkalemia
- Hypokalemia
- In large studies, a family history of sudden cardiac death among patients with Brugada syndrome does not appear to be a risk factor for sudden cardiac death in siblings.
- Procainamide (a diagnostic test agent)
- Propranolol intoxication
- Shaving due to vagal stimulation
- Sodium channel blockers (a diagnostic test agent)
- Tetracyclic antidepressants
- Tricyclic antidepressants
Risk Statification
- 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 [2][3]
Other groups have not reproduced the predictive value of these tests,[4][5] so the value of programmed electrical stimulation (PES) and inducibility remains controversial.
References
- ↑ Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, Gussak I, LeMarec H, Nademanee K, Perez Riera AR, Shimizu W, Schulze-Bahr E, Tan H, Wilde A (2005). "Brugada syndrome: report of the second consensus conference". Heart Rhythm : the Official Journal of the Heart Rhythm Society. 2 (4): 429–40. PMID 15898165. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Brugada J, Brugada R, Antzelevitch C, Towbin J, Nademanee K, Brugada P (2002). "Long-term follow-up of individuals with the electrocardiographic pattern of right bundle-branch block and ST-segment elevation in precordial leads V1 to V3". Circulation. 105 (1): 73–8. PMID 11772879. Retrieved 2012-10-13. Unknown parameter
|month=ignored (help) - ↑ 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) - ↑ Priori SG, Napolitano C, Gasparini M, Pappone C, Della Bella P, Giordano U, Bloise R, Giustetto C, De Nardis R, Grillo M, Ronchetti E, Faggiano G, Nastoli J (2002). "Natural history of Brugada syndrome: insights for risk stratification and management". Circulation. 105 (11): 1342–7. PMID 11901046. Retrieved 2012-10-13. Unknown parameter
|month=ignored (help) - ↑ 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)