Indian Pacing Electrophysiol. J.


   ISSN  0972-6292

Home Page Current Issue List of Editors

Indian Pacing Electrophysiol. J. 2003;3(3):91

Editorial



 

Brugada-Like Electrocardiographic Pattern

Johnson Francis, MD, DM*, Charles Antzelevitch, PhD, FACC**

*Associate Professor of Cardiology, Medical College Calicut, Kerala, India.

**Executive Director, Masonic Medical Research Laboratory, Utica, New York, USA

Address for correspondence: Dr. Johnson Francis, "Pulikkottil", Thondayad, P.O. Chevarambalam, Calicut -673017, Kerala, India. Email: johnsonf@vsnl.com

            The Brugada syndrome is characterized by a ST-segment elevation in the right precordial leads associated with right bundle branch block (RBBB) pattern and a propensity for life-threatening ventricular arrhythmias in the absence of structural heart disease.1 Mutations in a cardiac sodium channel gene have been linked to this syndrome2.

           
The mechanism underlying the RBBB and ST-segment elevation in right precordial leads in patients with the Brugada syndrome is thought to be an outward shift of the ionic currents during early repolarization causing a marked accentuation of the action potential notch in right ventricular epicardial but not endocardial cells. The outward shift of current ultimately leads to loss of the action potential dome causing marked abbreviation of the action potential in the right ventricular epicardial cells.3, 4,5

           
Local pressure applied to the right ventricular wall has also been reported to induce an ECG pattern similar to the Brugada syndrome. Tarin et al reported a patient with a mediastinal tumor and electrocardiographic findings similar to those described in the Brugada syndrome. This ECG pattern disappeared after tumor removal, thus suggesting that it was probably caused by compression of the right ventricular outflow tract by the mass.6 Another case of pericardial fluid and “tumour” compressing the right ventricle with Brugada-like ECG pattern in a patient with rheumatoid arthritis has also been reported7 During surgery the “tumour” was found to be organised haemopericardium. After the surgery the patient was well and had a normal ECG.

           
Nakazato et al describes a similar situation in this issue of the journal8. Compression of the right ventricular outflow tract by an abnormal infective mass, with/without focal pericardial inflammation was thought to be the mechanism of Brugada-like ST elevation in their patient.

           
The ability of local pressure to give rise to an ST segment elevation has been demonstrated experimentally in the arterially perfused right ventricular wedge preparation (Antzelevitch & Dumaine, 2002)9. Focal pressure was shown to cause loss of the action potential dome at some right epicardial sites but not others. The potential for this mechanism to give rise to closely coupled phase 2 reentrant extrasystoles and VT was also demonstrated in this experimental study.

            Several other instances of Brugada-like patterns have been reported. Ortega-Carnicer et al10 noted transient Brugada-type electrocardiographic abnormalities in renal failure which was reversed by dialysis. They reported a patient with a previous history of epilepsy treated with psychotropic drugs (with a sodium channel blocking effect) and chronic renal failure on haemodialysis who developed hyperkalaemia and ECG findings resembling Brugada syndrome. These ECG changes disappeared after haemodialysis when the potassium became normal. They concluded that hyperkalaemia along with cardiac membrane active drugs may cause ECG changes mimicking the Brugada syndrome.

           
Transient Brugada pattern has been observed repeatedly after recreational use of cocaine.11 Intravenous administration of procainamide and subsequent intravenous propranolol followed by noradrenaline failed to reproduce the Brugada in this case. Electrophysiologic study performed in the presence of the Brugada ECG pattern showed no inducible arrhythmias. Yet another report describes a patient in whom a typical Brugada ECG pattern developed in relation to fever but could not be reproduced at normal temperature on administration of flecainide12. This case suggests that in some patients a Brugada-like ECG may only manifest during a febrile state.

            All these reports of Brugada-like ECG pattern give us a better insight into the genesis of this pattern and possibly localize the abnormality to the right ventricular outflow tract. Heterogenous response of repolarization across the ventricular wall in the right ventricular outflow tract is thought to be responsible for accentuation of ST segment elevation in the right precordial leads.13

References

1. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol 1992; 20:1391–1396.

2. Chen Q, Kirsch GE, Zhang D, et al. Genetic basis and molecular mechanisms for idiopathic ventricular fibrillation. Nature 1998; 392:293–296.

3. Antzelevitch C. The Brugada syndrome: Diagnostic criteria and cellular mechanisms. Eur Heart J 2001; 22:356–363.

4. Antzelevitch, C. Late potentials and the Brugada syndrome. Journal of American College of Cardiology 2002;39:1996-1999.

5. Antzelevitch, C., Brugada, P., Brugada, J., Brugada, R., Shimizu, W., Gussak, I., & Perez Riera, A. R.  Brugada Syndrome: A Decade of Progress. Circulation Research 2002; 91:1114-1118.

6.  Tarin N, Farre J, Rubio JM, et al. Brugada-like electrocardiographic pattern in a patient with a mediastinal tumor. PACE 1999; 22:1264–1266.

7. Tomcsányi J, Simor T and Papp L. Haemopericardium and Brugada-like ECG pattern in rheumatoid arthritis. Heart 2002;87:234.

8.  Nakazato Y, Ohmura T, Shimada I, Daida H. Brugada-like Precordial ST Elevation on ECG by Anterior Mediastinal Infective Mass Lesion. Indian Pacing Electrophysiol. J. 2003;3:184  [ Free Full Text ]

9. Antzelevitch, C. & Dumaine, R. (2002). Electrical heterogeneity in the heart: Physiological, pharmacological and clinical implications. In Handbook of Physiology. The Heart., eds. Page, E., Fozzard, H. A., & Solaro, R. J., pp. 654-692. Oxford University Press, New York.

10.  Ortega-Carnicer J, Benezet J, Ruiz-Lorenzo F, Alcazar R. Transient Brugada-type electrocardiographic abnormalities in renal failure reversed by dialysis. Resuscitation 2002;55:215-9.

11.  Littmann L, Monroe MH, Svenson RH. Brugada-type electrocardiographic pattern induced by cocaine. Mayo Clin Proc 2000;75:845-9

12.  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 May;25(5):856-9.

13.  Shimizu W, Aiba T, Kurita T, Kamakura S. Paradoxic abbreviation of repolarization in epicardium of the right ventricular outflow tract during augmentation of Brugada-type ST segment elevation. J Cardiovasc Electrophysiol 2001;12:1418-21.

This article has been cited by other articles:


Home
Johnson Francis, C.G. Sajeev,  K. Venugopal
Brugada Syndrome: The Enigma
Calicut Medical Journal 2003;1(1):e3  [Full Text] 


Home Page Current Issue List of Editors