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CLINICAL REVIEW: June Edhouse and Francis Morris ABC of clinical electrocardiography: Broad complex tachycardiaPart II BMJ 2002; 324: 776-779 [Full text]

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Ventricular Tachycardia

Ranjan K Singh, --   (31 March 2002)

Brugada syndrome

Serdar KULA, Berna CANTER   (6 April 2002)

Ventricular Tachycardia 31 March 2002
Ranjan K Singh, Physician,District Hospital Daltonganj,Jharkhand,India. District Hospital Daltonganj,Jharkhand,India, -- Send response to journal: Re: Ventricular Tachycardia	Features suggesting ventricular tachycardia (v.tach.) in the article(1) are livid and justifying. In spite of these features sometimes it becomes difficult to deside whethere it is v.tach. or aberrant supraventricular tachycardia. In such situation clinical features like cannon waves in jugular vein and varying first heart sounds,vagal stimulation ie. carotid sinus pressure as well as valsava manoevre certainly help in differenciating broad QRS arrhythmia. Furthermore atrioventricular dissociation (AV dissociation)is a feature of v.tach.Details of AV dissociation is lacking in the article(1). Capture beats and fusion beats in v.tach. are always due to interference pattern of AV dissociation. AV dissociation (isorhythmic) has approximately same atrial and ventricular rates and P wave appears running over QRS complexes in the rhythm strip of ECG. Both kind of AV dissociations are seen in v.tach. Reference- 1.June Edhouse and Francis Morris.Broad Complex Tachycardia-Part- II.BMJ(2002);324:776-779.
Brugada syndrome 6 April 2002
Serdar KULA, Pediatrician and Pediatric Cardiologist Gazi University Medical School Department of Pediatric Cardiology, 06500 Besevler, Ankara, TURKEY, Berna CANTER Send response to journal: Re: Brugada syndrome	Dear editor, In your recently published review called “Broad complex tachycardia”, varieties of ventricular tachycardias were discussed. Brugada syndrome, which may be classified as an idiopathic ventricular fibrillation like long Q-T syndrome (LQTS) was not mentioned. This autosomal dominant disease, although more common in Asian countries, is seen worlwide and should be remembered as one of the causes of sudden cardiac death. Number of described cases so far exceeded 200 and new cases are being described everyday (1). ST segment elevation in V1 to V3 associated with right bundle branch blockis the typical ECG criteron of this syndrome; however it may not be evident all the time in some cases (2). Another important point that should be kept in mind is that although mutations in the cardiac Na channel gene SCN5A give rise to both congenital LQTS and Brugada syndrome, Na channel blockade using antiarrythmic drugs which improves Q-T interval prolongation in LQTS worsens the condition in Brugada syndrome (3). REFERENCES 1. Aligns M, Wilde A. Brugada syndrome: clinical data and suggested pathophysiological mechanism. Circulation 1999;99:666-673. 2. 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. 3. Brugada P, Brugada J. Further characterization of the syndrome of right bundle branch block, persistent ST segment elevation and sudden cardiac death. J Cardiovasc Electrophysiol 1997;8:325-331.