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European Heart Journal 1993 14(Supplement E):2-8; doi:10.1093/eurheartj/14.suppl_E.2
Copyright © 1993 by the European Society of Cardiology.
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© 1993 The European Society of Cardiology

Pathophysiology of supraventricular tachycardia

C. F. Shakespeare, M. Anderson and A. J. Camm

Department of Cardiology Sciences, St. Georges Hospital and Medical School Cranmer Terrace, London, U.K.

Correspondence: Dr Carl Shakespeare, Department of Cardiology. Royal London Hospital, Whitechapel Road, London E1 1BB. U.K.

Supraventricular tachycardia is due to altered automaticity, triggered activity or most commonly, reentry. Atrial flutter is most frequently due to reentry with counterclockwise activation in the right atrium with the left atrium acting as a bystander. The small wavefronts demonstrated during atrial fibrillation are less random than was previously thought. In the study of atrioventricular (AV) nodal reentrant tachycardia, recent evidence suggests that multiple pathways involving intranodal and perinodal tissue are probably involved. In the Wolff–Parkinson–White (WPW) syndrome, accessory pathways near the AV node have been demonstrated with decremental properties, suggesting conduction through accessory AV nodal tissue. The mechanism for atrial fibrillation in the WPW syndrome is poorly understood, but there is evidence that accessory pathways are branched and may themselves support micro-reentry. In Mahaim nodoventricular pathways, the atrium is not essential for reentry, unlike atriofascicular reentrant circuits. Atriofascicular pathways consist of AV node-like tissue and are usually located in the right atrial free wall.

Key Words: Mahaim fibres • atrioventricular nodal reentrant tacycardia • Wolff–Parkinson–White syndrome • triggered activity • altered automaticity • reentry


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