(Circulation. 2002;106:649.)
© 2002 American Heart Association, Inc.
Clinician Update |
From the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands.
Correspondence to Hein J.J. Wellens, MD, 21 Henric van Veldekeplein, 6211 TG Maastricht, The Netherlands. E-mail hwellens@xs4all.nl
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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History
In 1906, Einthoven made an electrocardiographic recording of AFl.1 In 1913, Lewis called attention to the typical saw tooth pattern and the negative deflections of the atrial waves in leads II and III.2
During the next 50 years, there was much discussion about whether AFl was caused by a rapidly firing atrial focus or is the result of a large circus movement involving the atria. After mapping atrial activation with endocardial and esophageal recordings, Puech et al3 concluded that the flutter cycle in the human heart involved activation of the whole right atrium. Stimulation studies by Waldo et al4 revealed that in postoperative AFl the arrhythmia was based on a reentry mechanism involving a large atrial area. They demonstrated the presence of an excitable gap that allowed the speeding up of the flutter rate during atrial pacing and termination of the arrhythmia by pacing.
Mechanism and Types of Macroreentrant Tachycardias
With the use of endocardial activation mapping and stimulation studies,
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