doi: 10.1161/01.RES.0000165653.83279.20
© 2005 American Heart Association, Inc.
Editorials |
Understanding Conduction System Development
A Hop, Skip and Jump Away?
From the Leon H. Charney Division of Cardiology, New York University School of Medicine, New York.
Correspondence to: Glenn I. Fishman, M.D. Leon H. Charney Division of Cardiology New York University School of Medicine 550 First Avenue, OBV A615 New York, New York, USA 10016 Tel: 212-263-3967 Fax: 212-263-3972 E-mail glenn.fishman@med.nyu.edu
See related article, pages 898–903
Key Words: cardiac conduction system • homeodomain only protein • transcription factors
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In the late 1800s, W.H. Gaskell demonstrated that impulse propagation from the atrium to the ventricle of the tortoise heart reflected conduction along myocardial tissue rather than nerve tissue.1 A decade later, Stanley Kent proposed, incorrectly as it turns out, that multiple muscular connections normally link the atria and ventricles of mammals,2 but it was not until the remarkably detailed report almost 100 years ago by Sunao Tawara, working in the laboratory of Ludwig Aschoff in Germany, that the histological identification and characterization of the atrioventricular node, the penetrating bundle of His, the left and right bundle branches and Purkinje fiber network was established.3 The notion that aberrant conduction between atria and ventricles might account for rhythm disturbances was first proposed in 1930, when the renowned American cardiologist Paul Dudley White and the English physicians John Parkinson and Louis Wolff reported on a series of patients with a short PR interval and apparent bundle branch block who were prone to paroxysmal tachycardia.4
During the past decade, there has been growing realization of the importance of diseases involving the cardiac conduction system (CCS), maladies that are now known to reflect diverse pathologic mechanisms including not only post-operative complications following surgical repair of congenital heart defects, but also immunological and metabolic disorders, degenerative processes and most recently - transcriptional dysregulation.5–9
Classically, the adult CCS is thought to encompass cells of the sinoatrial node, the atrioventricular node, common bundle of His, left and right bundle branches and distal Purkinje fiber network.10,11 Whether other
Related Article:
Circ. Res. 2005 96: 898-903.