Skip Navigation

Cardiovascular Research 2000 47(2):210-211; doi:10.1016/S0008-6363(00)00134-6
© 2000 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Kowey, P. R.
Right arrow Articles by Xu, X.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kowey, P. R.
Right arrow Articles by Xu, X.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2000, European Society of Cardiology

Familial hypertrophic cardiomyopathy: cornering the rat

Peter R. Koweya,b,*, Gan-Xin Yana,b and Xiaoping Xua,b

aLankenau Hospital and Institute for Medical Research, Main Line Health, Wynnewood, PA, USA
bJefferson Medical College, Philadelphia, PA, USA

* Corresponding author. Tel.: +1-610-649-6980; fax: +1-610-649-6990 prkowey@pol.net

Received 19 May 2000; accepted 19 May 2000

The first 10% of the full text of this article appears below.

See article by Frey et al. [8] (pages 254–264) in this issue.

Hypertrophic cardiomyopathy is a terrible disease [1]. It is associated with negative hemodynamic changes leading to pulmonary congestion and low output, and with severe ventricular arrhythmias that in many cases are lethal. We have learned a good deal about the electrophysiology of this disease [2]. Unlike ischemic heart disease that predisposes to conduction block and reentrant arrhythmias on that basis, the lesion of hypertrophy involves repolarization [3]. Hypertrophied cells have long and non-uniform repolarization times. This dispersion of action potential duration is a milieu in which early afterdepolarizations can generate sustained and highly disorganized ventricular arrhythmias, manifest on the . . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Eur Heart J SupplHome page
M.J. Janse and J.M.T. De Bakker
Arrhythmia substrate and management in hypertrophic cardiomyopathy: from molecules to implantable card ioverter-defibrillators
Eur. Heart J. Suppl., October 1, 2001; 3(suppl_L): L15 - L20.
[Abstract] [PDF]