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Cardiovascular Research 2000 47(2):210-211; doi:10.1016/S0008-6363(00)00134-6
© 2000 by European Society of Cardiology
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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]


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