© 2001 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
The role of altered intercellular coupling in arrhythmias induced by acute myocardial ischemia
aDepartment of Pediatrics, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110, USA
bDepartment of Medicine, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110, USA
cDepartment of Pathology, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110, USA
dCenter for Cardiovascular Research, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110, USA
* Corresponding author. Tel.: +1-314-362-7728; fax: +1-314-362-4096 saffitz@pathology.wustl.edu
Received 3 October 2000; accepted 13 November 2000
KEYWORDS Arrhythmia (mechanisms); Gap junctions; Ischemia; Sudden death
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1 Introduction |
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Sudden cardiac death occurs with unacceptably high incidence in patients with ischemic heart disease and cardiomyopathy. As Zipes and Wellens [1] have emphasized, sudden death arises from highly variable interactions between anatomic and/or functional myocardial substrates, transient initiating events and cellular/tissue arrhythmia mechanisms. In our view, a key strategy for developing mechanistic insights into sudden death is to first define the role of individual factors (including specific gene products) that contribute to arrhythmias, and to then understand how these factors interact to cause sudden death.
One of the most common disease settings leading to sudden cardiac death is the acute coronary syndromes. Acute ischemia is marked by alterations in cell metabolism, cell signaling, intercellular communication and electrical impulse propagation [2]. These changes produce a cascade of events that are adaptive in the sense that mechanisms are activated to mitigate injury, forestall cell death and isolate irreversibly injured myocytes from
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2 Connexins and electrical coupling |
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3 The Cx43 knockout mouse |
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4 Effects of diminished Cx43 expression on gap junction structure |
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5 Diminished intercellular coupling in the pathogenesis of arrhythmias induced by acute ischemia |
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6 Uncoupling and mechanisms of arrhythmias during acute ischemia |
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7 Conclusions |
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