© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Ins(1,4,5)P3 and cardiac dysfunction
aCellular Biochemistry Laboratory, Baker Medical Research Institute, Commercial Road, Prahran, Victoria, Australia
bRappaport Family Institute for Research in the Medical Sciences, Bruce Rappaport Faculty of Medicine, The Bernard Katz Center for Cell Biophysics, Technion—Israel Institute of Technology, Haifa, Israel
* Corresponding author. Tel.: +61-3-9522-4387; Fax: +61-3-9521-1362; E-mail: liz.woodcock@baker.edu.au
Received 18 February 1998; accepted 26 May 1998
KEYWORDS Arrhythmia (mechanisms); Calcium (cellular); Signal transduction; Reperfusion; Immunology
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1 Introduction |
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Cardiac related death occurs rapidly via the development of arrhythmias or more slowly by a progressive decline in mechanical performance reflecting decreased contractile activity as well as loss of viable myocytes. Pathological conditions such as myocardial ischaemia, inflammatory heart diseases and various forms of heart failure are associated with both sudden death and also with a more progressive decrease in cardiac function. Electrophysiological disturbances leading to malignant ventricular arrhythmias are the usual cause of sudden cardiac death, whereas a gradual loss of functional myocytes, or a decline in their performance, underlies heart failure ultimately leading to cardiac decompensation. The mechanisms initiating these scenarios are complex and multifactorial, involving both extracellular and intracellular factors. However, given the continued major contribution of cardiac deaths to overall mortality, understanding the processes which initiate these pathological events is of prime importance. The current review will focus on changes in the intracellular milieu and in
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2 Inflammatory heart disease |
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3 Ischaemia and reperfusion |
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4 Heart failure |
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5 Summary and conclusions |
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