© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Damage-induced arrhythmias: reversal of excitation–contraction coupling
Departments of Medicine, Physiology and Biophysics, The University of Calgary, Calgary, Alberta T2N 4N1, Canada
* Corresponding author. Tel.: +1-403-220-4521; fax: +1-403-270-0313; e-mail: Henk@cvrsun1.cvr.ucalgary.ca
Received 1 July 1998; accepted 24 August 1998
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1 Introduction |
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Sustained or self-terminating ventricular arrhythmias commonly arise as the oscillatory response of the mechanisms involved in re-entry to a premature beat in non-uniform working myocardium or conduction tissue. Non-uniformity of conduction in the human heart itself is often a result of myocardial ischemia or infarction due to coronary artery disease. Ischemic non-uniformity may further be aggravated by cardiac remodelling during development of congestive heart failure, thereby, providing a possible mechanism substrate for fatal arrhythmias which often cause the demise of patients with congestive heart failure [1, 2]. Most discussions of these arrhythmias emphasize the importance of electrical non-uniformity. Nevertheless, it is evident that myocardium that has been rendered non-uniform will also exhibit variations of mechanical stresses and strains from cell to cell as well as differences among cells in excitation contraction coupling, in addition to electrical non-uniformity.
Too little is known about the role played by non-uniform myocardial stress
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2 After-contractions and after-depolarizations and Ca2+ transients |
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3 Spontaneous Ca2+ release from the SR and Ca2+ waves in myocytes |
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4 Triggered propagated contractions in cardiac muscle |
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5 Triggered propagated contractions: damage and the initiating event |
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6 Propagation of TPCs |
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7 Mechanisms underlying initiation and propagation of Ca2+ waves and TPCs |
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7.1 Initiation of Ca2+ waves in myocytes
7.2 Initiation of TPCs in multicellular preparations
7.3 Propagation of Ca2+ waves in myocytes
7.4 Propagation of TPCs
7.5 Propagated Ca2+ release induces premature beats
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8 Premature beats and triggered arrhythmias resulting from TPCs |
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