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• W2108290469 abstract "Time for primary review 16 days 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 and strain distributions and by non-uniform excitation contraction coupling in mechanisms underlying premature beats that initiate an arrhythmia. Still, this knowledge is essential to the choice of treatment aimed at prevention of a premature beat versus treatment aimed at suppression of re-entry. An especially clinically important scenario in which arrhythmias occur is that of ischemic damage of myocardium. It is generally accepted that acute ischemic damage of myocardium leads after 20–30 min to Ca2+ overload of the damaged cells and their neighbours [3]. The arrhythmias of ischemic myocardium that occur in this phase may well be related to the Ca2+ overload [4]. Hence, it is conceivable that damage-induced premature beats may initiate re-entry arrhythmias and that abnormal cellular Ca2+ transport may play a crucial role in the initiation of the premature beat. The purpose of this paper is to … * Corresponding author. Tel.: +1-403-220-4521; fax: +1-403-270-0313; e-mail: Henk@cvrsun1.cvr.ucalgary.ca" @default.
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• W2108290469 date "1998-12-01" @default.
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• W2108290469 title "Damage-induced arrhythmias: reversal of excitation–contraction coupling" @default.
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• W2108290469 doi "https://doi.org/10.1016/s0008-6363(98)00263-6" @default.
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