Abstract
Myocardial infarction is usually the result of obstruction to flow in a coronary artery as a consequence of rupture of an atheromatous plaque and associated thrombosis. More rarely myocardial infarction (but often myocardial ischaemia) is related to an increased workload on the heart in the presence of limited blood flow. The major consequences are arrhythmias leading to sudden death, reduction of the ability of the myocytes to contract leading to heart failure, and cell necrosis leading to scar formation, remodelling of the residual myocardium and heart failure. Many of the key events, and, in particular, arrhythmias, early contractile failure and cell necrosis have been linked to alterations in ion homoeostatis within the myocardial cell. Indeed, some authors have argued that the ion changes associated with the metabolic consequences of reduced oxygen supply can account for almost all these observed effects. Alternatively it may be that during ischaemia damage to structures within the myocardial cell initiates cell damage and finally results in cell necrosis.
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Poole-Wilson, P.A. (1992). Ion Movements Early in Myocardial Ischaemia: Relation to Arrhythmias, Early Contractile Failure and Tissue Necrosis. In: Parratt, J.R. (eds) Myocardial Response to Acute Injury. Palgrave, London. https://doi.org/10.1007/978-1-349-12522-7_6
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DOI: https://doi.org/10.1007/978-1-349-12522-7_6
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