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Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 94))

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Abstract

Sudden release of a coronary artery occlusion is known to be a potent arrhythmogenic stimulus, often leading to ventricular fibrillation [1–4]. Although this phenomenon has been the subject of intense laboratory investigation, assessment of its clinical relevance has been difficult. The majority of patients with acute myocardial infarction undergoing coronary thrombolysis and/or angioplasty, or even those patients with Prinzmetal’s angina have not experienced significant reperfusion arrhythmias. This is not surprising as experimental data derived from dog studies suggest that the prevalence of reperfusion arrhythmias is related to a range of values for different variables that, if not satisfied, would minimize the expression of such arrhythmias. Practical considerations may reduce the risk for certain factors, such as duration of occlusion, myocardium at risk, and magnitude of reflow during reperfusion, resulting in a nominal risk for most patients [1–5]. Nonetheless, as patient access to thrombolytic therapy is accelerated, the duration of occlusion may be shortened, and expression of these arrhythmias may actually increase. More important, interaction among variables may occur, thereby altering the relationship between prevalence of arrhythmia and the value of a particular variable, so that expression of this arrhythmia may increase.

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© 1989 Kluwer Academic Publishers, Boston/Dordrecht/London

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Strauss, H.C., Yee, R., Hill, J.A., Wenger, T.L. (1989). Mechanisms of Reperfusion Arrhythmias. In: Rosen, M.R., Palti, Y. (eds) Lethal Arrhythmias Resulting from Myocardial Ischemia and Infarction. Developments in Cardiovascular Medicine, vol 94. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1649-7_5

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  • DOI: https://doi.org/10.1007/978-1-4613-1649-7_5

  • Publisher Name: Springer, Boston, MA

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