Journal
EUROPEAN HEART JOURNAL-ACUTE CARDIOVASCULAR CARE
Volume 8, Issue 2, Pages 142-152Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/2048872618812148
Keywords
Myocardial infarction; arrhythmias; myocardial reperfusion injury; pathophysiology
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Funding
- Hein Wellens Foundation, Maastricht, The Netherlands
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Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury.
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