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To understand the pathophysiology of myocardial infarction.
To review the imaging and biochemical biomarkers that measure infarct size.
To review the pharmacological and mechanical treatments available that impact infarct size.
Coronary artery disease is the leading cause of death worldwide, with ST segment elevation myocardial infarction (STEMI) an important contributor. Infarct size following STEMI is a determinant of heart failure and death. This article provides an update on key modalities used to determine infarct size, and recent advances in interventions used to reduce infarct size.
Determinants of infarct size and their pathophysiology
The area at risk (AAR) is the region of the myocardial bed supplied by the infarct related artery (IRA). In the era of reperfusion, not all the AAR will become infarcted. Depending on time to reperfusion and the exact location of occlusion, there will be a proportion of the AAR (jeopardised but not infarctedw1) that can be salvaged by reperfusion therapy. This can be calculated as AAR−infarct size (figure 1).
The cause of irreversible myocardial damage in STEMI can be divided into two categories: myocardial damage as a result of the myocardial ischaemic process itself; and myocardial damage as a result of reperfusion, termed reperfusion injury. It is difficult to separate out these two components (figure 2).
Following a coronary occlusion, the myocardial bed supplied …
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