Published in:
01-04-2017 | Letter to the Editor
ST-elevation no myocardial infarction
Authors:
Peter Damman, Robbert J. de Winter, Mitchell W. Krucoff
Published in:
Journal of Thrombosis and Thrombolysis
|
Issue 3/2017
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Excerpt
Acute coronary syndrome encompasses a clinical spectrum of signs and symptoms and that are most commonly caused by intracoronary atherosclerotic plaque rupture or erosion with superimposed thrombus formation and distal embolization [
1]. This intracoronary thrombus may lead to (partial) occlusion of the artery and a reduction in blood flow leading to clinical symptoms such as chest pain. Despite the common pathophysiological substrate, the clinical presentation of ACS is diverse. It ranges from ST-segment elevation myocardial infarction (STEMI), where the coronary artery is totally occluded by thrombus, to non-ST-segment elevation acute coronary syndrome characterized by a partially or intermittently occlusive thrombus. ST-segment elevation on electrocardiography, indicating but not limited to complete coronary occlusion, is the clinical hallmark of ST-elevation myocardial infarction (STEMI). Although myocardial cell injury can occur after 20–30 min of ischemia, it takes several hours for transmural myocardial necrosis to develop. Therefore, ST-segment elevation indicates a total occlusion of flow to a viable myocardial territory, not infarction and cell necrosis per se. The global standard for STEMI care includes early reperfusion of the infarct-related coronary artery by primary percutaneous coronary intervention in order to reduce infarct size. Earlier studies have shown a relation between shorter time to treatment and lower mortality. Therefore, “time is muscle” in STEMI. The time to treatment is determined by patient delay, and the pre- or inhospital system of care delay. …