ST-elevation no myocardial infarction

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. …