The pathogenesis of acute coronary syndromes (ACS) includes the rupture or erosion of a coronary atherosclerotic plaque with variable degrees of superimposed platelet aggregation inducing a thrombus.
1,2 ST-elevation myocardial infarction (STEMI) is often caused by a total coronary occlusion of the atherothrombotic plaque, whereas in non-ST-elevation myocardial infarction (NSTEMI) the thrombus is mainly nonocclusive or transiently occlusive causing less myocardial damage.
2 Conventional percutaneous coronary intervention (PCI) focuses on compressing the atherothrombotic plaque with the aim to normalise flow in the coronary artery and therefore restore perfusion of the ischaemic myocardium. However, embolisation of atherothrombotic material may occur spontaneously after plaque rupture or due to mechanical crushing of the culprit lesion during PCI.
3,4 This results in obstruction of distal vessels or the microcirculation in the down-stream bed of the ischaemiarelated artery.
4,5 Although normal epicardial flow may be achieved, this will lead to diminished myocardial perfusion, which is associated with larger infarct size, diminished left ventricular ejection fraction and increased mortality.
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