Abstract
Acute coronary syndrome (ACS) is a major health problem and leads to a large number of hospitalizations annually in Europe.1 ACS refers to a group of clinical conditions caused by myocardial ischaemia, including unstable angina pectoris, non-ST-segment elevation myocardial infarction (NSTEMI), ST-segment elevation myocardial infarction (STEMI), and sudden cardiac death. ACS results from a common underlying pathophysiological mechanism, i.e. plaques vulnerable to rupture or erosion, with different degrees of superimposed thrombosis and distal embolization. Vulnerable plaques that are likely to rupture or erode have evidence of inflammation, together with thin fibrous caps and large lipid cores. The platelet-rich thrombus, developed in association with pro-coagulant-vulnerable blood, can release vasoconstrictor substances such as serotonin and thromboxane A2 that may induce vasoconstriction at the site of plaque rupture or in the … *Corresponding author. Tel: +81 22 717 7153, Fax: +81 22 717 7156, Email: shimo{at}cardio.med.tohoku.ac.jp
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