Acute
Coronary Syndrome (ACS) is characterized by a complex multi factorial
pathogenesis, which involves an inflammatory response, immune damage, and the
activation of the blood clotting function. Thus far, researchers studying the fundamental mechanism of ACS have suggested that inflammation causes coronary atherosclerotic plaque instability and leads to the activation of endothelial cells, which results in the rupture of plaques and thrombus formation. In
addition, the progression of thrombus formation is associated with
inflammation, and the pro-inflammatory state appears to increase the risk of
coronary artery thrombosis, which suggests that the inflammatory response plays
an important role in the onset of ACS.
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