Abstract
Acute coronary syndrome (ACS), i.e. acute myocardial infarction (MI) and unstable angina, is a life threatening disease, and its treatment after onset has greatly improved; however, we are not satisfied with the long-term outcome of the patients with ACS. Furthermore, we cannot adequately prevent the onset of ACS, although we know many risk factors of ACS, e.g. diabetes mellitus, dyslipidemia, hypertension, obesity, and smoking. As plaque disruption and thrombosis is known as the major cause of ACS, many investigations to identify vulnerable plaques that are prone to disrupt have been performed but failed to identify high-risk lesions of future ACS event. Major reason for this failure may be that disruption of plaques does not always cause ACS and probably very few percentages of disrupted plaques may actually cause ACS. In order to know adequately about the mechanisms for the onset of ACS and to prevent it effectively, we have to clarify those missing factors that are essential for the disrupted plaques to cause ACS. In this chapter, we would like to elucidate and discuss on the known and unknown mechanisms for the onset of ACS from the angioscopic point of view.
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