Pathophysiology of the Unstable Atherosclerotic Plaque

摘要: Disruption of an atherosclerotic plaque with resultant intraluminal thrombosis is the principal mechanism rapid progression coronary atherosclerosis and fundamental process unstable angina, acute myocardial infarction many cases sudden death. The occurrence course largely unpredictable. It known that severity artery stenosis number diseased vessels are markers for future events. However, individuals identical or in degree angiographic stenoses, some live years without any symptoms while others experience life threatening heart attacks die suddenly unexpectedly. Recent observations indicate it not (i.e. volume) determines outcome, but composition extent collateral development. Patients ischemic disease have plaques their arteries, at least 10-fold more than judged from a angiogram, survival depends on common clinically silent non-flow limiting few stenotic ones [1]. Postmortem studies performed early 1980s revealed dangerous plaques/stenoses could be identified angiographically due to irregular borders and/or lucencies giving rise ‘complex ‘angiographic morphology [2]. A later, this was confirmed vivo culprit lesions responsible syndromes often angiography [3-5]. This chapter will review discuss pathoanatomic features mechanisms involve complex rupture plaques, those underlying syndromes.