ABSTRACT
APPLICATIONS, LIMITATIONS, TECHNICAL ASPECTS, PROPER EVALUATION (TIPS AND TRICKS), AND POTENTIAL COMPLICATIONS Detection of Thrombus and Disrupted Plaques The most important role of angioscopy is in the detection and classifi cation of disrupted plaques. Disrupted plaques can be subclassifi ed into ruptured plaques with a distinct crater and plaques with surface erosions. Because thrombosis at a disrupted plaque is the most frequent mechanism of acute coronary syndrome (ACS) (1-3), the detection of disrupted plaques is very important both for the identifi cation of the culprit lesion(s) in ACS and for investigating the mechanisms that lead a minority of such disrupted plaques to provoke a clinical event (Fig. 20.1; Video clip 20.1). We know from angioscopic studies that there are many disrupted plaques with active thrombus formation but without any clinical consequences; therefore, the disruption of vulnerable plaques must not be the only key step in the pathogenesis of an ACS. Other important factors involved in the process may be blood thrombogenicity (4) and the degree of luminal stenosis. However, we are still far from a comprehensive understanding of the pathophysiological mechanisms leading to ACS. To date, it is apparent that the majority of ACS events are caused by thrombosis at disrupted plaques, excluding a small percentage of events caused by vasospasm. Therefore, angioscopy has the potential to ascertain which lesion is the true culprit when patients with suspected symptoms of ACS have multiple stenotic lesions. In addition, the disrupted plaque is not always located at the site of the minimal lumen area (MLA) on angiography but is often found at a site somewhat proximal to the MLA site. The site of the disrupted plaque is called the “culprit site” of the “culprit lesion.” It has been suggested that it is important to implant a stent placing its both edges at angiographically normal segments in order to ensure complete lesion coverage rather than placing the stent edge in the midst of the disrupted plaque in order to minimize the risk of stent thrombosis or of stenosis progression at the stent edges.
