Previous Brief Review in this Series:• Choudhury RP, Fuster V, Badimon JJ. Fisher EA, Fayad ZA. MRI and characterization of atherosclerotic plaque: emerging appliations and molecular imaging. 2002;22:1065-1074.• Bonetti PO, Lerman LO, Lerman A. Endothelial dysfunction: a marker of atherosclerotic risk. 2003;23:168 -175.• Oliver JJ, Webb DJ. Noninvasive assessment of arterial stiffness and risk of atherosclerotic events. 2003;23:554 -566.
Finding Vulnerable Atherosclerotic Plaques Is It Worth the Effort?Mohammad Madjid, Alireza Zarrabi, Silvio Litovsky, James T. Willerson, Ward Casscells Abstract-Techniques to identify and treat vulnerable plaques are the focus of enormous research. Some have questioned the benefit of locating individual vulnerable plaque in a multifocal disease. On autopsy, it is found that most deaths are caused by thrombotic occlusion of a single plaque; simultaneous occurrence of 2 occlusive thrombi is rare, but a second vulnerable plaque is common, particularly in acute myocardial infarction (MI). Angiographic progression is poorly predicted by risk factors, and angiographic progression is a weak predictor of MI or death. Intravascular ultrasonography (intravascular ultrasound [IVUS]) studies find plaque rupture in most MI patients and in approximately half with unstable angina, but in only a minority of patients with stable angina. IVUS identifies a second vulnerable plaque in many patients with unstable angina, and in most MI patients. Angioscopy reveals a very low incidence of a second vulnerable plaque compared with angiography and IVUS, but identifies additional yellow plaques in many patients with stable angina and in most patients with unstable angina or MI. Using thermography catheters and a temperature cutoff of 0.1°C, approximately half the patients with stable angina have Ͼ1 hot lesion; however, if the cutoff is 0.2°C, only Ϸ15% have a second hot lesion. New imaging techniques may detect additional characteristics of plaques and new predictive models may assess the risk of vulnerable plaques and patients. This approach enables physicians to "buy time" by application of local therapies until systemic therapies stabilize plaques. This may also reduce the risk in subjects in whom systemic therapies do not work. tions of coronary heart disease, whereas superimpositions of thrombi over the plaques lead to acute coronary syndromes. To date, angiography has been the method of choice for detecting these problematic arterial lesions. However, this diagnostic technique, which approximately compares the degree of stenosis of arterial lesions relative to the proximal segments of the artery, does not provide insight into the disease state within the artery, and often fails to detect those lesions prone to thrombosis. A series of landmark angiographic studies in the mid 1980s demonstrated that nearly two-thirds of all MI originate at atherosclerotic lesions that lack hemodynamic significance. 2-6 Unfortunately, these "culprit" lesions, which have been termed vulnerable plaques, are undetectable...