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Brief Reviews |
From the Department of Internal Medicine/Division of Cardiology (M.M., A.Z.) and Department of Pathology (S.L.), School of Medicine, University of TexasHouston Health Science Center and Texas Heart Institute, Houston, Tex; the Department of Internal Medicine and President of the University of Texas Health Science Center at Houston (J.T.W.), Medical Director, Texas Heart Institute, and Chief of Cardiology at St. Lukes Episcopal Hospital, Houston, Tex; the Department of Internal Medicine/Division of Cardiology and Public Health (W.C.), Vice President of Biotechnology, School of Medicine, University of TexasHouston Health Science Center, and Associate Director of Cardiology Research Texas Heart Institute/St. Lukes Episcopal Hospital, Houston, Tex, and Division of Cardiology/Department of Internal Medicine, Medical School, The University of Texas Health Science Center at Houston, The Texas Heart Institute at St. Lukes Episcopal Hospital, and President Bush Center for Cardiovascular Health at Memorial Hermann Hospital, Houston, Tex.
Correspondence to Dr Ward Casscells, The University of Texas Medical School at Houston, 6431 Fannin Street, MSB 1.252, Houston, TX 77030. E-mail s.ward.casscells{at}uth.tmc.edu
Series Editor: William Haynes
ATVB in Focus
Noninvasive Assessment of Atherosclerosis: from Structure to Function
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;22:10651074.
Bonetti PO, Lerman LO, Lerman A. Endothelial dysfunction: a marker of atherosclerotic risk. 2003;23:168175.
Oliver JJ, Webb DJ. Noninvasive assessment of arterial stiffness and risk of atherosclerotic events. 2003;23:554566.
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 >1 hot lesion; however, if the cutoff is 0.2°C, only
15% 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.
Techniques to identify and treat vulnerable plaques are the focus of enormous research. Here, we discuss the potential benefit of locating individual vulnerable plaques. We review the multifocal nature of the disease in autopsy series and studies using angiography, IVUS, thermography, and angioscopy. The use of new imaging techniques and the development of predictive models may enable physicians to identify plaques that may benefit from local therapies.
Key Words: plaque rupture atherosclerosis stents coronary imaging
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