Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp suitable animal model for vulnerable plaque has considerably hampered progress in the research into understanding this field. Therefore, significant advances in our understanding and natural history of plaque formation and progression can only be achieved by improving our ability to accurately identify and locate these lesions in the clinical setting. Detection based on morphology alone has been proposed using intracoronary imaging modalities such as intravascular ultrasound (IVUS), optical coherence tomography (OCT), and coronary angioscopy (CAS). In this review, we provide a short description of their techniques, validations, clinical utility, and limitations for detecting vulnerable plaques, especially those that are prone to rupture.
IVUSIVUS is a catheter-based imaging modality that provides highresolution cross-sectional images of the coronary arterial walls. High-frequency (20-40 MHz) IVUS is capable of visualizing the 3 layers of the muscular arterial wall, such as that of the coronary arteries. In normal adult human arteries, the inner bright acoustic reflection layer is derived from the interface of blood with the intima and internal elastic lamina and the second bright interface (third layer) is from the external elastic lamina and adventitia, and the middle echolucent zone reflects the media. 3 Therefore, grayscale IVUS allows qualitative measurements of luminal and vessel areas in vivo.Observation of focal arterial enlargement at the site of anagement of coronary artery disease (CAD) has 2 goals: to reduce ischemia and symptoms, and to prevent acute coronary syndrome (ACS) and death. These are controlled by different mechanisms: symptoms and ischemia, by the reduced oxygen supply/demand ratio (usually because of coronary atherosclerosis), and ACS and death, usually by disruption of vulnerable plaques.Medical management is pivotal in all patients with CAD. The first step is to identify and treat any associated diseases that can precipitate angina by increasing myocardial oxygen demand (eg, tachycardia and hypertension) or by decreasing the amount of oxygen delivered to the myocardium (eg, heart failure, pulmonary disease, or anemia). The second step is to manage CAD risk factors (eg, smoking cessation, blood pressure control, and lipid and diabetes management), as well as to prevent myocardial infarction with lifestyle changes and pharmacological treatment.It is now widely recognized that plaque rupture with subsequent thrombus formation is the most frequent cause of ACS. 1 It has been postulated that thin-cap fibroatheromas (TCFA), which are characterized by a large necrotic core with an overlying thin fibrous cap measuring <65 μm, are the precursor of plaque rupture. 2 A greater understanding of the mechanisms of vulnerable plaque formation is necessary for advancement in the diagnosis, treatment, and prevention of ACS. A good animal model would help us to understand not only how plaque progresses and ...