INFLAMMATORY MEDIATORS LEAD TO CAROTID PLAQUE INSTABILITY AND RUPTURE

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The goal of this project is to fill major gaps in our knowledge regarding the process of carotid plaque instability and rupture. Carotid artery disease is an important cause of cerebrovascular disease and continues to be a major health care problem, contributing to at least 200,000 cases of stroke each year the United States. In almost half of these cases, death follows within a year. The mechanism for these events is via carotid plaque instability, rupture, and atheroembolization. Increasing evidence suggests that factors other than the degree of carotid stenosis are involved in the risk of ischemic stroke. Carotid atherosclerotic plaques have traditionally been characterized as "stable" or "unstable" by the clinical presentation of the patient. Plaque stability relates to the unlikely event of atheroembolization, while "instability" or plaque vulnerability, invokes the greater potential for plaque rupture and ocular or cerebral hemispheric events. Even though some of these plaque differences can be appreciated sonographically, no good biochemical markers exist. Furthermore, the pathogenesis which leads a stable carotid plaque towards an unstable one is poorly understood. We have obtained IRB approval at various hospitals in the area to study the role that inflammatory mediators play in carotid atherosclerotic plaque progression from a stable to a vulnerable, unstable plaque. Furthermore, we aim to study the key molecular differences between stable and unstable carotid plaques.