Abstract 2995: Natural History Of Carotid Atherosclerotic Plaque Remodeling After Tia And Stroke
Background Thrombosis of carotid vulnerable atherosclerotic plaques is the pathological substrate for cerebrovascular events such as transient ischemic attacks (TIA) and stroke. However, the natural history of symptomatic plaque remodeling following a clinical event is unknown.
Methods Atherosclerotic carotid plaques were obtained from 547 patients undergoing endarterectomy. Plaques were analyzed for the presence of macrophages, smooth muscle cells (SMC), collagen, calcification, thrombus and lipid core size. In plaques, inflammatory status was determined by measuring cytokines Interleukin-2 (IL-2), IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, IFN-gamma, TNF-alfa and TGF-beta with FACS analysis. Results were related to the time elapsed between the initial event and the atherosclerotic plaque dissection.
Results In patients who suffered from a stroke (n=166), presence of macrophages decreased (p=0.01) and SMC tended to increase with time after the event. After major stroke (n=23) plaques demonstrated a stronger reduction of macrophages, whereas plaques after TIA did not show histological changes in relation to time after an event. At protein level, pro-inflammatory IL-6 and IL-8 significantly reduced with time since the clinical event. Other cytokines did not show a relation.
Conclusions Symptomatic carotid lesions restore into more stable plaques with time, with a decrease in macrophage infiltration and lower expressions of IL-6 and IL-8. The severity of the event is positively associated with the degree of stabilization. These findings provide new insights in the natural history of the progression of atherosclerotic disease.