Please click here to obtain permission to reproduce this image.
Click on image to view larger version.
Figure 7 Proposed Natural History of Coronary Atherosclerosis
The initiating process of atherosclerosis in an atherosclerosis-prone host is a low endothelial shear stress (ESS) environment, leading to the formation of an early fibroatheroma, which might be diffuse. The vascular response to that early fibroatheroma likely determines the nature of the subsequent natural history of that plaque. If there is local compensatory expansive remodeling, then the local ESS is normalized, the hemodynamic stimulus for further plaque progression is resolved, and the early lesion evolves to a quiescent plaque with limited inflammation. However, in the presence of certain local, systemic, and genetic factors, the local vascular wall might undergo excessive expansive remodeling. In this context the local low ESS environment persists, promoting further plaque progression and vessel expansion. A self-perpetuating vicious cycle is established among local low ESS, excessive expansive remodeling, and plaque inflammation, transforming the early fibroatheroma to a thin cap fibroatheroma. The stenotic plaques might either evolve with a phenotype promoting fibroproliferation consistently throughout their natural history course or represent an end-stage of scarring in the setting of prior inflamed thin cap fibroatheroma through repetitive microruptures and healing. Also, the stenotic plaques might infrequently undergo local erosion or develop calcified nodules and lead to local thrombus formation and manifestation of an acute coronary syndrome. The percentages reported in the figure are based on intravascular ultrasound studies (23,110,111).
|
