ABSTRACT
Introduction The role of immune cells and inflammatory mediators in cardiovascular disease has been well documented. Atherosclerosis has been described as a chronic inflammatory syndrome, a systemic disorder characterized by focal lesions throughout the vasculature (1,2). Immune cells such as T-cells and macrophages are recruited to the vascular wall where they and their signaling molecules play important roles at all stages of lesion development including plaque initiation, progression, and rupture leading to thrombotic events (3,4). Compositionally, varying sections of the plaque may be engorged with soft, pliable lipid (cholesterol ester) and immune components such as foam-cell-like macrophages, typical of either newly formed or shoulder regions of mature lesions versus regions with more stable transformations comprised of proliferated smooth muscle cells (SMCs), fibroblasts, and matrix (5-7). With growth and maturation, remodeling occurs with thickening and breakdown of the architecture and function of the vascular wall, ultimately impinging on the size of the lumen and reducing blood flow. It is these larger lesions, those more easily identified by angiography, that are typically treated with interventional procedures.
