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The complex molecular and cellular biology of the inflammatory process that promotes atherosclerosis has been elucidated through years of extensive experimental and clinical research. Vascular injury from inflammation initiates plaque formation and dictates the downstream clinical sequelae of atherosclerotic disease. It is essential that interventional cardiologists understand the natural history and pathologic processes of atherosclerosis, as well as the vascular biologic consequences of therapies employed during coronary intervention. This chapter describes (1) the pathophysiology of atherosclerosis; (2) the mechanisms responsible for an unstable plaque in acute coronary syndrome (ACS); and (3) the biology of vascular remodeling leading to restenosis, differences between balloon and stent injury, and therapies for restenosis.

A Response to Injury

Atherosclerosis is a result of risk factors and chronic arterial inflammation that promote sustained vascular injury.1 Several risk factors (Table 9-1) for atherosclerosis have been identified, including metabolic conditions such as sustained exposure to low-density lipoprotein (LDL) or hyperglycemia and insulin resistance associated with diabetes mellitus or metabolic syndrome. However, additional factors, including age, family history, physical factors (eg, uncontrolled hypertension resulting in changes in shear stress), environmental factors (eg, tobacco smoke), and infectious disease, also contribute to the development of atherosclerotic plaque. Vascular injury results from an inflammatory response that involves a complex sequence of interactions between endothelial and smooth muscle cells, leukocytes, inflammatory cells (eg, macrophages) and their secreted growth factors, and cytokines, which combine with lipoproteins and components of the vascular wall to form a mature atherosclerotic plaque. Inflammation plays a central role in pathogenesis of atherosclerosis; numerous studies have demonstrated a correlation between circulating inflammatory biomarkers (eg, C-reactive protein [CRP]) and an increased risk for atherosclerosis and adverse coronary events.2,3,4

Table 9-1Risk factors for Vascular Injury and Atherosclerosis


The biologic mechanisms in atherosclerotic plaque formation include intimal lipid accumulation, leukocyte recruitment, foam cell formation, neointimal growth, and vessel remodeling (Fig. 9-1).


Stages of atherosclerotic plaque growth. A. Initial stage of atherosclerosis involves injury to the vessel wall with subsequent expression of inflammatory adhesion molecules, which leads to leukocyte recruitment. B. Intermediate lesions involve macrophages imbibing oxidized low-density lipoprotein, leading to foam cell formation. There is continued leukocyte recruitment, formation of an early lipid core, and smooth muscle cell proliferation and migration. C. The advanced or mature atherosclerotic plaque consists of a necrotic lipid core with foam cells, necrotic debris, and ...

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