ABSTRACT
Higher prevalence rates of tobacco use, hypertension, and dyslipidemia are currently being observed in the developing world, and, concurrently, morbidity and mortality from atherosclerotic disease are also increasing.1 Previously conceived as a ‘natural’ degenerative process of aging because of its higher prevalence with advancing age, our understanding of atherosclerosis now holds it to be a pathologic malady that occurs in the context of chronic vascular injury. The body’s response to injury is inflammation, and decades of research into the pathogenesis of atherosclerosis have ultimately converged upon a unifying model of chronic inflammation that now serves as our present paradigm of understanding of this disease. Through the prism of inflammation, one may begin to understand more fundamental mechanisms that contribute to the development of atherosclerosis and the causal relationship of various traditional and emerging risk factors. A more rigorous understanding of the molecular mechanisms of vascular wall inflammation will undoubtedly yield new pharmacologic targets that might retard or halt development of the atheroma. Moreover, indices of inflammation that associate with atherosclerosis may predict future morbid or mortal events and response to therapy. This chapter will review the fundamental molecular mechanisms of inflammation as they pertain to atherosclerosis, and thoroughly explore the mounting evidence, both laboratory and clinical, that underlies this model.
