The Heat Is on

Abstract

It is common knowledge that atherosclerosis is a multifactorial disease, and the disease-promoting role of classic risk factors for atherosclerosis, such as high serum cholesterol levels, diabetes, hypertension, smoking, and various types of infections, has been proven in innumerable clinical studies. Despite the fact that we are dealing with a chronic disease, however, there is a surprising scarcity of reports dealing with the very first stages of atherogenesis, ie, those that are not yet leading to clinical symptoms. It is now evident that inflammatory/immunologic processes play a major role in the development of atherosclerosis. The correlation between the presence and amount of inflammatory surrogate markers and the occurrence of sonographically demonstrable early arterial changes becomes more significant the earlier in the course of the disease that these analyses are performed. Although complicated atherosclerotic lesions, as the name implies, are composed of many different cellular and extracellular constituents, the earliest lesions are characterized by intimal infiltration by mononuclear cells often still without the presence of foam cells, especially in those instances in which risk factors other than high serum cholesterol levels are operative. In this context, it is important to remember that the first intima-infiltrating cells in early, clinically nonapparent lesions are lymphoid cells, followed by blood-borne monocytes, and finally smooth muscle cells immigrating from the media.1 Later, both the scavenger receptor–expressing macrophages and smooth muscle cells may transform into foam cells accompanied by fibroblast and myofibroblast proliferation with collagenous and noncollagenous extracellular matrix protein deposition leading to the paradigmatic hardening of the arterial wall. The antigenic specificity of early intima-infiltrating lymphoid cells is still to be determined. Article p 886 In this issue of Circulation , Park et al2 address the possible role of heat shock protein (HSP) 27 in atherogenesis. HSPs have risen to prominence in atherosclerosis …