Abstract
For many years atheroma, or atherosclerosis as it is more commonly denoted, has been regarded as a disease exclusively affecting the tunica intima. In later years this misconception has been slowly eroded, and it is now generally recognized that this disorder affects all three coats of the arterial wall. Apart from the prominent medial thinning, advanced disease typically exhibits a triad of changes in the adventitia, namely fibrosis, increased vascularity, and a prominent cellular infiltrate which is predominantly lymphocytic. The frequent granulomatous foci of advanced human plaques, together with the lymphocytic infiltration (1–3) are but two overt histologic manifestations of the inflammatory nature of human atherosclerosis. Additionally, in both human and experimental atherosclerosis, and in experimentally-induced hypercholesterolemia, an enhanced monocyte macrophage recruitment to the arterial intima has been observed (4–16).
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Schwartz, C.J., Sprague, E.A., Valente, A.J., Kelley, J.L., Edwards, E.H., Suenram, C.A. (1990). Inflammatory Components of the Human Atherosclerotic Plaque. In: Glagov, S., Newman, W.P., Schaffer, S.A. (eds) Pathobiology of the Human Atherosclerotic Plaque. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-3326-8_7
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DOI: https://doi.org/10.1007/978-1-4612-3326-8_7
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