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The Central Nervous System and Atherogenesis: Interrelationships

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Tobacco Smoking and Atherosclerosis

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 273))

Abstract

Despite almost a century of scientific study since Anitschkov and Chalatov1 observed that cholesterol feeding produced arterial lesions in rabbits, the etiology and pathogenesis of atherosclerosis (AS) remain unknown. In humans, clinical complications and sequelae occur when the lesions have evolved to produce the fibrous plaque. The main histologic features of this stage are lipid accumulation and fibroelastic and fibromuscular thickening, which initially are present in a patchy distribution but later become more diffuse as individual plaques coalesce. A fatty streak stage, characterized by lipid accumulation within intimal cells, either of monocyte/ macrophage or arterial smooth muscle cell (ASMC) origin, to give them a “foam cell” appearance in histologic sections, is considered by some to represent an intermediate step in the development of the final lesion.2

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Authors and Affiliations

  1. Department of Pathology, New York Medical College, Valhalla, N.Y., 10595, USA

    William H. Gutstein

  2. Department of Biochemistry, New York Medical College, Valhalla, N.Y., 10595, USA

    Joseph M. Wu

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  1. William H. Gutstein
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Editors and Affiliations

  1. Tobacco and Health Research Institute, University of Kentucky, Lexington, Kentucky, USA

    John N. Diana

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Gutstein, W.H., Wu, J.M. (1990). The Central Nervous System and Atherogenesis: Interrelationships. In: Diana, J.N. (eds) Tobacco Smoking and Atherosclerosis. Advances in Experimental Medicine and Biology, vol 273. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5829-9_34

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  • DOI: https://doi.org/10.1007/978-1-4684-5829-9_34

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