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Absence of atherosclerosis evolution in the coronary arterial segment covered by myocardial tissue in cholesterol-fed rabbits

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Abstract

The evolution of atherosclerotic lesions is suppressed in the intima of the human coronary artery, beneath myocardial bridges. To elucidate the mechanism of the protective effect, we investigated morphological changes using the rabbit coronary artery as a model. Rabbits fed a 1%-cholesterol diet were killed at intervals up to 20 weeks. Two short segments of the left coronary arteries running in the epicardial adipose tissue (EpiLAD) and subsequently running in the myocardium (MyoLAD) were compared morphologically. The intima of the EpiLAD had flat endothelial cells with a polygonal shape, and demonstrated raised atherosclerotic lesions with increase in serum cholesterol level. In contrast, the intima of the MyoLAD was free of atherosclerotic lesions throughout the study, and the endothelial cells were spindle-shaped and engorged. While ferritin particles reached only the surroundings of the internal elastic lamina in the MyoLAD, they permeated into the media of the EpiLAD. We suggest that myocardial bridges suppress coronary atherosclerosis by an alteration of endothelial permeability, which may be due to changes in haemodynamic force tending towards a higher shear stress. The data provide an insight into the relationship between haemodynamics and the development of coronary atherosclerosis.

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Authors and Affiliations

  1. Department of Pathology, Hachioji Medical Center, Tokyo Medical College, 1163 Tatemachi, 193, Hachioji City, Tokyo, Japan

    Yukio Ishikawa, Noriko Asuwa & Shigeru Masuda

  2. Department of Pathology, School of Medicine, Toho University, Tokyo, Japan

    Toshiharu Ishii

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  1. Yukio Ishikawa
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  2. Toshiharu Ishii
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  3. Noriko Asuwa
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  4. Shigeru Masuda
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Ishikawa, Y., Ishii, T., Asuwa, N. et al. Absence of atherosclerosis evolution in the coronary arterial segment covered by myocardial tissue in cholesterol-fed rabbits. Virchows Archiv 430, 163–171 (1997). https://doi.org/10.1007/BF01008038

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  • DOI: https://doi.org/10.1007/BF01008038

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