title: Absence of atherosclerosis evolution in the coronary arterial segment covered by myocardial tissue in cholesterol-fed rabbits.
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. Rabbit 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.
authors.affiliation: Department of Pathology, Hachioji Medical Center, Tokyo Medical College, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ishikawa
authors.forename: T
authors.initials: T
authors.lastname: Ishii
authors.forename: N
authors.initials: N
authors.lastname: Asuwa
authors.forename: S
authors.initials: S
authors.lastname: Masuda
mesh_terms: D000818:Animals; D001055:Apolipoproteins B / Q000032:analysis; D002467:Cell Nucleus / Q000648:ultrastructure; D002791:Cholesterol, Dietary / Q000493:pharmacokinetics*; D003324:Coronary Artery Disease / Q000139:chemically induced / Q000209:etiology / Q000473:pathology*; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology*; D003593:Cytoplasm / Q000737:chemistry / Q000648:ultrastructure; D004727:Endothelium / Q000378:metabolism / Q000648:ultrastructure; D005487:Foam Cells / Q000737:chemistry / Q000648:ultrastructure; D007150:Immunohistochemistry; D008297:Male; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D009000:Monocytes / Q000648:ultrastructure; D009206:Myocardium / Q000473:pathology*; D010496:Pericardium / Q000473:pathology; D011817:Rabbits; D017539:Tunica Intima / Q000648:ultrastructure
chemical_list: D001055:Apolipoproteins B; D002791:Cholesterol, Dietary