Bookshelf

A, Dissected left coronary artery from a 31-year-old male who died of head injuries. The artery shows no radiographic evidence of atherosclerosis. B-H are contiguous segments of the main left coronary artery, as labeled in A. B, Normal appearing intima (thin arrows) and media. C, Same coronary segment as B, but directly opposite on the other side of the lumen. The intima here is thicker (bracket), with a small focus of relative acellularity (open arrows). D, Slightly increased intimal thickening (bracket) and an increased area of acellularity (open arrows) compared to C. E, Marked increase in intimal thickness (bracket) with loss of tissue and cells (open arrows) consistent with focal degeneration. Lipid-laden SMCs (long arrows) surround this area of degeneration. F, Further increase in intimal thickness (bracket) with areas of acellularity and lipid-laden SMCs (long arrows). No areas of degeneration can be identified. G & H, Intimal thickening (bracket) is decreasing distally from F, but with more prominent and more numerous lipid-laden SMCs (long arrows). White asterisk = lumen, fat arrows = media. Hematoxylin & Eosin (H & E) stain in all photos.

A, Proximal CIRC coronary artery from a 43-year-old white male who died in the hospital of cardiogenic shock following an AMI. The asymmetric plaque is calcified and contains two necrotic foci (asterisks), and the adventitia overlying this plaque is thickened in a rather uniform manner. The adventitia is not thickened over normal, uninvolved wall. B, High-power view of rectangle B in A showing heavy Tcell infiltrates in a thickened adventitia (short fat arrows) and associated with a similar infiltrate in the intima (long arrows). The intimal fibrous tissue adjacent to inflammatory infiltrates appears to be undergoing digestion. The media appear to be intact (open arrows). A large adventitial arteriole is close by (white asterisk). MSB stain. C, High-power view of rectangle C in A. The intima (white arrow) is of normal thickness and is not involved with atherosclerosis. The media (open arrow) and the adventitia appear normal without injury, thickening, inflammation, or increased vascularity. MSB stain. D, High-power view of rectangle D in A, containing a small portion of the intima (asterisk), the internal elastic lamina (solid arrows), the media (open arrows), and the adventitia (bracket). The adventitia is composed of layers of thick collagen fibers, often wavy in appearance and oriented in a circumferential direction. Relatively few cells are present and typical intimal SMCs cannot be identified in the adventitia. H & E stain.

A, Crescent-shaped atherosclerotic plaque in the proximal LAD coronary artery of a 53-year-old white male. Red and blue injection mass has mixed in the lumen (asterisk). Note the major part of the plaque is composed of whitish material (fat arrows), and microscopic examination shows this white material to be the necrotic core. The fibrous cap is made up of what appears to be clear or transparent tissue (thin arrows) and varies in thickness from one side of the plaque to the other. The fibrous cap is quite thin at the plaque shoulder near the bottom of the photograph (open arrow). B, High-power view of the plaque shown in A. The necrotic core is identified by a black asterisk, and the arterial lumen by a white asterisk. The fibrous cap has structure similar to that shown in Figures 3A and 3B, is adjacent to the lumen. The fibrous tissue (arrows) between the lumen and the necrotic core has undergone partial degeneration and necrosis. MSB stain. C, SMC actin stain of a fibrous plaque surrounding a necrotic core (asterisk) from another patient. The tissue adjacent to the necrotic core has undergone degeneration with loss of SMCs, but the basic fibrous structure remains (Bracket 1). The next layer outward from the necrotic core (Bracket 2), shows the SMCs are still apparently viable and stain appropriately with the SMC actin stain, but many are lipid-laden (long arrows), of different size, with several small lipid lakes and with early degeneration of tissue at the right side of the photograph (open arrows). Beyond this second layer is a layer of cellular fibrous tissue (Bracket 3) composed of viable-appearing SMCs, and only occasional small lipid-laden SMCs (short arrows).

A, Typical fibrous plaque in a 65-year-old white male. Note the spindle-shaped, lipid-laden, SMCs (small arrows). These cells vary greatly in size, and some appear to be coalescing with neighboring cells (long arrows). The SMC nucleus is flattened along one side of the lacunar spaces (open arrows). There are relatively few cells present, but a large amount of fibrous tissue. H & E stain. B, High-power view of the subendothelial area in the same section as A. There are foam cells (white arrows) and other lipid- containing cells just beneath the endothelium. Two very large, lipid-filled spaces, apparently formed by the joining of adjacent, but dead, SMCs are present (black arrows). Asterisk = Lumen. H & E stain. C, A small fibrous plaque in a 50-year-old female, stained with SMC actin, showing the lipid-laden cells (arrows) within the lacunar spaces are, in fact, SMCs. Asterisk = Lumen. D, Intimal hyperplasia in a 75-year-old white female who received PTCA at this site 9 months earlier. Note the hypercellularity, the disorganization of these cells, the presence of stellate cells (arrow), and the absence of any lipid-laden SMCs. H & E stain. E, Intimal hypercellularity in a 6-month-old vein bypass graft in a 53-year-old white male. The SMCs are oriented parallel to the endothelial surface, and none appear to be lipid-laden. Note the hypercellularity near the endothelial surface (arrows). Asterisk = Lumen. H & E stain. F, Oil Red O stain of a fibrous plaque showing the fibrous tissue diffusely infiltrated with lipid droplets, giving the fibers a granular appearance. Note the scattered cholesterol crystals (arrows).