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Pathological Coronary Lesions

1. Common atherosclerotic plaques were present on the three main coronary trunks in 60% of cases, with two different pat­terns: either young plaques consisting in macrophages, foamy cells, and a small amount of extracellular lipid deposit (Fig.

1), or adult eccentric plaque with a lipid core surrounded by a fibrous wall consisting in macrophages, fibroblasts, smooth muscle cells, a few lymphocytes, elastic fibers, and collagenous fibers. Stenosis occluded 75% or more of the lumen (Figs. 2-4). In one case, the right coronary artery was completely occluded by a massive thrombosis (Fig. 5).

2. Uncommon intimal thickening which was diffuse, circular, and concentric through­out the whole length of every coronary trunk affected all patients, occluding over 40% of the vascular lumen. Collage­nous and microelastic fibers were admixed with smooth muscle cells, macrophages, rare foam cells, and fibrob­lasts, without lymphocytes (Figs. 6-9).

3. Unusual and original lesions consisting in proliferation of smooth muscle cells mixed with numerous packed elastic fibers, which formed mamillated

Fig. 1 Common atherosclerotic young plaque. Col HPS ?100

Fig. 2 Adult eccentric plaque.

Col HPS, ?25

Fig. 3 Adult eccentric plaque. Col HPS, ?25

Fig. 4 Adult eccentric plaque. Col HPS, ?25

Fig. 5 Complete occlusion by fibrous organized plaque. Col HPS, ?25

Fig.6 Intimal diffuse and circular thickness

Fig.7 Intimal diffuse and circu­lar thickness.

Col HPS, ?25

Fig. 8 Intimal diffuse and circular thickness. Col HPS, ?100

Fig. 9 Intimal diffuse and circular thickness with foamy cells. Col HPS, ?100

endoluminal protrusions resembling veg­etations, were present in 40% of cases (Figs. 10-12).

The distal coronary network of intramu­ral arterioles was also the site of a diffuse concentric intimal wall thickening occlud­ing more than 80% of the lumen in 25% of cases (Figs. 13-15). Immunohistochemical data allowed true identification of smooth muscle cells (alpha-actin and vimentin expression) as the main elements of diffuse intimal layer thickening. The expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1-alpha (IL-1α) in these cells was significantly greater than in smooth muscle cells of the underlying media. Fibro- cytes and fibroblasts were scarcely dissemi­nated on the periphery of atherosclerotic plaques, mixed with smooth muscle cells and some lymphocytes. CD68 expression identified macrophages, proving also TNF-α and IL-1 expression and Factor VIII expres­sion appeared on endothelial cells. Coro­nary lesions in AIDS patients have some of the characteristics of common atherosclero­sis such as eccentric fibro-lipidic plaques; however, they also present similarities with coronary lesions following heart transplan­tation (so-called chronic rejection) such as diffuse concentric intimal thickening occur­ring in coronary trucks and in the distal net­work [12].

Fig. 10 Mamillated endoluminal pro­trusion. Col HPS, ?25

Fig. 11 Mamillated endoluminal pro­trusion. Col HPS, ?100

Fig.12 Mamillated endoluminal pro­trusion. Col Weigert, ?25

Fig. 13 Distal coronary network. Col HPS, ?25

Fig. 14 Distal coronary network. Col HPS, ?100

Fig. 15 Distal coronary network. Col HPS, ?100

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Source: Barbaro Giuseppe, Boccara Franc (eds.). Cardiovascular Disease in AIDS. 2nd edition. — Springer,2009. — 169 p.. 2009
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