Abstract
The aim of this study was to determine the ultrastructural characteristics of cell populations and extracellular matrix components in the wall of ruptured atherosclerotic abdominal aortic aneurysm (AAA). We analyzed 20 samples of ruptured AAA. For orientation to the light microscopy, we used routine histochemical techniques by standard procedures. For ultrastructural analysis, we applied transmission electron microscopy (TEM). Our results have shown that ruptured AAA is characterized by the remains of an advanced atherosclerotic lesion in the intima followed by a complete absence of endothelial cells, the disruption of basal membrane and disruption of internal elastic lamina. On plaque margins as well as in the inner media we observed smooth muscle cells (SMCs) that posses a euchromatic nucleus, a well-developed granulated endoplasmic reticulum around the nucleus and reduced myofilaments. The remains of the ruptured lipid core were acellular in all samples; however, on the lateral sides of ruptured plaque we observed a presence of two types of foam cells (FCs), spindle- and star-shaped. Fusiform FCs possess a well-differentiated basal lamina, caveolae and electron dense bodies, followed by a small number of lipid droplets in the cytoplasm. Star-shaped FCs contain a large number of lipid droplets and do not possess basal lamina. On the inner margins of the plaque, we observed a large number of cells undergoing apoptosis and necrosis, extracellular lipid droplets as well as a large number of lymphocytes. The media was thinned out with disorganized elastic lamellas, while the adventitia exhibited leukocyte infiltration. The presented results suggest that atherosclerotic plaque in ruptured AAA contains vascular SMC synthetic phenotype and two different types of FCs: some were derived from monocyte/macrophage lineage, while others were derived from SMCs of synthetic phenotype. The striking plaque hypocellularity was the result of apoptosis and necrosis of different cell populations.
Highlights
An aneurysm is a local dilatation of the artery that arises due to congenital or acquired damage to the wall, especially the tunica media, causing a consequent weakness of the wall
On the margins of the ruptured plaques, there was a heterogeneous cell population composed of foam cells (FCs) and smooth muscle cells (SMCs) of different shapes and characteristics, as well as cell detritus
In the ruptured intima of atherosclerotic abdominal aortic aneurysm (AAA) are the remains of complicated atherosclerotic lesions classified as type VI
Summary
An aneurysm is a local dilatation of the artery that arises due to congenital or acquired damage to the wall, especially the tunica media, causing a consequent weakness of the wall. Usually localized in the abdominal area (abdominal aortic aneurysm - AAA), mainly from the distal opening of the renal arteries. It rarely occurs in the thoracic aorta or in the upper abdominal aorta. The most common pathological processes that cause aneurysm development are hereditary metabolic disorders of connective tissue, primarily a congenital defect in the synthesis of collagen III, and dystrophic changes, atherosclerosis, inflammation and trauma (Bengtsson et al, 1996). Ulceration of the plaque conjoined with parietal thrombus formation, which is a common feature of advanced atherosclerotic lesion, could further promote the development of aneurysms (Zhao et al, 2004; Stary et al, 1995)
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