APOLIPOPROTEIN-B, APOLIPOPROTEI(A), AND APOLIPOPROTEIN-E ACCUMULATE IN THE MORPHOLOGICALLY EARLY LESION OF DEGENERATIVE VALVULAR AORTIC-STENOSIS

Citation
Kd. Obrien et al., APOLIPOPROTEIN-B, APOLIPOPROTEI(A), AND APOLIPOPROTEIN-E ACCUMULATE IN THE MORPHOLOGICALLY EARLY LESION OF DEGENERATIVE VALVULAR AORTIC-STENOSIS, Arteriosclerosis, thrombosis, and vascular biology, 16(4), 1996, pp. 523-532
Citations number
64
Categorie Soggetti
Cardiac & Cardiovascular System","Peripheal Vascular Diseas
ISSN journal
10795642
Volume
16
Issue
4
Year of publication
1996
Pages
523 - 532
Database
ISI
SICI code
1079-5642(1996)16:4<523:AAAAAI>2.0.ZU;2-S
Abstract
Nonrheumatic aortic stenosis of trileaflet aortic valves has been cons idered to be a ''degenerative'' process, but the early lesion of aorti c stenosis contains the chronic inflammatory cells, macrophages and T lymphocytes. Because lipoprotein deposition is prominent in atheroscle rosis, another chronic inflammatory process, this study examined wheth er lipoproteins accumulate in aortic valve lesions. Immunohistochemica l studies were performed to detect apolipoprotein (ape) B, apo(a), apo E, macrophages, and a-actin-expressing cells on 18 trileaflet aortic v alves that ranged from normal to stenotic. All three apolipoproteins w ere detected in early through end-stage lesions of aortic stenosis bur not in histologically normal regions. Comparison with oil red O stain ing suggested that most of the extracellular neutral lipid in these va lves was associated with either plasma-derived or locally produced apo lipoproteins. Thus, in early through end-stage aortic valve lesions, a polipoproteins accumulate and are associated with the majority of extr acellular valve lipid. These results are consistent with the hypothesi s that lipoprotein accumulation in the aortic valve contributes to pat hogenesis of aortic stenosis.