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
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.