O'Brien K D, Reichenbach D D, Marcovina S M, Kuusisto J, Alpers C E, Otto C M
Department of Medicine and Pathology, University of Washington, Seattle, WA 98195-6422, USA.
Arterioscler Thromb Vasc Biol. 1996 Apr;16(4):523-32. doi: 10.1161/01.atv.16.4.523.
Nonrheumatic aortic stenosis of trileaflet aortic valves has been considered to be a "degenerative" process, but the early lesion of aortic stenosis contains the chronic inflammatory cells, macrophages and T lymphocytes. Because lipoprotein deposition is prominent in atherosclerosis, another chronic inflammatory process, this study examined whether lipoproteins accumulate in aortic valve lesions. Immunohistochemical studies were performed to detect apolipoprotein (apo) B, apo(a), apoE, macrophages, and alpha-actin-expressing cells on 18 trileaflet aortic valves that ranged from normal to stenotic. All three apolipoproteins were detected in early through end-stage lesions of aortic stenosis but not in histologically normal regions. Comparison with oil red O staining suggested that most of the extracellular neutral lipid in these valves was associated with either plasma-derived or locally produced apolipoproteins. Thus, in early through end-stage aortic valve lesions, apolipoproteins accumulate and are associated with the majority of extracellular valve lipid. These results are consistent with the hypothesis that lipoprotein accumulation in the aortic valve contributes to pathogenesis of aortic stenosis.
三叶主动脉瓣的非风湿性主动脉瓣狭窄一直被认为是一个“退行性”过程，但主动脉瓣狭窄的早期病变包含慢性炎症细胞、巨噬细胞和T淋巴细胞。由于脂蛋白沉积在动脉粥样硬化（另一种慢性炎症过程）中很突出，本研究检测了脂蛋白是否在主动脉瓣病变中积聚。对18个从正常到狭窄的三叶主动脉瓣进行免疫组织化学研究，以检测载脂蛋白（apo）B、apo(a)、apoE、巨噬细胞和表达α-肌动蛋白的细胞。在主动脉瓣狭窄的早期至终末期病变中均检测到所有三种载脂蛋白，但在组织学正常区域未检测到。与油红O染色的比较表明，这些瓣膜中的大多数细胞外中性脂质与血浆来源或局部产生的载脂蛋白有关。因此，在主动脉瓣病变的早期至终末期，载脂蛋白积聚并与大多数细胞外瓣膜脂质相关。这些结果与以下假设一致，即主动脉瓣中的脂蛋白积聚促成了主动脉瓣狭窄的发病机制。
