Intimal Cell Density in Postangioplasty Versus Primary Coronary and Peripheral Lesions: A Systematic Study on Human Atherectomy Samples

Abstract

Our knowledge ofthe identity and functional significance ofthe pathogenic mechanisms responsible,f'or restenosis and arteriosclerosis in man is still limited. Among others, phenotypic conversion, migration, and proliferation qf smooth muscle cells have been suggested to lead to hypercellular neointima. In the present study, w*e examined intimul cell numbers and cell types in tissue of 23 postangioplasty lesions biop.ried by directional utherectorn~. using histohgy and transmission electron microscopv. Cornparative tissue analysis was p e t j h n e d f i r 53 primar?; lesions. Ti.ssue specimens obtained from coronaty ( n = 32) and peripheral lesions (n = 44) of 69 svrnptornatic patients were analyzed. Histological assessment of cell density showed intra-and interlesionol iwriability. A marked1.y ( P < 0.001) higher cellularity wus found in postangioplasty compared to primary lesions, irrespectiiv of coronary or peripheral origin. Cell density in renarrowed tissue following angioplasty ( 2 to 30 months) did riot significantly decrease regardless of previous balloon dilatation or atherectorry. When categorizing intimal cell density, postangioplasty lesion hypercellularity (7Sth percentile; > 514 cells/mm') was observed in 12/23 lesions (52%), but hvpocellularity (25th percentile; < 76 cells/mni') in none. In contrast. primary lesions were more inricible, with hypercellularity in 7/53 plaques (13%). and hypocetlularity in 19/53 (36%). Trunsmission electron microscopic analysis of subcellular features revealed hypocellulctr plaques to have an extensive build-up of extracellular matrix, with only sparsely embedded smooth muscle cells (SMCs). These SMCs haw a range qf' intermediate to microfilament-rich contractile phenotypes. thereby indicating only marginal metabolic cicti\,ity. I n contrust, hypercellular plaque regions contained predoniiriantly organelle-filled SMCs. irrespective qf po.c.tungiaplasty or primary origin. In conclusion, increased SMC density was observed predominantly in most renarrowed lesions encompassing classical restenoses (2 to 6 months post angioplasty) as well a.s late recurrent lesions (7 to 30 months postangioplasty). Concordundy, primary lesion hypercellularity is suggested to be related to the formation and progression of nutiw arteriosclerosis. (J Interven Cardiol 1991; 10:417-425)

Pathogen Burden, Inflammation, Proliferation and Apoptosis in Human In-Stent Restenosis

“…Another characteristic feature of human ISR was its pronounced hypercellularity (table 2) that significantly differed from primary lesion cell density, consistent with previous reports of others and our group [6, 23, 34]. Hypercellular neointima formation has been attributed to smooth muscle cell migration, proliferation and mitigated apoptosis [23, 34].…”

“…Hypercellular neointima formation has been attributed to smooth muscle cell migration, proliferation and mitigated apoptosis [23, 34]. Likewise, in the present study, ISR tissue was predominantly composed of α-SM actin-positive cells.…”

Local Delivery of Therapeutics for Percutaneous Coronary Intervention

“…Restenotic lesions differ from primary lesions in that they are much more fibrous while native atherosclerotic lesions have a higher amount of cholesterol [6]. Both primary and restenotic lesions are high in cell density with smooth muscle cells (SMCs) being in excess in restenosis [7].…”