Morimoto S, Mizuno Y, Hiramitsu S, Yamada K, Kubo N, Nomura M, Yamaguchi T, Kitazume H, Kodama K, Kurogane H
Department of Internal Medicine, Fujita Health University School of Medicine, Japan.
Jpn Circ J. 1990 Jan;54(1):43-56. doi: 10.1253/jcj.54.43.
Restenosis was studied histopathologically by serial step sectioning of 22 coronary arteries from 21 patients in whom percutaneous transluminal coronary angioplasty (PTCA) had been performed (9 arteries from patients who had died shortly after PTCA and 13 from those who had died considerably later). Nine of the 13 arteries from the patients who had died long after PTCA were immunohistochemically stained using anti-actin antibody for examination of spindle-shaped cells proliferating in the intima. In the patients who had died shortly after PTCA, all 9 arteries showed fresh thrombus formation. In the patients who had died considerably later after PTCA, however, there was fragmentation of the internal elastic lamina (IEL) in 9 arteries. In each of these 9 arteries, a remarkable proliferation of intimal cells was observed on the intimal side, mainly at the site of the IEL fragmentation. These spindle-shaped cells were identified as smooth muscle cells (SMC) because they stained reddish-brown with Masson's trichrome, and because immunohistochemical staining with anti-actin antibody was also positive. In 2 arteries, proliferation of SMC and elastic fibers was observed on the luminal side of the intima, despite absence of fragmentation in the IEL. Proliferation of SMC in false lumens was identified in 2 patients with medial dissection. From the above findings, the following 4 forms of restenosis after PTCA have been identified: 1. thrombus formation; 2. proliferation of SMC on the intimal side, mainly around fragmentation in the IEL; 3. proliferation of SMC on the luminal side of the intima where there was no fragmentation of the IEL; and 4. proliferation of SMC in dissected false lumen. The proliferation of SMC on the intimal side of the disrupted IEL was thought to have been a result of migration of SMC from the media to the intima, because SMC proliferation was seen around the disrupted region.
对21例行经皮腔内冠状动脉成形术（PTCA）患者的22条冠状动脉进行连续阶梯切片，通过组织病理学研究再狭窄情况（其中9条动脉来自PTCA术后不久死亡的患者，13条来自术后很久才死亡的患者）。对PTCA术后很久才死亡患者的13条动脉中的9条，使用抗肌动蛋白抗体进行免疫组织化学染色，以检查内膜中增殖的梭形细胞。在PTCA术后不久死亡的患者中，所有9条动脉均显示有新鲜血栓形成。然而，在PTCA术后很久才死亡的患者中，9条动脉出现内弹性膜（IEL）断裂。在这9条动脉的每一条中，在内膜侧均观察到内膜细胞显著增殖，主要位于IEL断裂部位。这些梭形细胞被鉴定为平滑肌细胞（SMC），因为它们用Masson三色染色呈红棕色，并且用抗肌动蛋白抗体进行免疫组织化学染色也呈阳性。在2条动脉中，尽管IEL没有断裂，但在内膜腔侧观察到SMC和弹性纤维增殖。在2例中膜夹层患者的假腔中发现了SMC增殖。根据上述发现，已确定PTCA术后再狭窄有以下4种形式：1. 血栓形成；2. 内膜侧SMC增殖，主要围绕IEL断裂处；3. IEL未断裂的内膜腔侧SMC增殖；4. 夹层假腔内SMC增殖。IEL破裂的内膜侧SMC增殖被认为是SMC从外膜迁移到内膜的结果，因为在破裂区域周围可见SMC增殖。
