Mechanisms of constrictive remodeling at the site of restenosis after PTCA

初步成功的经皮冠状动脉腔内成形术(PTCA)后再狭窄仍然是一个重要的临床问题。再狭窄背后的机制仍不清楚。最初的报告记录了增殖的细胞反应是主要的病理特征。最近，所谓的晚期重构被引入作为一种机制，尽管引起这种现象的过程仍然不清楚。目前的研究表明，在PTCA部位的新生内膜形成过程中，平滑肌细胞表现出表型的变化，表明平滑肌肌球蛋白重链的表达发生了变化(循环96：82-90,1997)。此外，本研究还发现，血管紧张素转换酶和内皮素转换酶在PTCA术后新生内膜形成过程中表达上调，尤其是在新生内膜形成的早期。(发行量96：3328-3337,1997；J.Hyperten，15：1295-1302；发行量96：I-348,1997)。此外，本研究还发现，在PTCA部位的新生内膜平滑肌细胞中，内皮素A型受体的表达也上调(Circularion 98：I-734,1998)。

Restenosis after an initial successful percutaneous transluminal coronary angioplasty (PTCA) remains a signifiant clinical problem. The mechanisms that underlie restenosis are still unclear. Initial reports have documented a proliferative cellular response as the main pathological feature. More recently, so-called late remodeling has been introduced as a mechanism, although the processes causing this phenonenon are unclear still.The present study demonstrates that, during neointimal formation at the site of PTCA, smooth muscle cells show phenotypic changes, indicated by altered expression of smooth muscle myosin heavy chain (Circulation 96 : 82-90, 1997). The present study, moreover, documents that up-regulation of angiotensin converting enzyme and endothelin converting enzyme occurs during neointimal formation after PTCA, especially at the early stage of neointimal formation. (Circulation 96 : 3328-3337, 1997 ; J.Hypertens, 15 : 1295-1302 ; Circulation 96 : I-348, 1997). Furthermore, The present study reveals that the expression of endothelin type A receptor is also up-regulated in neointimal smooth muscle cells at the site of PTCA (Circularion 98 : I-734, 1998)