Hoffmann R, Mintz G S, Dussaillant G R, Popma J J, Pichard A D, Satler L F, Kent K M, Griffin J, Leon M B
Intravascular Ultrasound Imaging and Cardiac Catheterization Laboratories, Washington Hospital Center, Washington, DC, USA.
Circulation. 1996 Sep 15;94(6):1247-54. doi: 10.1161/01.cir.94.6.1247.
Studies have suggested that restenosis within Palmaz-Schatz stents results from neointimal hyperplasia or chronic stent recoil and occurs more frequently at the articulation.
Serial intravascular ultrasound (IVUS) was performed after intervention and at follow-up in 142 stents in 115 lesions. IVUS measurements (external elastic membrane [EEM], stent, and lumen cross-sectional areas [CSAs] and diameters) were performed, and plaque CSA (EEM lumen in reference segments and stent lumen in stented segments), late lumen loss (delta lumen), remodeling (delta EEM in reference segments and delta stent in stented segments), and tissue growth (delta plaque) were calculated. After intervention, the lumen tended to be smallest at the articulation because of tissue prolapse. At follow-up, tissue growth was uniformly distributed throughout the stent; the tendency for greater neointimal tissue accumulation at the central articulation reached statistical significance only when normalized for the smaller postintervention lumen CSA. In stented segments, late lumen area loss correlated strongly with tissue growth but only weakly with remodeling. Stents affected adjacent vessel segments; remodeling progressively increased and tissue growth progressively decreased at distances from the edge of the stent. These findings were similar in native arteries and saphenous vein grafts and in lesions treated with one or two stents. There was no difference in the postintervention or follow-up lumen (at the junction of the two stents) when overlapped were compared with nonoverlapped stents.
Late lumen loss and in-stent restenosis were the result of neointimal tissue proliferation, which tended to be uniformly distributed over the length of the stent.
研究表明，Palmaz-Schatz支架内再狭窄是由新生内膜增生或慢性支架回缩引起的，且在关节处更频繁地发生。
对115处病变中的142个支架进行干预后及随访时的系列血管内超声（IVUS）检查。进行IVUS测量（外弹力膜[EEM]、支架和管腔横截面积[CSA]及直径），并计算斑块CSA（参考节段的EEM管腔和支架节段的支架管腔）、晚期管腔丢失（Δ管腔）、重塑（参考节段的ΔEEM和支架节段的Δ支架）以及组织生长（Δ斑块）。干预后，由于组织脱垂，关节处的管腔往往最小。随访时，组织生长在整个支架中均匀分布；仅在对干预后较小的管腔CSA进行标准化时，中央关节处新生内膜组织积累更多的趋势才具有统计学意义。在支架节段，晚期管腔面积丢失与组织生长密切相关，但与重塑的相关性较弱。支架影响相邻血管节段；在距支架边缘一定距离处，重塑逐渐增加，组织生长逐渐减少。这些发现在天然动脉和隐静脉移植物以及用一个或两个支架治疗的病变中相似。重叠支架与非重叠支架相比，干预后或随访时的管腔（在两个支架的连接处）没有差异。
晚期管腔丢失和支架内再狭窄是新生内膜组织增殖的结果，新生内膜组织增殖倾向于在支架长度上均匀分布。
