Dilcher Christian E, Chan Rosanna C, Pregowski Jerzy, Kalinczuk Lukasz, Mintz Gary S, Kotani Jun-ichi, Kruk Mariusz, Shah Vivek M, Canos Daniel A, Weissman Neil J, Waksman Ron
Cardiovascular Research Institute (CRI), Washington Hospital Center, 110 Irving Street NW, Washington, DC 20010, USA.
Cardiovasc Radiat Med. 2002 Jul-Dec;3(3-4):190-2. doi: 10.1016/s1522-1865(03)00107-0.
Positive remodeling and decreased neointima proliferation are among the causes for Late Stent Malapposition (LSM). It was our interest to investigate a possible relationship between dose and incidence of LSM.
Index and follow up IVUS examinations of 238 patients (152 treated with Intravascular Brachytherapy (IVBT), 86 control) enrolled in IVBT trials were reviewed to identify patients with LSM. 7.2% of patients treated with IVBT and 2.3% of patients in the control group were found to have LSM on their 6-month follow-up IVUS. Using the index IVUS study. Dose Volume Histograms (DVH) were constructed for a segment of the adventitia comprising an arc deep to the area where LSM is present at follow up. For control, two areas: an arc deep to complete apposition (Control 1) and a segment within the stent but 5 mm apart from the LSM (Control 2). Volumes were defined by IVUS images that were 1 mm apart and the media-adventitial contour was taken to be 0.5 mm thick from the border.
DVH of 90% and 50% adventitial volume of LSM area received a significantly (p < .05) higher dose compared to both controls. Calculated are 12 LSM sites in 9 patients and 9 control sites. At all 12 sites Mean Cross Sectional Area of External Elastic Membrane (EEM CSA) was significantly larger in the LSM group at follow up compared to index (p-.001).
DVH analysis showed a positive correlation between radiation dose to the adventitia and incidence of LSM. The myofibroblasts in the adventitia are known to be the target for irradiation. Proliferation of myofibroblasts leads to neointima formation. LSM may be due to the higher dosages delivered to 50% and 90% of the adventitia volume (LSM area) which may have led to profound neointima suppression. In turn the neointima could not compensate positive remodeling reflected by an increase in EEM CSA.
正向重塑和新生内膜增殖减少是晚期支架贴壁不良(LSM)的原因之一。我们感兴趣的是研究LSM的剂量与发生率之间可能存在的关系。
回顾了参加血管内近距离放射治疗(IVBT)试验的238例患者(152例接受血管内近距离放射治疗,86例为对照组)的首次及随访血管内超声(IVUS)检查,以确定患有LSM的患者。在6个月的随访IVUS检查中,发现接受IVBT治疗的患者中有7.2%以及对照组中有2.3%的患者存在LSM。利用首次IVUS研究,为外膜的一段构建剂量体积直方图(DVH),该段外膜为随访时LSM所在区域深部的一段弧形。作为对照,选取两个区域:完全贴壁深部的一段弧形(对照1)和支架内但距LSM 5 mm的一段(对照2)。通过间隔1 mm的IVUS图像定义体积,从中膜-外膜轮廓到边界的厚度取为0.5 mm。
与两个对照组相比,LSM区域外膜体积的90%和50%的DVH接受的剂量显著更高(p < 0.05)。计算得出9例患者中有12个LSM部位和9个对照部位。在所有12个部位,随访时LSM组的外弹力膜平均横截面积(EEM CSA)与首次检查相比显著更大(p = 0.001)。
DVH分析显示外膜接受的辐射剂量与LSM的发生率之间呈正相关。已知外膜中的肌成纤维细胞是辐射的靶点。肌成纤维细胞的增殖会导致新生内膜形成。LSM可能是由于传递到外膜体积(LSM区域)的50%和90%的较高剂量,这可能导致了新生内膜的显著抑制。反过来,新生内膜无法补偿由EEM CSA增加所反映的正向重塑。