Losordo D W, Rosenfield K, Pieczek A, Baker K, Harding M, Isner J M
Department of Medicine, St. Elizabeth's Hospital, Boston, MA 02135.
Circulation. 1992 Dec;86(6):1845-58. doi: 10.1161/01.cir.86.6.1845.
Previous studies regarding the mechanism by which balloon angioplasty increases luminal patency have generally used animal models or postmortem specimens from occasional fatal cases of angioplasty performed in human patients. In either case, conclusions regarding participatory mechanisms have relied exclusively on nonserial, postangioplasty histopathological examination.
In the present study, intravascular ultrasound examination was performed before and after balloon angioplasty in 40 consecutive patients with iliac artery stenoses. The areas of the arterial wall, plaque, lumen, and areas resulting from angioplasty-induced plaque fractures were measured immediately after angioplasty in vivo and compared with findings recorded immediately before angioplasty. Angioplasty increased luminal cross-sectional area (CSA) from 11.5 +/- 0.6 mm2 before angioplasty to 25.4 +/- 1.2 mm2 after angioplasty (p = 0.0001). CSA of the portion of the postangioplasty neolumen contained within angioplasty-induced plaque fractures measured 10.0 +/- 0.8 mm2; the neolumen excluding the area contributed by these plaque fractures measured 15.4 +/- 0.8 mm2. Thus, the area contained within plaque fractures accounted for 10.0 mm2 (71.9%) of the 13.9-mm2 increase in luminal CSA after angioplasty. Analysis of CSA occupied by atherosclerotic plaque disclosed that plaque CSA decreased from 33.8 +/- 1.8 mm2 before angioplasty to 22.5 +/- 1.5 mm2 after angioplasty (p = 0.0001). Plaque CSA was thus reduced ("compressed") by 11.3 +/- 1.1 mm2. Total artery CSA increased ("stretched") slightly from 45.3 +/- 2.6 mm2 before angioplasty to 47.8 +/- 2.0 mm2 after angioplasty (p = 0.0025).
In vivo analysis of iliac stenoses by intravascular ultrasound immediately before and after angioplasty demonstrates that plaque fractures and "compression" of atherosclerotic plaque are the principal factors responsible for increased luminal patency resulting from balloon angioplasty. "Stretching" of the arterial wall provides an additional, but minor, contribution.
以往关于球囊血管成形术增加管腔通畅性机制的研究,通常采用动物模型或对人类患者偶尔发生的血管成形术致死病例的尸检标本。在这两种情况下,关于参与机制的结论完全依赖于血管成形术后的非系列组织病理学检查。
在本研究中,对40例连续的髂动脉狭窄患者在球囊血管成形术前后进行了血管内超声检查。在血管成形术后立即在体内测量动脉壁、斑块、管腔以及血管成形术引起的斑块破裂区域的面积,并与血管成形术前立即记录的结果进行比较。血管成形术使管腔横截面积(CSA)从血管成形术前的11.5±0.6mm²增加到血管成形术后的25.4±1.2mm²(p = 0.0001)。血管成形术引起的斑块破裂区域内的血管成形术后新生管腔部分的CSA为10.0±0.8mm²;不包括这些斑块破裂区域的新生管腔面积为15.4±0.8mm²。因此,斑块破裂区域内的面积占血管成形术后管腔CSA增加的13.9mm²中的10.0mm²(71.9%)。对动脉粥样硬化斑块所占CSA的分析显示,斑块CSA从血管成形术前的33.8±1.8mm²减少到血管成形术后的22.5±1.5mm²(p = 0.0001)。因此,斑块CSA减少(“压缩”)了11.3±1.1mm²。动脉总CSA从血管成形术前的45.3±2.6mm²略有增加(“拉伸”)到血管成形术后的47.8±2.0mm²(p = 0.0025)。
通过血管内超声在血管成形术前后立即对髂动脉狭窄进行体内分析表明,斑块破裂和动脉粥样硬化斑块的“压缩”是球囊血管成形术导致管腔通畅性增加的主要因素。动脉壁的“拉伸”提供了额外但较小的作用。