Kinney T B, Chin A K, Rurik G W, Finn J C, Shoor P M, Hayden W G, Fogarty T J
Radiology. 1984 Oct;153(1):85-9. doi: 10.1148/radiology.153.1.6236478.
We quantitatively determined the relative contribution of various factors leading to arterial lumen enlargement during transluminal angioplasty. Mechanical tests were conducted on both normal and atherosclerotic artery necropsy specimens. In our range of dilating pressures (0-3.4 atm or 0-50 lb/in2), content extrusion of fluid from the plaque accounted for 6-12% of the overall lumen area increase, while compaction of the plaque accounted for only 1-1.5%. The majority of the increase, 86.8-93%, was due to plaque and arterial wall disruption. The mechanism of disruption began with shearing of the plaque from the underlying artery at relatively low dilating pressures and continued with longitudinal tearing and stretching of the arterial wall at higher pressures. Diseased arteries dilated significantly more than nondiseased arteries at dilating pressures greater than or equal to 1.36 atm or 20 lb/in2 (P less than .05). In the range of stenoses that were tested (10-50%), the mean dilating pressure required to increase the lumen cross-sectional area by 50% was approximately 1.5 atm or 22 lb/in2.
我们定量测定了经腔血管成形术期间导致动脉管腔扩大的各种因素的相对贡献。对正常和动脉粥样硬化动脉尸检标本进行了力学测试。在我们的扩张压力范围（0 - 3.4个大气压或0 - 50磅/平方英寸）内，斑块中液体的内容物挤出占管腔总面积增加的6 - 12%，而斑块的压实仅占1 - 1.5%。增加的大部分，即86.8 - 93%，是由于斑块和动脉壁破裂。破裂机制始于在相对较低的扩张压力下斑块与下层动脉的剪切，并在较高压力下继续伴随着动脉壁的纵向撕裂和拉伸。在大于或等于1.36个大气压或20磅/平方英寸的扩张压力下，患病动脉的扩张明显大于未患病动脉（P小于0.05）。在测试的狭窄范围内（10 - 50%），将管腔横截面积增加50%所需的平均扩张压力约为1.5个大气压或22磅/平方英寸。
