Mondy J S, Williams J K, Adams M R, Dean R H, Geary R L
Department of Surgery, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC, USA.
J Vasc Surg. 1997 Nov;26(5):875-83. doi: 10.1016/s0741-5214(97)70103-4.
The relationship between lumen narrowing, intimal hyperplasia, and wall remodeling after angioplasty was explored in a nonhuman primate model of atherosclerosis.
Cynomolgus monkeys (n = 37) used in long-term atherosclerosis studies underwent left iliac artery balloon injury. The uninjured right iliac artery served as a reference segment for intraanimal comparisons. One month later iliac arteries were fixed by perfusion (100 mm Hg) and removed for cross-sectional analysis to determine mean values for lumen area (LA), intimal area (IA), internal elastic lamina area (IELA), plaque burden (IA/IELA), and depth of wall injury. Values for each balloon-injured iliac artery were normalized to the contralateral uninjured iliac artery (percent of control), and linear regression analysis was performed comparing LA with IA, with IELA, and with depth of injury. Comparisons were also made between those arteries that remained dilated 1 month after balloon injury (LA > or = 140%; n = 13) and those that renarrowed (LA < or = 100%; n = 14).
For all 37 animals, LA 1 month after balloon injury correlated well with IELA (r = 0.72; p < 0.001) but not with IA (r = 0.10; p = 0.54), suggesting that changes in artery size rather than neointimal mass determined lumen caliber. When comparing arteries that remained dilated (n = 13) with those that renarrowed (n = 14), there were no differences in depth of wall injury (injury depth: 0, no injury; 1, intima; 2, IEL; 3, media; 4, EEL; 2.1 +/- 0.3 vs 1.6 +/- 0.3; p = 0.12), neointimal accumulation (IA, 507% +/- 118% vs. 421% +/- 81% of control; p = 0.55), or plaque burden (IA/IELA, 0.39 +/- 0.04 vs 0.37 +/- 0.06; p = 0.71), respectively. However, wall size defined as IELA was significantly smaller in arteries that renarrowed than in those that remained dilated (IELA, 115% +/- 14% vs 230% +/- 19% of control; p < 0.001).
Restenosis after angioplasty has been attributed to intimal hyperplasia, equating loss of lumen caliber with neointimal mass. The data presented herein suggest that lumen narrowing after arterial wall injury may have little to do with intimal mass per se, but rather that a change in wall caliber or wall narrowing is the cause of restenosis.
在动脉粥样硬化的非人灵长类动物模型中探讨血管成形术后管腔狭窄、内膜增生和血管壁重塑之间的关系。
用于长期动脉粥样硬化研究的食蟹猴（n = 37）接受左髂动脉球囊损伤。未受伤的右髂动脉作为动物体内比较的参照节段。1个月后，通过灌注（100 mmHg）固定髂动脉并取出进行横断面分析，以确定管腔面积（LA）、内膜面积（IA）、内弹力膜面积（IELA）、斑块负荷（IA/IELA）和血管壁损伤深度的平均值。将每条球囊损伤髂动脉的值相对于对侧未受伤髂动脉进行标准化（对照百分比），并进行线性回归分析，比较LA与IA、IELA以及损伤深度。还对球囊损伤后1个月仍保持扩张的动脉（LA≥140%；n = 13）和发生再狭窄的动脉（LA≤100%；n = 14）进行了比较。
对于所有37只动物，球囊损伤后1个月的LA与IELA相关性良好（r = 0.72；p < 0.001），但与IA相关性不佳（r = 0.10；p = 0.54），这表明动脉大小的变化而非新生内膜质量决定了管腔内径。比较仍保持扩张的动脉（n = 13）和发生再狭窄的动脉（n = 14）时，血管壁损伤深度（损伤深度：0，无损伤；1，内膜；2，内弹力层；3，中膜；4，外弹力层；2.1±0.3 vs 1.6±0.3；p = 0.12）、新生内膜积累（IA，为对照的507%±118% vs. 421%±81%；p = 0.55）或斑块负荷（IA/IELA，0.39±0.04 vs 0.37±0.06；p = 0.71）均无差异。然而，定义为IELA的血管壁大小在发生再狭窄的动脉中显著小于仍保持扩张的动脉（IELA，为对照的115%±14% vs 230%±19%；p < 0.001）。
血管成形术后再狭窄归因于内膜增生，将管腔内径的减小等同于新生内膜质量。本文给出的数据表明，动脉壁损伤后的管腔狭窄可能与新生内膜质量本身关系不大，而是血管壁内径的变化或血管壁狭窄是再狭窄的原因。
