Luo H, Nishioka T, Eigler N L, Forrester J S, Fishbein M C, Berglund H, Siegel R J
Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, Calif. 90048, USA.
Arterioscler Thromb Vasc Biol. 1996 Nov;16(11):1393-8. doi: 10.1161/01.atv.16.11.1393.
Therapies that inhibit intimal hyperplasia do not prevent restenosis after coronary artery balloon angioplasty, suggesting that additional mechanisms may be responsible for restenosis in humans. Using an intravascular ultrasound (Hewlett-Packard Sonos Intravascular Imaging System). 3.5F, 30-MHz (Boston Scientific) monorail imaging catheter, we studied 17 patients with clinical and angiographic restenosis at an average (mean +/- SD) of 7 +/- 6 months after balloon angioplasty (13 men age, 71 +/- 10 years; 12 left anterior descending coronary arteries, 4 right coronary arteries, and 1 left circumflex coronary artery) The lumen area (L.A), vessel wall area (VWA), and total cross-sectional area (CSA) within the external elastic lamina were measured at the restenosis site and at proximal and distal reference sites, which were defined as adjacent segments with the least amount of plaque. Consistent with coronary angiography findings, decreased LA at the restenotic site was detected in all 17 patients. The unique finding was that total CSA at the restenotic site was significantly decreased compared with both proximal and distal reference sites (10.1 +/- 2.4 versus 14.8 +/- 3.2 mm2 and 10.1 +/- 2.4 versus 13.8 +/- 3.1 mm2, respectively, P < .001), whereas VWA (intima plus media) was slightly increased at the angioplasty site compared with both proximal and distal reference sites (8.0 +/- 2.3 versus 7.6 +/- 2.3 mm2 and 8.0 +/- 2.3 versus 6.7 +/- 2.3 mm2, respectively, P = NS). Eighty-three percent of the loss in LA at the restenotic site was due to constriction of the total CSA, while the increase in VWA at the restenotic site accounted for only a 17% loss in LA. We then compared these results with the morphology of coronary artery segments in 14 patients without restenosis. These coronary artery segments had been previously treated with balloon angioplasty (7 +/- 5 months). Unlike that in restenotic lesions, the total CSA within the external elastic lamina at the sites of previous angioplasty was similar to that in distal and proximal reference sites (P = NS). Significant and consistent reduction in arterial CSA, with a minor increase in VWA, characterizes human coronary lesions that cause angiographic restenosis. These data suggest that in humans, "recoil" and/or vascular contraction with healing in response to balloon injury is a major contributor to restenosis after balloon angioplasty.
抑制内膜增生的疗法并不能预防冠状动脉球囊血管成形术后的再狭窄，这表明可能存在其他机制导致人类再狭窄。我们使用血管内超声（惠普Sonos血管内成像系统，3.5F，30兆赫（波士顿科学公司）单轨成像导管），研究了17例临床和血管造影显示再狭窄的患者，这些患者在球囊血管成形术后平均（均值±标准差）7±6个月（13名男性，年龄71±10岁；12支左前降支冠状动脉，4支右冠状动脉，1支左旋支冠状动脉）。在再狭窄部位以及近端和远端参考部位（定义为斑块最少的相邻节段）测量了外弹力膜内的管腔面积（L.A）、血管壁面积（VWA）和总横截面积（CSA）。与冠状动脉造影结果一致，所有17例患者在再狭窄部位均检测到管腔面积减小。独特的发现是，与近端和远端参考部位相比，再狭窄部位的总CSA显著减小（分别为10.1±2.4对14.8±3.2平方毫米和10.1±2.4对13.8±3.1平方毫米，P<0.001），而血管成形术部位的VWA（内膜加中膜）与近端和远端参考部位相比略有增加（分别为8.0±2.3对7.6±2.3平方毫米和8.0±2.3对6.7±2.3平方毫米，P=无显著性差异）。再狭窄部位管腔面积损失的83%是由于总CSA的收缩，而再狭窄部位VWA的增加仅占管腔面积损失的17%。然后我们将这些结果与14例无再狭窄患者的冠状动脉节段形态进行了比较。这些冠状动脉节段此前已接受球囊血管成形术治疗（7±5个月）。与再狭窄病变不同，先前血管成形术部位外弹力膜内的总CSA与远端和近端参考部位相似（P=无显著性差异）。动脉CSA显著且持续减小，同时VWA略有增加，这是导致血管造影再狭窄的人类冠状动脉病变的特征。这些数据表明，在人类中，“回缩”和/或球囊损伤后愈合过程中的血管收缩是球囊血管成形术后再狭窄的主要原因。
