Hirshfeld J W, Schwartz J S, Jugo R, MacDonald R G, Goldberg S, Savage M P, Bass T A, Vetrovec G, Cowley M, Taussig A S
University of Pennsylvania, Cardiac Catheterization Laboratory, Philadelphia 19104.
J Am Coll Cardiol. 1991 Sep;18(3):647-56. doi: 10.1016/0735-1097(91)90783-6.
The Multi-Hospital Eastern Atlantic Restenosis Trial group obtained follow-up angiography in 510 patients with 598 successfully dilated coronary lesions who were enrolled in a controlled trial of the effects of a single dose of 1 g of methylprednisolone on restenosis after coronary angioplasty. The overall restenosis rate was 39.6%. The strongest univariate relations to the restenosis rate were found for lesion location (saphenous vein graft, 68%; left anterior descending artery, 45%; left circumflex artery and right coronary artery, 32%; p = 0.002); lesion length (less than or equal to 4.6 mm, 33%; greater than 4.6 mm, 45%; p = 0.001); percent stenosis before angioplasty (less than or equal to 73%, 25%; greater than 73%, 43%; p = 0.005), percent stenosis after angioplasty (less than or equal to 21%, 33%; greater than 21%, 46%; p = 0.017) and arterial diameter (less than 2.9 mm, 44%; greater than or equal to 2.9 mm, 34%; p = 0.036). Two multivariate models to predict restenosis probability were developed with use of stepwise logistic regression. The preprocedural model, which included only variables whose values were known before angioplasty, entered lesion length, vein graft location, left anterior descending artery location, percent stenosis before angioplasty, eccentric lesion and arterial diameter. The postprocedural model, which also included variables whose values were known after angioplasty was performed, was similar to the preangioplasty model except that it also entered postangioplasty percent stenosis and "optimal" balloon sizing but did not enter eccentric lesion. These data indicate that the probability of restenosis after angioplasty is determined predominantly by the characteristics of the lesion being dilated. They are consistent with the known intimal proliferative mechanism of restenosis, offer a means of identifying lesions at unusually high or low risk of restenosis, and of predicting the likelihood that a particular lesion will restenose after angioplasty and provide a rationale for stratification by restenosis probability in the design of future studies of restenosis.
东大西洋多医院再狭窄试验组对510例患者的598处成功扩张的冠状动脉病变进行了随访血管造影，这些患者参加了一项关于单剂量1克甲泼尼龙对冠状动脉成形术后再狭窄影响的对照试验。总体再狭窄率为39.6%。发现与再狭窄率最密切的单变量关系为病变部位（大隐静脉移植血管，68%；左前降支动脉，45%；左旋支动脉和右冠状动脉，32%；p = 0.002）；病变长度（小于或等于4.6毫米，33%；大于4.6毫米，45%；p = 0.001）；血管成形术前狭窄百分比（小于或等于73%，25%；大于73%，43%；p = 0.005），血管成形术后狭窄百分比（小于或等于21%，33%；大于21%，46%；p = 0.017）和动脉直径（小于2.9毫米，44%；大于或等于2.9毫米，34%；p = 0.036）。使用逐步逻辑回归建立了两个预测再狭窄概率的多变量模型。术前模型仅包括血管成形术前已知值的变量，纳入了病变长度、静脉移植血管部位、左前降支动脉部位、血管成形术前狭窄百分比、偏心病变和动脉直径。术后模型也包括血管成形术后已知值的变量，与术前模型相似，不同之处在于它还纳入了血管成形术后狭窄百分比和“最佳”球囊尺寸，但未纳入偏心病变。这些数据表明，血管成形术后再狭窄的概率主要由被扩张病变的特征决定。它们与已知的再狭窄内膜增生机制一致，提供了一种识别再狭窄风险异常高或低的病变的方法，预测特定病变在血管成形术后再狭窄的可能性，并为在未来再狭窄研究设计中按再狭窄概率进行分层提供了理论依据。
