Califf R M, Fortin D F, Frid D J, Harlan W R, Ohman E M, Bengtson J R, Nelson C L, Tcheng J E, Mark D B, Stack R S
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.
J Am Coll Cardiol. 1991 May;17(6 Suppl B):2B-13B. doi: 10.1016/0735-1097(91)90933-z.
Despite substantial basic and clinical efforts to address the problem of restenosis after percutaneous coronary intervention, effective preventive therapies have not yet been developed. Nevertheless, the accumulated information has provided much insight into the process of restenosis in addition to allowing standards to be developed for adequate clinical trials. The pathophysiology of restenosis increasingly appears to be distinct from that of primary atherosclerosis. Restenosis involves elastic recoil, incorporation of thrombus into the lesion and fibrocellular proliferation in varying degrees in different patients. Lack of an animal model that satisfactorily mimics restenosis is a major impediment to further understanding of the process. Clinical studies are hampered by difficulties in finding a single unifying definition of restenosis and by variable methods of reporting follow-up. Reporting of clinical outcomes of all patients in angiographic substudies would allow a more satisfactory interpretation of the results of clinical trials. Current noninvasive test results are not accurate enough to substitute for angiographic and clinical outcome data in intervention trials. In the majority of observational studies, only diabetes and unstable angina have emerged as consistently associated with restenosis; whereas most of the standard risk factors for atherosclerosis have a less consistent relation. Disappointingly, the new atherectomy and laser technologies have not affected restenosis rates. The one possible exception is coronary stenting, as a result of the larger luminal diameter achieved by the placement of the stent. In conclusion, although substantial continued effort is necessary to explore the basic aspects of cellular proliferation and mechanical alteration of atherosclerotic vessels, attention to the principles of clinical trials and observation are required to detect the impact of risk factors and interventions on the multifactorial problem of restenosis. Adequate sample sizes, collection of clinical and angiographic outcomes and factorial study designs hold promise for unraveling this important limitation of percutaneous intervention.
尽管为解决经皮冠状动脉介入治疗后的再狭窄问题进行了大量基础和临床研究，但尚未开发出有效的预防疗法。然而，积累的信息除了有助于制定充分的临床试验标准外，还为再狭窄过程提供了许多见解。再狭窄的病理生理学越来越明显地不同于原发性动脉粥样硬化。再狭窄在不同患者中涉及弹性回缩、血栓融入病变以及不同程度的纤维细胞增殖。缺乏能令人满意地模拟再狭窄的动物模型是进一步了解该过程的主要障碍。临床研究因难以找到再狭窄的单一统一定义以及报告随访的方法各异而受到阻碍。在血管造影亚研究中报告所有患者的临床结局将有助于更满意地解释临床试验结果。目前的非侵入性检测结果不够准确，无法替代干预试验中的血管造影和临床结局数据。在大多数观察性研究中，只有糖尿病和不稳定型心绞痛一直被认为与再狭窄相关；而动脉粥样硬化的大多数标准危险因素的关联则不太一致。令人失望的是，新的旋切术和激光技术并未影响再狭窄率。一个可能的例外是冠状动脉支架置入术，因为置入支架可获得更大的管腔直径。总之，尽管有必要持续付出大量努力来探索动脉粥样硬化血管细胞增殖和机械改变的基本方面，但也需要关注临床试验和观察原则，以检测危险因素和干预措施对再狭窄这一多因素问题的影响。足够的样本量、临床和血管造影结局的收集以及析因研究设计有望解决经皮介入治疗的这一重要局限性。
