Feldman L J, Riessen R, Steg P G
Unité Physiopathologie du Coeur et des Artères, Faculté Bichat, Paris, France.
Fundam Clin Pharmacol. 1995;9(1):8-16. doi: 10.1111/j.1472-8206.1995.tb00259.x.
Restenosis after coronary angioplasty, the main limitation of interventional cardiology, remains an unsolved issue. The failure to-date of all pharmacological attempts at prevention has prompted the development of alternative strategies. A mechanistic approach to the problem of restenosis is based on the assumption that creating a more satisfactory acute angioplasty result would reduce the development of restenosis. With the exception of coronary stenting, however, none of the new angioplasty devices have convincingly reached this goal. Furthermore, recent advances in the field of vascular biology have opened new avenues for a molecular approach of restenosis. Better understanding of the pathophysiology of restenosis, in conjunction with high-pace development of catheter, polymer, and virus technologies, provide opportunities to deliver agents--drugs, genes, or antisense oligonucleotides--locally, at the site of angioplasty to interfere specifically with the restenosis process. Some of these molecular strategies are currently being investigated in animal models. Clinical application of a molecular approach to prevent restenosis, however, will require close collaboration between physicians, molecular biologists, and bio-engineers.
冠状动脉血管成形术后再狭窄是介入心脏病学的主要局限，至今仍是一个未解决的问题。迄今为止，所有预防再狭窄的药物尝试均告失败，这促使人们开发替代策略。对再狭窄问题的一种机制性方法基于这样的假设，即创造更令人满意的急性血管成形术结果将减少再狭窄的发生。然而，除冠状动脉支架置入术外，没有一种新的血管成形术器械令人信服地实现了这一目标。此外，血管生物学领域的最新进展为再狭窄的分子治疗方法开辟了新途径。对再狭窄病理生理学的更好理解，以及导管、聚合物和病毒技术的快速发展，为在血管成形术部位局部递送药物、基因或反义寡核苷酸等药剂提供了机会，以特异性干扰再狭窄过程。目前正在动物模型中研究其中一些分子策略。然而，预防再狭窄的分子方法的临床应用需要医生、分子生物学家和生物工程师之间密切合作。
