Bauters C, Hamon M, Van Belle E, Dupuis B, Lablanche J M, Bertrand M E
Service de cardiologie B, hôpital Cardiologique, Lille.
Arch Mal Coeur Vaiss. 1993 Jan;86 Spec No 1:47-56.
Restenosis is the main complication of coronary angioplasty. Many experimental models have been developed over the last few years, reflecting very active research work in this field. The value of experimental models may be discussed under two headings: improvement in our understanding of the mechanisms of restenosis and the development of preventing strategies. The smooth muscle cell is the main cause of restenosis, experimental models having demonstrated a triple response which has been observed clinically: proliferation, migration to the intima and synthesis of the extracellular matrix. The mechanisms controlling this response are not fully understood, the most likely candidates being desendethelialisation, platelets and other circulating components of the blood, vasopressive hormones especially the renin-angiotensin system, growth factors and finally the degree of direct trauma to the smooth muscle cells. Experimental models also allow evaluation of therapeutic strategies elaborated to reduce the frequency of restenosis in clinical practice: three strategies are identifiable: systemic treatment, local treatment and genetic therapy. At the present time, none of these approaches has been clearly shown to be effective clinically though some positive results have been observed in the animal.
再狭窄是冠状动脉血管成形术的主要并发症。在过去几年中已建立了许多实验模型,这反映了该领域非常活跃的研究工作。实验模型的价值可从两个方面进行讨论:增进我们对再狭窄机制的理解以及开发预防策略。平滑肌细胞是再狭窄的主要原因,实验模型已证明了临床上观察到的三重反应:增殖、向内膜迁移以及细胞外基质的合成。控制这种反应的机制尚未完全明了,最有可能的因素是内皮剥脱、血小板及血液中的其他循环成分、血管加压激素尤其是肾素-血管紧张素系统、生长因子,最后还有平滑肌细胞直接损伤的程度。实验模型还可用于评估为降低临床实践中再狭窄发生率而制定的治疗策略:可确定三种策略:全身治疗、局部治疗和基因治疗。目前,尽管在动物实验中观察到了一些阳性结果,但这些方法在临床上均未明确显示有效。