Tcheng J E
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.
Tex Heart Inst J. 1998;25(1):49-56.
During the past 2 decades, advances in molecular and cellular biology have greatly expanded our understanding of the critical role of platelets in the pathogenesis of acute coronary syndromes. This work has suggested that aggressive platelet inhibition might reduce cardiovascular morbidity and mortality rates beyond the reductions already achieved with aspirin and other conventional therapies. Researchers in basic science laboratories have identified a specific platelet receptor, the glycoprotein IIb/IIIa integrin, which serves as the mediator, or final common pathway, leading to platelet aggregation. This glycoprotein receptor is a logical target for the development of antagonists to inhibit thrombosis. A number of these antagonists have been tested in clinical trials involving coronary intervention, unstable angina, and acute myocardial infarction. Herein, I present some of the rationale behind the investigation of these agents, as well as some issues to be considered with regard to the future of this exciting new class of drugs.
在过去的20年里，分子和细胞生物学的进展极大地扩展了我们对血小板在急性冠脉综合征发病机制中关键作用的理解。这项工作表明，积极的血小板抑制可能会降低心血管发病率和死亡率，超出阿司匹林和其他传统疗法已经实现的降低幅度。基础科学实验室的研究人员已经确定了一种特定的血小板受体，即糖蛋白IIb/IIIa整合素，它是导致血小板聚集的介质或最终共同途径。这种糖蛋白受体是开发抑制血栓形成拮抗剂的合理靶点。其中一些拮抗剂已经在涉及冠状动脉介入治疗、不稳定型心绞痛和急性心肌梗死的临床试验中进行了测试。在此，我介绍这些药物研究背后的一些基本原理，以及关于这一令人兴奋的新型药物未来需要考虑的一些问题。
