作者: Matthew D. Linden , Huyen A. Tran
DOI: 10.3109/10408363.2012.731377
关键词:
摘要: People with diabetes have an increased risk of life-threatening cardiovascular disease compared to the general population. Furthermore, people are at greatly not responding standard anti-platelet therapy, such as aspirin, for prevention atherothrombotic events. This phenomenon is often referred treatment failure. Those who events despite aspirin therapy can be prospectively identified by a variety laboratory measures residual on-treatment platelet function, known resistance. However, there little agreement among laboratories on approaches these measurements, and insufficient data guide clinical management diabetes-associated resistance if it identified. review provides critical appraisal different detection evidence mechanisms which contribute this phenomenon, well potential effectiveness overcoming failure in diabetes. Potential include elevated turnover that results immature fraction able synthesise uninhibited therapeutic target cyclooxygenase-1 (COX-1); thromboxane production both COX-1-dependent COX-1-independent pathways; up-regulation aspirin-insensitive pathways adenosine diphosphate signalling; underlying atherosclerotic burden hyper-reactivity. High on-aspirin reactivity may related glycemic control. controlling modifiable factors achieve effective control, guided increases dose or frequency administration, use additional antiplatelet therapies. While suggests altering particularly increasing overcome incomplete inhibition synthesis, no studies date assessed preventing breakthrough atherothrombosis. some clinicians currently alter basis theoretical benefit strategies following identification laboratory, yet supported benefit, clear guidelines lacking.