PubMed · 9883018
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J Castillo. 1998. [Clopidogrel].. https://pubmed.ncbi.nlm.nih.gov/9883018/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Membranous nephropathy with nephrotic syndrome occurred in a patient with anterior myocardial infarction 2 months after the start of clopidogrel treatment. Sensitisation by prior treatment with ticlopidine is discussed.
An extensive body of research conducted in the past 25 years has helped foster understanding of the mechanisms and pathogenesis of the acute coronary syndromes and occlusive disease. Thus, it is well established that thrombosis is caused by vascular injury and that immediate lysis of the arterial thrombus and subsequent prevention of thrombotic reocclusion are critical to the treatment of these disorders. Remarkable progress in the understanding of the biological and molecular mechanisms involved in vascular-wall-platelet interactions, platelet-platelet interactions, and coagulation has led to the identification of multiple targets for drug discovery and the development of numerous antithrombotic drugs. The purpose of this article is to review emerging antithrombotic therapies, introduce potential future molecular targets for drug discovery efforts, and discuss novel strategies for managing patients with coronary disease.
Ticlopidine has become an established therapy in patients with stroke, and during stenting in patients with coronary artery disease. Clopidogrel, another thienopyridine, is a safe and promising alternative, that irreversibly inhibits ADP-induced platelet aggregation, and reduces formation of both arterial and venous thrombi. In a recent, large, well-controlled trial (CAPRIE), clopidogrel has been shown to be superior to aspirin in terms of prevention of ischaemic stroke, myocardial infarction and death in patients with atherosclerotic vascular disease. Clopidogrel provides a safe opportunity to enhance reperfusion when administered during stent placement, by protecting platelets from excessive activation. However, the ability of clopidogrel to be superior to ticlopidine in terms of its antiplatelet properties in the clinical setting of coronary stenting, is unknown. The effects of clopidogrel versus ticlopidine on platelet and endothelial function are yet to be determined and may strongly affect the outcome, benefits, and complications following coronary stent placement. Further clinical trials, well-designed, and carefully conducted, should elucidate possible benefits of clopidogrel during coronary interventions, especially in conjunction with new and aggressive reperfusion techniques. The benefits of clopidogrel in an expanding array of clinical conditions, including myocardial infarction, may be directly related to platelet inhibition. Moreover, marginal clinical benefits, and recently reported severe bleeding events in some patients after oral platelet glycoprotein IIb/IIIa therapy, may advance clopidogrel as a safe, and efficient alternative during coronary interventions. This review summarises the latest, and often confusing data on the effects of thienopyridines on certain haemostatic characteristics in interventional cardiology. 1999 Academic Press.