Inhibition of platelets and thrombin: implications for treatment of coronary artery thrombosis.
Molecular biology approaches have brought considerable progress to the development of novel plasminogen activators and antithrombin agents. While the modification of t-PA itself and the construction of chimeras between t-PA and pro-urokinase by molecular techniques have not resulted in enhanced efficacy, this can be achieved by constructing hybrids consisting of plasminogen activator domains and domains of monoclonal "targeting" antibodies. This and alternative approaches offer the promise of improved therapy in the future. Of equal importance is effective anticoagulant therapy through new antithrombin agents, platelet fibrinogen receptor inhibitors, or alternative approaches, among them gene therapy. Prevention of short-term thrombotic complications of invasive procedures such as PTCA or stent implantation may be better attained with the new antithrombins, while prevention of longer term complications (restenosis) may require inhibition of the thrombin receptor.
Runge
M S
MS
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.
Bode
C
C
D015906:Angioplasty, Balloon, Coronary; D003131:Combined Modality Therapy; D003328:Coronary Thrombosis / Q000097:blood / Q000188:drug therapy*; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects*; D010980:Platelet Membrane Glycoproteins / Q000037:antagonists & inhibitors; D011994:Recombinant Proteins / Q000627:therapeutic use; D013917:Thrombin / Q000037:antagonists & inhibitors*; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use
D010980:Platelet Membrane Glycoproteins; D011994:Recombinant Proteins; D013917:Thrombin; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator