By A. Michael Lincoff
This considerably revised moment variation includes new chapters at the position of GPIIb/IIIa blockade in the course of acute coronary syndromes or with fibrinolytic remedy in the course of acute myocardial infarctions, and up-to-date and increased details at the newest trials of GP IIb/IIIa inhibition in the course of percutaneous coronary intervention. extra advancements contain a brand new bankruptcy on results with persistent oral GP IIb/IIIa blockade following acute coronary syndromes, dialogue of GPIIb/IIIa blockade with different platelet and thrombin inhibitors, and a overview of the aptitude results past inhibition of platelet aggregation. Platelet Glycoprotein IIb/IIIa inhibitors in heart problems, moment version bargains trendy physicians, cardiologists, emergency room medical professionals, and uncomplicated scientists the main whole and authoritative evaluation of the cutting-edge in glycoprotein Iib/IIIa receptor inhibitor use.
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Additional info for Platelet Glycoprotein IIb IIIa Inhibitors in Cardiovascular Disease (Contemporary Cardiology) 2nd Edition
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Blood 1990;76:345–353. 136. Agbanyo FR, Sixma JJ, de Groot PG, Languino LR, Plow EF. Thrombospondin-platelet interactions. Role of divalent cations, wall shear rate, and platelet membrane glycoproteins. J Clin Invest 1993;92: 288–296. 38 Part I / Basic Principles Chapter 3 / GPIIb/IIIa in Platelet Aggregation 3 39 Glycoprotein IIb/IIIa in Platelet Aggregation and Acute Arterial Thrombosis Patrick Andre, PhD and David R. Phillips, PhD CONTENTS INTRODUCTION GPIIb/IIIa IN THROMBOGENESIS GPIIb/IIIa STRUCTURE LIGAND BINDING PROPERTIES OF GPIIb/IIIa STIMULUS-INDUCED GPIIb/IIIa ACTIVATION OUTSIDE-IN GPIIb/IIIa SIGNAL TRANSDUCTION GPIIb/IIIa POLYMORPHISMS AS A CARDIOVASCULAR RISK FACTOR GPIIb/IIIa IN INFLAMMATION ADDITIONAL FUNCTIONS FOR GPIIb/IIIa NEW PERSPECTIVES FOR GPIIb/IIIa IN ANTITHROMBOTIC THERAPIES GLOSSARY REFERENCES INTRODUCTION Glycoprotein (GP) IIb/IIIa antagonists have been shown to therapeutically regulate platelet function to prevent, for example, the thrombotic complications associated with coronary artery disease (1).
Shah PK. New insights into the pathogenesis and prevention of acute coronary syndromes. Am J Cardiol 1997;79:17–23. 36. Lundberg B. Chemical composition and physical state of lipid deposits in atherosclerosis. Atherosclerosis 1985;56:93–110. 37. Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation 1996;92:657–671. 38. Davies MJ, Richardson PD, Woolf N, Katz DR, Mann J. Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content.
Kirchhofer D, Riederer MA, Baumgartner HR. Specific accumulation of circulating monocytes and polymorphonuclear leukocytes on platelet thrombi in a vascular injury model. Blood 1997;89: 1270–1278. 19. Ott J, Neumann FJ, Gawaz M, Schmitt M, Schomig A. Increased neutrophil-platelet adhesion in patients with unstable angina. Circulation 1996;94:1239–1246. 20. Sixma JJ, de Groot PG. Platelet adhesion. Br J Haematol 1990;75:308–312. 21. Lopez-Fernandez M, Ginsberg MH, Ruggeri ZM, Batlle FJ, Zimmerman TS.
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