title: [Therapeutic inhibition of platelets in a acute coronary syndrome and in coronary intervention: mechanisms and clinical results].
abstract: Platelets play a crucial role in the pathogenesis of atherosclerosis and especially in the final ischemic consequences such as acute coronary syndromes. Furthermore, platelets are central mediators of acute or subacute complications of coronary interventions. Therefore, therapeutic inhibition of platelet function is of major interest in cardiology. The following review describes three different therapeutic strategies for platelet inhibition and provides a representative overview on the clinical results of studies based on these strategies. First, the mechanism of acetylsalicylic acid is described and the strong meta-analytic data demonstrating a convincing positive clinical effect is discussed. Second, the mode of action of the thienopyridines is described and initial clinical results are discussed. Third, the inhibition of the platelet integrin receptor GP IIb/IIIa is described as a potent way to block the final common pathway of platelet stimulation. The structural description of GP IIb/IIIa is followed by a structural classification of the available GP IIb/IIIa inhibitors. Clinical studies, meanwhile including several thousands of patients, are discussed based on representative examples. Finally, unresolved issues regarding the various GP IIb/IIIa inhibitors, such as differences in receptor affinity and specificity, intrinsic activation and GP IIb/IIIa inhibitor induced thrombocytopenia are, discussed.
authors: Innere Medizin III Albert-Ludwigs-Universität Freiburg. peter@med1.ukl.uni-freiburg.de
authors: K
authors: K
authors: Peter
authors: T
authors: T
authors: Nordt
authors: C
authors: C
authors: Bode
mesh_terms: D000077284:Abciximab; D000208:Acute Disease; D000328:Adult; D000787:Angina Pectoris / Q000188:drug therapy; D000789:Angina, Unstable / Q000188:drug therapy; D015906:Angioplasty, Balloon, Coronary; D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D001792:Blood Platelets / Q000187:drug effects*; D000077144:Clopidogrel; D017023:Coronary Angiography; D001026:Coronary Artery Bypass; D003327:Coronary Disease / Q000188:drug therapy*; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D015201:Meta-Analysis as Topic; D051379:Mice; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D016032:Randomized Controlled Trials as Topic; D018048:Receptors, Purinergic P2 / Q000187:drug effects; D015607:Stents; D013577:Syndrome; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use
chemical_list: D000911:Antibodies, Monoclonal; D016861:Cyclooxygenase Inhibitors; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D018048:Receptors, Purinergic P2; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin; D000077284:Abciximab