title: Platelets in atherothrombosis--diagnostic and prognostic value of platelet activation in patients with atherosclerotic diseases.
abstract: Platelets and their activation have a pivotal role in the development of atherosclerotic diseases such as acute myocardial infarction (AMI), stroke and peripheral arterial occlusion. Biomarkers of platelet activation are making inroads into clinical studies and may serve as promising agents upstream to established downstream markers of myocardial necrosis such as troponin and creatin kinase. Targeting the degree of platelet activation assessed by the key collagen receptor of platelet activation, glycoprotein VI (GPVI), may have diagnostic and prognostic value for the assessement of high-risk groups of patients with symptomatic coronary artery disease and ischemic stroke and may be worthwhile to help to facilitate clinical decision-making and to rapidly initiate adequate therapy. The concert of platelet count, platelet activation, platelet aggregation and subsequent inflammation has had a significant impact on the clinical outcome in patients with atherosclerotic diseases. For a therapeutical approach to ameliorate prognosis, the use of antiplatelet treatment in particular in AMI patients with low response to clopidogrel has partly been overcome by novel second antiplatelet drugs on top of aspirin such as prasugrel and ticagrelor. Antiplatelet therapy may be adapted according to a GPVI-based platelet activity monitoring along with aggregometry of residual platelet aggregation. Other approaches using protease-activated receptor- 1 antagonists vorapaxar or atopaxar, which inhibit the platelet thrombin receptor, soluble GPVI called Revacept©, which blocks the collagen binding sites at the vascular lesion and anopheline saliva protein derived from the malaria vector mosquito, a platelet adhesion inhibitor independent of a GPVI mechanism, still wait for their breakthrough.
authors.affiliation: Medizinische Klinik III Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Otfried-Muller-Str. 10, 72070 Tübingen, Germany. boris.bigalke@med.uni-tuebingen.de
authors.forename: Boris
authors.initials: B
authors.lastname: Bigalke
authors.forename: Andreas
authors.initials: A
authors.lastname: Schuster
authors.forename: Kateryna
authors.initials: K
authors.lastname: Sopova
authors.forename: Thomas
authors.initials: T
authors.lastname: Wurster
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Stellos
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D050197:Atherosclerosis / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D001792:Blood Platelets / Q000378:metabolism*; D004359:Drug Therapy, Combination; D006801:Humans; D009203:Myocardial Infarction / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D058729:Peripheral Arterial Disease / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D015539:Platelet Activation; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use; D011379:Prognosis; D020521:Stroke / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D013927:Thrombosis / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D010975:Platelet Aggregation Inhibitors