Acute occlusion of a large coronary artery by a @entity1423 is a life-threatening event. Intravasal @entity715 generation in most cases is caused by a disturbed interaction between platelets and the vessel wall, with accompanying @entity1423 , local adhesion to the vessel wall, activation and aggregate formation after binding of soluble fibrinogen to the activated @entity1427 /IIIa-receptor. Conventional antiplatelet agents, such as @entity117 or @entity1396 / @entity1397 , inhibit uncontrolled local agonist-induced signal transduction within the platelet by interfering with the @entity2404 and @entity857 pathway, respectively. This results in an activation of the platelet @entity1427 /IIIa-receptor and, finally, in a reduced capacity of fibrinogen binding. Antiintegrins inhibit cell-cell and cell-matrix interactions. Antagonists of the platelet @entity1428 ( @entity1427 /IIIa) (eg. Abciximab, Eptifibatide, @entity6541 ) inhibit platelet adhesion and aggregation via their RGD (KGD) binding sequence, resulting in reduced fibrinogen binding. The significance of inhibition of other RGD-containing adhesion molecules ( @entity2880 Factor, @entity4732 ) with respect to the clinical efficacy of these compounds is stil under debate. @entity1427 /IIIa-antagonists are the most effective inhibitors of platelet function and in high doses, may cause complete inhibition of @entity1423 and maximum prolongation of bleeding time. The clinical efficacy of @entity1427 /IIIa-antagonists for acute percutaneous coronary interventions and in the management of the @entity1187 is established. Whether Abciximab and low-molecular weight intravenous compunds (Eptifibatide, Tirofiban, @entity50600 ) are equipotent, remains to be demonstrated by controlled comparative studies. Orally active low-molecular-weight compounds (Sibrafiban, Xemilofiban and others) are currently undergoing clinical trials. Whether these substances are superior to oral @entity117 and/or @entity1397 in long-term prevention of @entity432 remains to be determined.

[Anti-integrins--new platelet function inhibitors for therapy and prevention of XXXX ].

@entity1187 :: ('MESH:D054058', 'Disease') :: ['acute coronary syndrome'] @entity1396 :: ('MESH:D013988', 'Chemical') :: ['ticlopidine'] @entity1423 :: ('MESH:D001791', 'Disease') :: ['platelet thrombus', 'platelet aggregation', 'platelet hyperreactivity'] @entity2404 :: ('MESH:D013928', 'Chemical') :: ['thromboxane A2'] @entity1397 :: ('MESH:C055162', 'Chemical') :: ['clopidogrel'] @entity117 :: ('MESH:D001241', 'Chemical') :: ['aspirin'] @entity6541 :: ('CHEBI:9605', 'Chemical') :: ['Tirofiban'] @entity50600 :: ('MESH:C084062', 'Chemical') :: ['Lamifiban'] @entity1428 :: ('3690', 'Gene') :: ['integrin alpha IIB/beta 3'] @entity1427 :: ('3674', 'Gene') :: ['GP IIb'] @entity432 :: ('MESH:D001157', 'Disease') :: ['acute arterial vessel occlusions'] @entity715 :: ('MESH:D013927', 'Disease') :: ['thrombus'] @entity857 :: ('MESH:D000244', 'Chemical') :: ['ADP'] @entity4732 :: ('7448', 'Gene') :: ['Vitronectin'] @entity2880 :: ('MESH:D014842', 'Disease') :: ['von Willebrand']
@entity1187 :: (MESH:D054058,Disease) :: ['acute coronary syndrome']
