Platelet–Monocyte Aggregates Bridging Thrombosis and Inflammation

摘要: Thrombus formation within a coronary vessel is the precipitating event in unstable syndromes. The angiographic severity of stenoses may not predict sites subsequent acute events, inasmuch as rupture atheromatous plaque with thrombosis relatively mildly stenosed vessels underlie many intact endothelium normally prevents platelet activation, but intimal injury associated endothelial denudation and exposes subendothelial collagen von Willebrand factor, which support prompt adhesion activation. Circulating platelets can adhere either directly to or indirectly, via binding glycoprotein Ib/IX complex. Local activation promotes thrombus additional recruitment by supporting cell surface thrombin releasing potent agonists, such adenosine 5′-diphosphate, serotonin, thromboxane A2. central role syndromes supported increased platelet-derived prostaglandin metabolites detected patients syndromes1 clear clinical benefit treatment aspirin for prevention events.2 See p 2166 The importance platelet-dependent has made aggregate common therapeutic target Recently, therapies have included use aspirin, thienopyridines, direct IIb/IIIa inhibitors. Although mechanism action these various agents differs, they all inhibit fibrinogen-dependent platelet–platelet associations (ie, aggregation). However, highlighted recent disappointing results trials using oral inhibitors,3 merely preventing process aggregation always translate into efficacy. Recent data suggest that only interactions between (homotypic aggregates) also leukocytes (heterotypic detectable circulating blood. These aggregates form when are …