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Coagulation activation and expression of CD40 ligand on platelets upon in vitro lipopolysaccharide-challenge in patients with unstable angina

2005; Elsevier BV; Volume: 111; Issue: 2 Linguagem: Inglês

10.1016/j.ijcard.2005.08.001

1874-1754

Thorsten Kälsch, Xuan Duc Nguyen, Elif Elmas, Nadine Grebert, Tim Süselbeck, Harald Klüter, Martin Borggrefe, Carl Erik Dempfle,

Atherosclerosis and Cardiovascular Diseases

Background Elevated markers of inflammation and coagulation are found in patients with coronary heart disease. A role of inflammatory stimulation on coagulation time and expression of CD40 ligand on platelets in acute coronary syndromes has not been described yet. Methods and results Whole blood samples of 9 patients with coronary heart disease and stable angina, 10 patients with unstable angina, 7 patients with acute myocardial infarction and 7 patients without coronary heart disease were incubated with lipopolysaccharide (LPS). Coagulation time was measured in arterial and coronary blood with the ReoRox®, a viscometric whole blood coagulometer. CD40L and CD62P expression on platelets and platelet–monocyte aggregates were measured by flow cytometry. Without LPS, patients with unstable angina showed a significantly decreased coagulation time in arterial and coronary blood compared to patients without coronary heart disease. After incubation with LPS, in patients with unstable angina, a significantly decreased coagulation time in coronary blood was observed compared to patients with stable angina or patients without coronary heart disease. CD40L expression on platelets in patients with unstable angina was significantly higher in arterial and coronary blood compared to patients with stable angina. No significant differences between the patient groups were observed concerning CD62P expression on platelets, tissue factor binding on monocytes, platelet–monocyte aggregates and plasma levels of platelet factor 4. Conclusions Patients with unstable angina show an enhanced coagulation activation and an upregulation of CD40L on platelets. This may be of importance in the understanding of coronary plaque rupture and formation of coronary thrombosis.