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Blood, 15 September 2005, Vol. 106, No. 6, pp. 1992-1994.
Prepublished online as a Blood First Edition Paper on June 14, 2005; DOI 10.1182/blood-2005-03-1247.


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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Brief report

Tumor necrosis factor-{alpha} as trigger of platelet activation in patients with heart failure

Pasquale Pignatelli, Luciano De Biase, Luisa Lenti, Giuliano Tocci, Alessandra Brunelli, Roberto Cangemi, Silvia Riondino, Susanna Grego, Massimo Volpe, and Francesco Violi

From the Divisione IV Clinica Medica, Dipartimento di Medicina Sperimentale e Patologia, Policlinico Umberto I, Università "La Sapienza" di Roma; Dipartimento di Scienze dell'Invecchiamento, Policlinico Umberto I, Università "La Sapienza" di Roma; Ospedale Sant'Andrea, Cardiologia, II Facoltà di Medicina e Chirurgia, Università "La Sapienza" di Roma.

The clinical history of patients with heart failure (HF) is complicated by arterial thromboembolism. Platelet activation is reported in this population, but the underlying mechanism has not been clarified. Forty-two patients with HF scored according to New York Heart Association (NYHA) classification had higher levels of collagen-induced platelet aggregation, platelet tumor necrosis factor-{alpha} (TNF-{alpha}) receptor expression, and serum thromboxane B2 and higher circulating levels of TNF-{alpha} than 20 healthy subjects. Coincubation of platelets from HF patients with an inhibitor of TNF-{alpha} receptors significantly reduced collagen-induced platelet aggregation. In vitro study demonstrated that TNF-{alpha} amplified the platelet response to collagen; this effect was inhibited by TNF-{alpha} receptor antagonist and inhibitors of arachidonic acid metabolism. This study showed that TNF-{alpha} behaves as a trigger of platelet activation through stimulation of the arachidonic acid pathway.


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