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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.
Previous Article | Next Article 
Submitted March 28, 2005
Accepted May 20, 2005
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*
Divisione IV Clinica Medica, Policlinico Umberto I, Universita "La Sapienza" di Roma, Rome, Italy
Ospedale Sant'Andrea, Cardiologia, II Facolta di Medicina e Chirurgia, Universita "La Sapienza" di Roma, Rome, Italy
Dipartimento di Medicina Sperimentale e Patologia, Policlinico Umberto I, Universita "La Sapienza" di Roma, Rome, Italy
Dipartimento di Scienze dell'Invecchiamento, Policlinico Umberto I, Universita "La Sapienza" di Roma, Rome, Italy
* Corresponding author; email: francesco.violi{at}uniroma1.it.
Clinical history of patients with Heart Failure (HF) is complicated by arterial thromboembolism. Platelet activation was reported in this setting, but the underlying mechanism has not been clarified.
42 patients with HF scored according to NYHA classification had higher collagen-induced platelet aggregation, platelet tumor necrosis factor-alpha (TNF- ) receptor expression, serum thromboxane B2 and circulating levels of TNF- than 20 healthy subjects.
Coincubation of platelets from HF patients with an inhibitor of TNF- receptors significantly reduced collagen induced platelet aggregation. In vitro study demonstrated that TNF- amplified the platelet response to collagen; this effect was inhibited by (a) TNF- receptor antagonist and (b) inhibitors of arachidonic acid metabolism.
This study shows that TNF- behaves as a trigger of platelet activation via stimulation of the arachidonic acid pathway.

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