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-α (TNF-α) receptor expression, and serum thromboxane B 2 and higher circulating levels of TNF-α than 20 healthy subjects. Coincubation of platelets from HF patients with an inhibitor of TNF-α receptors significantly reduced collagen-induced platelet aggregation. In vitro study demonstrated that TNF-α amplified the platelet response to collagen; this effect was inhibited by TNF-α receptor antagonist and inhibitors of arachidonic acid metabolism. This study showed that TNF-α behaves as a trigger of platelet activation through stimulation of the arachidonic acid pathway.
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