Protein Z is a vitamin K-dependent plasma protein that acts as a cofactor for the inactivation of activated factor X by forming a complex with a specific plasma protein Zdependent protease inhibitor [1]. Over the past years, protein Z has been investigated in different prothrombotic conditions, ranging from ischaemic cerebrovascular disease through pregnancy complications to coronary artery disease, and a role for altered levels of this protein has been reported [2][3][4]. However, some uncertainties regarding the real role of this protein on the occurrence of such diseases still remain. In particular, the relationship between this protein and the inflammatory pathway has been scarcely investigated. Only two previous studies have analysed the interaction between protein Z and proinflammatory cytokines: in 1999 Undar et al. showed an inverse correlation between protein Z and interleukin-6 in patients with haematological malignancies [5], while in 2002 Vasse et al., in an 'in-vitro' study, demonstrated that protein Z biosynthesis by hepatic cells was only weakly affected by some inflammatory cytokines [6]. Actually, the very broad range of protein Z levels shown within the normal population suggests that protein Z may act as an acute phase protein, possibly being regulated by inflammatory cytokines. However, no clear data regarding the interplay between inflammatory reactants and protein Z in patients with atherosclerotic diseases are present.The aim of this study was to evaluate the time-course of protein Z and interleukin-6 during and after an acute coronary event, in order to give an insight into the relationship between protein Z and the acute-phase state. We therefore enrolled and prospectively followed 10 patients (eight men, two women; median age, 64 years) with acute coronary syndrome who underwent primary percutaneous coronary intervention (PCI) at the Catheterization Laboratory of the Department of Heart and Vessels of the University of Florence. All the patients were followed up over several time-points [baseline (i.e. before PCI), 36 h, 72 h, 1 month and 3 months after PCI], remaining free from any adverse events throughout the follow-up period, and receiving standard therapy that included aspirin, clopidogrel, low-molecular-weight heparin, intravenous nitrates, statins, b-blockers and angiotensin-converting enzyme inhibitors where appropriate. Study approval was granted by the institutional ethics committee and all patients gave written informed consent. None of the patients were under anticoagulant treatment or reported a positivity to factor V Leiden mutation or antiphospholipid antibodies.Fasting blood samples were withdrawn at each visit. Protein Z plasma levels were measured as previously described [4]. The intra-assay coefficient of variation was 4.9% and the interassay coefficient of variation was 8.4%. Interleukin-6 plasma levels were measured using a commercial enzyme-linked immunosorbent assay (highsensitivity interleukin-6 human, Biotrak ELISA system; Amersham Biosciences, Little Chalfont, ...