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Protein Z Decreases During Follow-up of Patients with Acute Coronary Syndromes

Abstract number: P0658

Sofi F, Cesari F, Fedi S, Fatini C, Tellini I, Valente S, Vigiani S, Beconcini S, Abbate R, Gensini GF

Protein Z (PZ) is a vitamin K-dependent glycoprotein that serves as a cofactor for the control of the coagulation factor Xa by the protein Z-dependent protease inhibitor. Over the last years, some reports have been published regarding the role of PZ in vascular disorders such as ischemic stroke, and acute coronary syndromes. However, only one paper that evaluated PZ levels during and after the acute phase of the ischemic event is available in the literature. Aim of the present study was to compare PZ plasma levels at the time of an acute coronary event (T0) and after a follow-up time (median time: 12; range: 6–16 months) (T1). PZ plasma levels were determined in 144 patients (102M; 42F) who underwent a percutaneous coronary intervention at the Coronary Unit of the University of Florence. Exclusion criteria were liver or renal dysfunction and warfarin therapy. None showed a positivity for antiphospholipid antibodies or for factor V Leiden mutation. PZ plasma levels at T1 were significantly (P < 0.0001) lower (1204.2 ± 655.1 ng/mL) than those reported at T0 (1815.1 ± 848.2 ng/mL). Mean decrease percentage of PZ plasma levels during the follow-up was 37.0 ± 17.9%. A major adverse cardiac event (MACE) defined as restenosis, new myocardial infarction or need for target vessel revascularization occurred in 34/144 (23.6%) patients during the follow-up. Interestingly, PZ levels measured during follow-up were found to be lower (1012.2 ± 582.9 ng/mL) in patients with MACE respect to those without (1246.1 ± 667.3 ng/mL). Similarly, patients who occurred MACE had a higher decrease of PZ during the follow-up (-36.9% vs -34.1%) respect to those who remained free of events. In conclusion, these results support the hypothesis of the role of PZ in atherosclerosis and indicate a possible relationship between decrease of PZ levels and a subsequent coronary event.

To cite this abstract use the following format:

Journal of Thrombosis and Haemostasis 2005; Volume 3, Supplement 1: abstract number

Session Details

Date: 01/08/2007
Time: 00:00-00:00
Session name: XXIst ISTH Congress
Subject: Posters Session – Tuesday
Location: Oxford, UK
Presentation type:
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