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Low protein Z plasma levels are independently associated with acute coronary syndromes

Sandra Fedi1, Francesco Sofi, Daria Brogi

  • 1Department of Medical and Surgical Critical Care, Section of Clinical Medicine and Cardiology, University of Florence, and Thrombosis Center, Azienda Ospedaliera Careggi, Viale G. Morgagni 85, 50134 Florence, Italy. frasofi@hotmail.com

Thrombosis and Haemostasis
|December 4, 2003
PubMed

Insights

Low levels of Protein Z (PZ), a vitamin-K-dependent glycoprotein, are associated with an increased risk of acute coronary syndromes (ACS). This finding suggests PZ may play a role in arterial thrombosis development.

Area of Science:

  • Biochemistry
  • Cardiology
  • Hematology

Background:

  • Protein Z (PZ) is a vitamin-K-dependent glycoprotein synthesized in the liver.
  • PZ acts as a cofactor, inhibiting coagulation by facilitating the inactivation of factor Xa.
  • Conflicting data exists regarding plasma PZ levels in ischemic stroke patients.

Purpose of the Study:

  • To investigate the potential role of Protein Z (PZ) in the pathogenesis of acute coronary syndromes (ACS).

Main Methods:

  • Plasma PZ levels were measured in 223 ACS patients and 265 healthy controls.
  • Exclusion criteria included oral anticoagulation, antiphospholipid antibodies, liver, and kidney dysfunction.
  • Multivariate analysis was used to assess the association between PZ levels and ACS risk.

Main Results:

  • Mean PZ plasma levels were significantly lower in ACS patients (1508 ± 730 ng/mL) compared to controls (1728 ± 594 ng/mL).
  • PZ levels below the 5th percentile (565 ng/mL) were observed in 15.7% of patients versus 4.9% of controls.
  • Low PZ levels (< 565 ng/mL) were independently associated with ACS (OR=3.3), and this risk was amplified by smoking (OR=9.5).

Conclusions:

  • Reduced plasma Protein Z levels may contribute to the development of arterial thrombosis in acute coronary syndromes.
  • PZ deficiency, particularly in combination with smoking, represents a significant risk factor for ACS.
  • Further research is warranted to elucidate the precise mechanisms of PZ in thrombogenesis.

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