AI Article Synopsis

  • The study investigates plasma protein Z (PZ) levels in patients with acute myocardial infarction (AMI) and chronic coronary atherosclerosis disease (CCAD) to assess its clinical relevance.
  • Plasma PZ concentrations were significantly lower in AMI patients compared to those with CCAD and healthy controls, suggesting that lower PZ levels may correlate with heart injury and inflammation.
  • Increased risk for AMI and CCAD is associated with PZ levels below a certain threshold, indicating that monitoring PZ could be a useful predictor for these conditions.

Article Abstract

Objectives: To examine plasma protein Z (PZ) levels in acute myocardial infarction (AMI) and chronic coronary atherosclerosis disease (CCAD) patients without history of AMI and explore its potential clinical significance.

Methods: Plasma PZ concentrations were measured in 90 AMI patients (Group A), 87 CCAD patients without AMI history who remained free of major clinical events at least one year (Group B), and 88 clinically healthy controls (Group C).

Results: PZ was found to be significantly lower (P<0.001) in Group A (1508.5±486.2ng/mL) compared with Group B (1823.0±607.8ng/mL) and C (2001.7±733.0ng/mL) and in Group A+B compared with Group C (Group A+B 1663.1±570.0 ng/mL, P<0.001). No statistically significant difference was reached between Group B and C (P=0.081). PZ level was significantly correlated with concentration of creatine kinase MB, high sensitive-cardiac troponin T, high sensitive C reactive protein, D-dimer and coagulation factor II and may be a useful predictor for AMI (OR: 1.38, 95% CI: 1.13-1.77, P=0.03). Subgroup analysis showed PZ concentration below the lowest tertile (<1398ng/mL) had a significantly increased risk for AMI and CCAD (OR: 3.39; 95% CI: 1.12-10.31; P=0.03 and OR: 7.39; 95% CI: 2.62-20.79; P<0.001 respectively).

Conclusions: PZ deficiency is found in AMI patients and could potentially reflect the myocardium injury, local coagulation activation and inflammation response during the acute phase of coronary atherosclerosis disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5154850PMC
http://dx.doi.org/10.1016/j.thromres.2016.10.010DOI Listing

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