Low protein Z plasma level is a risk factor for acute myocardial infarction in coronary atherosclerosis disease patients

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 (Gro...

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Veröffentlicht in:Thrombosis research 2016-12, Vol.148, p.25-31
Hauptverfasser: Liu, Baoxin, Li, Yong, Luo, Jiachen, Dai, Liming, Zhao, Jinlong, Li, Hongqiang, Jie, Qiqiang, Wang, Dongzhi, Huang, Xin, Wei, Yidong
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Sprache:eng
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Zusammenfassung: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 A (1508.5 ± 486.2 ng/mL) compared with B (1823.0 ± 607.8 ng/mL) and C (2001.7 ± 733.0 ng/mL) groups and in A + B compared with C Group (A + B 1663.1 ± 570.0, P < 0.001). No statistically significant difference was reached between B and C groups ( 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 (< 1398 ng/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.
ISSN:0049-3848
1879-2472
DOI:10.1016/j.thromres.2016.10.010