Serum prolidase activity in patients with cardiac syndrome X

被引:3
|
作者
Aciksari, Gonul [1 ]
Demir, Bulent [2 ]
Uygun, Turgut [3 ]
Gedikbasi, Asuman [4 ]
Kutlu, Orkide [5 ]
Atici, Adem [1 ]
Baycan, Omer Faruk [1 ]
Kocak, Mehmet [6 ]
Kul, Seref [1 ]
机构
[1] Istanbul Medeniyet Univ, Dept Cardiol, Gortepe Training & Res Hosp, Istanbul, Turkey
[2] Bakirkoy Dr Sadi Konuk Training & Res Hosp, Dept Cardiol, Istanbul, Turkey
[3] Konya Training & Res Hosp, Dept Cardiol, Konya, Turkey
[4] Bakirkoy Dr Sadi Konuk Training & Res Hosp, Dept Biochem, Istanbul, Turkey
[5] Okmeydani Training & Res Hosp, Dept Internal Med, Istanbul, Turkey
[6] Fatih Sultan Mehmet Training & Res Hosp, Dept Emergency Med, Istanbul, Turkey
关键词
Cardiac syndrome X; collagen; serum prolidase activity; CORONARY-ARTERY-DISEASE; ANGINA-PECTORIS; CHEST-PAIN; EXTRACELLULAR-MATRIX; OXIDATIVE STRESS; ASSOCIATION;
D O I
10.14744/nci.2020.09086
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVE: Although the underlying mechanism is not yet fully understood, Cardiac Syndrome X (CSX) is defined as microvascular dysfunction. Prolidase plays a role in collagen synthesis. Increased serum prolidase activity (SPA) has been shown to correlate with collagen turnover. Augmented collagen turn-over may be associated with vascular fibrosis and microvascular dysfunction. In this study, we assessed whether there was a correlation between CXS and prolidase activity. METHODS: This case-control study included 45 consecutive CSX patients (mean age 50.7 +/- 6.5 years, 27 women) and 40 healthy controls (mean age 51.2 +/- 6.5 years, 25 women). Prolidase activity was determined with the Human Xaa-Pro Dipeptidase/Prolidase enzyme-linked immunosorbent assay kit (Cusabio Biotech Co. Ltd, China). RESULTS: Mean prolidase activity was 898.8 +/- 639.1 mU/mL in the CSX group and 434.1 +/- 289.8 mU/mL in the control group (p<0.001). In ROC analysis, it was found that the SPA value above 350 mU/mL sympathizes with the diagnosis of CSX. CONCLUSION: Increased SPA in CXS patients may play an essential role in the pathophysiology of CSX, leading to augmented oxidative stress and vascular fibrosis, endothelial dysfunction, and increased microvascular resistance.
引用
收藏
页码:471 / 477
页数:7
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