Changes in ADMA and TAFI levels after stenting in coronary artery disease patients

Khalifa,Nouran   M.; Gad,Mohamed  Z.; Hataba,Alaa   A.; Mahran,Laila   G.

doi:10.3892/mmr.2012.985

Changes in ADMA and TAFI levels after stenting in coronary artery disease patients

Authors:
- Nouran M. Khalifa
- Mohamed Z. Gad
- Alaa A. Hataba
- Laila G. Mahran
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Affiliations: Department of Pharmacology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt, Department of Biochemistry, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt, Cardiology Department, Kobry El Kobba Military Hospital, Cairo, Egypt
Published online on: July 11, 2012 https://doi.org/10.3892/mmr.2012.985
Pages: 855-859

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Abstract

The aim of this study was to examine the contribution of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS) and a novel marker of vascular endothelial dysfunction, and thrombin-activatable fibrinolysis inhibitor (TAFI), a risk factor for venous thrombosis, to the predisposition of coronary restenosis following stent implantation in coronary artery disease (CAD) patients. Thirty-seven patients with CAD were recruited from the Kobry El Obba Military Hospital, Cairo, Egypt. The patients were hospitalized for coronary angiography and coronary stenting (CS). Overnight fasting blood samples were collected from patients prior to CS and four months later for the determination of plasma ADMA and TAFI levels. The patients underwent follow-up coronary angiography to reveal in-stent restenosis. The results showed that plasma ADMA levels in CAD patients were significantly higher than those reported for healthy subjects. ADMA levels were significantly increased by 30% in CAD patients four months following CS. CAD patients who developed in-stent restenosis had a 35% increase in ADMA levels following CS. TAFI levels were not significantly changed after CS in CAD patients or in any of the subgroups. In conclusion, ADMA, but not TAFI, is linked to the predisposition of in-stent restenosis following CS.

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