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    Coron Artery Dis. 2013 May;24(3):201-8. doi: 10.1097/MCA.0b013e32835e5c86.

    Association between serum γ-glutamyltransferase levels and coronary microvascular function.


    Departments of aCardiology bCardiovascular Surgery, Konya Application and Research Center cBiochemistry dGastroenterology, Baskent University Faculty of Medicine, Ankara eDepartment of Cardiology, Medeniyet University Faculty of Medicine, Istanbul, Turkey.



    Serum γ-glutamyltransferase (GGT) level is an independent risk factor for cardiovascular (CV) disease, and there is a strong association between serum GGT levels and most CV risk factors. However, the role of the serum GGT level as an independent risk factor for coronary microvascular function remains controversial.


    We aimed to determine whether the serum GGT level is independently and specifically associated with coronary flow reserve (CFR) impairment in normal individuals.


    We examined healthy individuals who did not have any major CV risk factors (277), of whom CFR was achieved in 263 (95%). They were divided into three groups according to serum GGT levels. In each participant, CFR was measured using an Acuson Sequoia C256 Echocardiography System.


    Participants with high GGT levels had significantly impaired CFR compared with those with intermediate and low GGT levels (2.82±0.49 vs. 2.71±0.51 and 2.44±0.48 U/l; P<0.0001). After adjusting for potential confounders, including sex, BMI, blood pressure, lipids, and glucose, we found that the serum GGT and high-sensitivity C-reactive protein levels were associated independently with CFR impairment (b=-0.205, P=0.007; b=-0.172, P=0.024). We also found that the serum GGT level was a good predictor of low CFR at the receiver-operating characteristic curve. The area under the curve was 75% [95% confidence interval, 0.65-0.86], and the serum GGT level was significantly predictive of a low CFR (P<0.0001).


    These results support a role for the serum GGT level as an independent marker of coronary microvascular damage and inflammation in normal individuals without concomitant risk factors.

    [PubMed - in process]

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