Abstract
BackgroundRecent studies have shown that increased circulating concentrations of fibroblast growth factor 21 (FGF21) are associated with obesity, metabolic disorder, and atherosclerosis. However the relationship between FGF21 and coronary artery disease (CAD) is controversial This study was planned to investigate the role of FGF21 in CAD development and CAD severity.MethodsSeventy-eight patients with stable angina pectoris (SAP) (lesion positive) and 40 control patients (lesion negative) with similar cardiovascular risk factors were included in the study. Serum FGF21 levels were measured by ELISA method. CAD severity was evaluated by using SYNTAX and GENSINI risk scores.ResultsFGF21 concentrations were found significantly higher in the SAP group than in the control group. [101.18 ± 141.62 vs. 47.93 ± 58.74 pg/mL; p = 0.03], no correlation was found between the SYNTAX (r = 0.146 and p = 0.134) and GENSINI (r = 0.211 and p = 0.084) scores with serum FGF21 levels. There was a negative relationship between serum FGF21 and serum HDL-C levels in correlation analysis (r = - 0.272; p = 0.026).ConclusionsThe serum FGF21 levels are different between SAP and control patients. FGF21 is a marker for CAD diagnosis, but not for the evaluation of CAD severity.
Highlights
Cardiovascular diseases (CVDs) are among the most common causes of morbidity and mortality [1]
fibroblast growth factor 21 (FGF21) concentrations were found significantly higher in the stable angina pectoris (SAP) group than in the control group. [101.18 ± 141.62 vs. 47.93 ± 58.74 pg/mL; p = 0.03], no correlation was found between the SYNTAX (r = 0.146 and p = 0.134) and GENSINI (r = 0.211 and p = 0.084) scores with serum FGF21 levels
Serum FGF21 levels were found higher in patients with unstable angina pectoris than in the SAP and control group, and there was no difference between serum FGF21 levels in SAP and control subjects unlike to our study [19]
Summary
Cardiovascular diseases (CVDs) are among the most common causes of morbidity and mortality [1]. Despite the developments in evidence-based medical treatments and revascularisation strategies, CVD still continues to be a global health problem and leads to a significant burden on the health system [2, 3]. Atherosclerosis has been assumed to be a chronic inflammatory process, and the immune system’s response to oxidised lipoproteins, in particular, initiates this process [4, 5]. Especially cytokines, have been investigated for the prevention and early detection of CVD [2, 6]. These adipokines affect the metabolism, and have many effects on the cardiovascular system [3].
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