Serum concentrations of galectin-3 in patients with cardiac syndrome X

- In the current study, we demonstrate for the first time that novel cardiac marker.
- Galectin-3 serum concentrations are significantly higher in patients with CSX.
- This finding suggests that cardiovascular fibrosis may also contribute the pathogenesis of CSX.
- CSX may not be as innocuous as considered.
- Moreover, galectin-3 can be a useful marker for identifying CSX patients at high risk of cardiovascular disease in the future.

Objective: Microvascular dysfunction has been reported in cardiac syndrome X (CSX), even though the underlying mechanisms still remain uncertain. Galectin-3 has been recently recognized as a biomarker of cardiovascular fibrosis and inflammation. We sought to investigate the role of galectin-3 in the CSX. Methods: We studied 115 consecutive CSX patients (mean age 55.43 ± 8.71 years, 36 men) and 74 healthy controls (mean age 54.53 ± 10.07 years, 31 men). Serum concentrations of galectin-3 and high-sensitive C-reactive protein (hs-CRP) were measured on the blood samples. Results: Galectin-3 concentrations were significantly higher in patients with CSX compared to controls (0.90 ng/ml; IQR, 0.40-1.70 ng/ml vs 0.40 ng/ml; IQR, 0.36-0.44 ng/ml, p < 0.0001). Although, the prevalence of diabetes mellitus, hypertension and family history of coronary artery disease (CAD) were significantly higher among patients with CSX, following adjustment for diabetes mellitus, hypertension, and family history of CAD, serum galectin-3 concentrations were still found significantly increased in patients with CSX. Galectin-3 concentrations correlated positively with hs-CRP (r = 0.16, p = 0.03). In addition, concentrations of galectin-3, hs-CRP, fasting glucose, uric acid and family history of CAD were determined as independent predictors of the CSX. Conclusion: It was found that galectin-3 serum concentrations are higher in patients with CSX compared to healthy controls. Further studies on larger population are needed to confirm the relation between the fibrosis and the CSX, as well as to explore the potential role of galectin-3 in the CSX.