Key result
Lower serum fetuin-A strongly linked to acute coronary syndrome independent of heart valve calcification.
Why the study?
The relationship among serum fetuin-A levels, heart valve calcification, and biomarkers of inflammation in patients with acute coronary syndrome was not well characterized.
Are serum fetuin-A levels associated with acute coronary syndrome, heart valve calcification, and inflammatory biomarkers?
Case-Control (n=176)
Are serum fetuin-A levels associated with acute coronary syndrome, heart valve calcification, and inflammatory biomarkers?
Odds Ratio: 0.015 (95% CI 0–0.52)
Absolute Event Rate: 0.76% vs 1.1%
p-value: p=0.020
Serum fetuin-A levels are significantly decreased in patients with acute coronary syndromes and are inversely associated with inflammatory markers and valve calcification, suggesting it acts as a negative acute phase protein.
Association of fetuin-A with valve calcification in ACS remains hypothesis-generating; prospective studies needed before clinical consideration.
PURPOSE: Fetuin-A is a multifunctional hepatic secretory protein that inhibits dystrophic vascular and valvular calcification. Our aim was to evaluate the relationship among fetuin-A levels, heart valve calcification and other biomarkers of inflammation in patients with acute coronary syndrome (ACS). METHODS: The associations among serum fetuin-A concentrations, mitral annular (MAC) and aortic valve calcification and other biomarkers of inflammation (hs-CRP, ferritin, fibrinogen, white blood cell count (WBC), erythrocyte sedimentation rate (ESR), albumin levels) were evaluated in ACS patients and healthy controls. The study included 95 patients (mean age 61.8 ± 12.10 years) and 81 healthy controls (mean age 48.33 ± 9.19 years). RESULTS: Fetuin-A levels were significantly lower in patients with ACS than in healthy controls (0.76 ± 0.23 and 1.10 ± 0.45 g/L, respectively; p < 0.001). Fetuin-A was lower in patients with mitral annular calcification (p = 0.007) and aortic (p = 0.001) valve calcification. In patients with ACS, there was a negative correlation among serum urea (r = -0.377; p < 0.001) and creatinine (r = -0.232; p = 0.024) levels and fetuin-A, and a negative correlation among WBC (r = -0.156; p = 0,132), ESR (r = -0.214; p = 0.037), hs-CRP (r = -0.220; p = 0.032) levels and fetuin-A. A positive correlation was seen between albumin and fetuin-A (r = 0.362; p < 0.001). Multivariate logistic regression analysis revealed that fetuin-A was the variable that had a significant effect on ACS (p = 0.020 OR = .015; (95% CI)(0.000-0.520). CONCLUSION: Fetuin-A levels decrease in patients with acute coronary syndromes, independent of heart valve calcification. Fetuin-A may therefore act as a negative acute phase protein after myocardial infarction.
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Afşar et al. (2012) conducted a case-control in Acute coronary syndrome (n=176). Serum fetuin-A levels vs. Healthy controls was evaluated on Acute coronary syndrome (OR 0.015, 95% CI 0.000-0.520, p=0.020). Lower serum fetuin-A levels were significantly associated with acute coronary syndrome (OR 0.015; 95% CI 0.000-0.520; p=0.020), independent of heart valve calcification.
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