Key result
Baseline serum fetuin-A levels <0.72 g/L were associated with a significantly higher increase in aortic valve calcification scores compared to higher levels (34.6% vs 10.0%, P<0.001).
Why the study?
Are baseline fetuin-A serum levels associated with the progression of aortic valve calcification in non-dialyzed patients with aortic valve disease?
Cohort (n=77)
Are baseline fetuin-A serum levels associated with the progression of aortic valve calcification in non-dialyzed patients with aortic valve disease?
Absolute Event Rate: 34.6% vs 10%
p-value: p=<0.001
Lower serum levels of fetuin-A are associated with faster progression of aortic valve calcification and increased risk of MACE in non-dialyzed patients with aortic valve disease.
Low fetuin-A may mark faster AVC progression in non-dialyzed AV disease; hypothesis-generating and requires prospective validation before clinical use.
AIMS: Fetuin-A has been identified as a potent circulating inhibitor of ectopic calcification. We investigated the relationship between baseline fetuin-A serum levels and the rate of progression of aortic valve calcification (AVC) in non-dialyzed patients with aortic valve disease (AVD). METHODS AND RESULTS: Seventy-seven patients (mean age 70 +/- 8 years) with echocardiographically proven AVD were collected. In all patients, serum fetuin-A levels, creatinine, calcium, lipid parameters, and C-reactive protein were measured at baseline. For quantification of AVC progression, all patients underwent multislice spiral computed tomography examinations at baseline and after a mean follow-up of 12.6 +/- 1.4 months (range 7-18 months). In a multifactorial analysis of covariance including fetuin-A levels, baseline AVC score, the covariables sex, age, body mass index, C-reactive protein, glomerular filtration rate, serum lipids, diabetes, smoking status, and hypertension, only serum fetuin-A levels significantly predict the progression of AVC (P < 0.001). Post hoc analysis demonstrated that patients with baseline fetuin-A levels lower than the median of the cohort (0.72 g/L) showed a significantly higher increase of AVC scores (34.6 +/- 31.4%) than patients with fetuin-A levels larger than the median (10.0 +/- 11.2%, P < 0.001) despite comparable baseline AVC scores. In addition, fetuin-A levels were associated with major adverse clinical events (MACE; P = 0.03). CONCLUSION: Serum levels of the calcification inhibitor fetuin-A are associated with the progression of AVC and MACE, independent of the renal function and inflammation.
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Koós et al. (2009) conducted a cohort in Aortic valve disease (n=77). Baseline fetuin-A serum levels <0.72 g/L vs. Baseline fetuin-A serum levels ≥0.72 g/L was evaluated on Progression of aortic valve calcification (increase of AVC scores) (p=<0.001). Baseline serum fetuin-A levels <0.72 g/L were associated with a significantly higher increase in aortic valve calcification scores compared to higher levels (34.6% vs 10.0%, P<0.001).
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