Serum cystatin C is associated with early stage coronary atherosclerotic plaque morphology on multidetector computed tomography.

OBJECTIVE

Cystatin C, a novel marker of kidney function, has been reported to be a predictor of adverse cardiovascular outcomes in patients without established chronic kidney disease. However, the relationship between serum cystatin C concentrations and early stage coronary atherosclerotic plaque morphology among patients with preserved kidney function has not been fully evaluated.

METHODS AND

RESULTS

405 outpatients with early coronary artery disease with estimated glomerular filtration rate (eGFR) ≥ 60ml/min/1.73m(2) and <50% stenosis on 64-slice CT coronary angiography were enrolled. Subjects were categorized into quartiles by serum cystatin C (quartile I: ≤ 0.88mg/L - quartile IV: ≥ 1.16mg/L). Plaques in coronary segments were categorized as calcified or noncalcified. Multiple linear regression analysis revealed that lower eGFR, higher age, increasing numbers of noncalcified and calcified plaques, lower high-density lipoprotein cholesterol, and female gender were statistically significant predictors of increased cystatin C concentrations. The risk for presence of noncalcified plaques increased significantly with increasing quartiles of cystatin C. Compared with those in the lowest quartile, patients in each subsequent quartile were at steadily increased risk of having noncalcified plaque (quartile IV: OR 5.6; 95% CI 2.3-13.9, p-value <0.001). Both number of segments with calcified plaque and Agatston score were highly correlated with cystatin C concentrations (both p<0.001), but when adjusted for segments with noncalcified plaque and other risk factors, calcified plaque segments were no longer independently predictive.

CONCLUSION

Higher serum cystatin C concentrations were correlated with early stage coronary atherosclerotic plaques among patients without established chronic kidney dysfunction. Noncalcified plaques increased with serum cystatin C concentrations, an association independent of eGFR and other cardiovascular risk factors.