Abstract
Objectives: High cystatin C(CysC) levels are associated with impaired cardiovascular outcome. Whether CysC levels are independently related to the atherosclerosis burden is still controversial. Methods: We enrolled 31 non-ST-segment elevation acute coronary syndrome patients undergoing percutaneous coronary intervention. Patients were divided into 2 groups on the basis of median value of serum CysC. Using the high CysC group as a dependent variable, univariable and multivariable analyses were used to evaluate the association between CysC and three different features of atherosclerosis: 1) coronary plaque vulnerability as assessed by optical coherence tomography (OCT), 2) coronary artery calcium (CAC) by means of computed tomography scan, and 3) aortic wall metabolic activity, as assessed using 18F-Fluorodeoxyglucose-positron emission tomography (18F-FDG-PET). Results: After univariable and multivariable analyses, 18F-FDG uptake in the descending aorta (DA) was independently associated with a low level of CysC [(Odds Ratio = 0.02; 95%CI 0.0004–0.89; p = 0.044; 18F-FDG uptake measured as averaged maximum target to blood ratio); (Odds Ratio = 0.89; 95%CI 0.82–0.98, p = 0.025; 18F-FDG uptake measured as number of active slices)]. No trend was found for the association between CysC and characteristics of OCT-assessed coronary plaque vulnerability or CAC score. Conclusions: In patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS), 18F-FDG uptake in the DA was associated with a low level of serum CysC. There was no relation between CysC levels and OCT-assessed coronary plaque vulnerability or CAC score. These findings suggest that high levels of CysC may not be considered as independent markers of atherosclerosis.
Highlights
Cystatin C, a 13-kDa protein, is a member of a family of competitive inhibitors of lysosomal cysteine proteases synthesized in all nucleated cells at a constant rate [1]
Since elastolytic cysteine proteases and their inhibitors are involved in the pathogenesis of atherosclerosis, it has been suggested that cystatin C levels may be directly linked to the development and progression of atherosclerosis [8,9]
The study population comprised 31 NSTE-ACS patients treated with percutaneous coronary intervention (PCI)
Summary
Cystatin C, a 13-kDa protein, is a member of a family of competitive inhibitors of lysosomal cysteine proteases synthesized in all nucleated cells at a constant rate [1]. The mechanisms linking increased cystatin C levels and impaired cardiovascular outcome are not completely understood, so far, renal dysfunction is a definite plausible link. Studies suggested that raised cystatin C levels identify a ‘preclinical’ kidney dysfunction that may be associated with adverse clinical outcomes [6]. Shlipak et al [7], in a large meta-analysis of 11 general-population studies and 5 studies with subjects suffering from chronic renal disease, showed that use of cystatin C for estimation of the glomerular filtration rate (eGRF) improved the role of renal function in risk classification with reference to all-cause mortality, cardiovascular mortality, and renal failure. Since elastolytic cysteine proteases and their inhibitors are involved in the pathogenesis of atherosclerosis, it has been suggested that cystatin C levels may be directly linked to the development and progression of atherosclerosis [8,9]
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