Abstract
Objective The underlying mechanisms by which cystatin C affects cardiovascular disease (CVD) are not very clear. Metabolic syndrome (MetS) is a cluster of risk factors that increase the risk of CVD. Here, we aimed to investigate the association of cystatin C with metabolic syndrome and cardiovascular outcomes in non-ST-segment elevation acute coronary syndrome (NSTE-ACS) with preserved renal function. Methods In total, 422 NSTE-ACS patients with preserved renal function were enrolled to examine the association of cystatin C with MetS. MetS was defined based on the NCEP-ATP-III guidelines. Major adverse cardiovascular events (MACEs) were also evaluated, which included cardiac death, nonfatal myocardial infarction (MI), target vessel revascularization (TVR), heart failure, and nonfatal stroke. All patients underwent a 12-month follow-up for MACEs after admission. Results Cystatin C was significantly correlated with metabolic risk factors and inflammation markers. The prevalence of MetS and MACEs correlated with cystatin C levels. Cystatin C showed a strong diagnostic performance for cardiovascular risk factors and outcomes in ROC analysis. After adjustment for multiple risk factors, cystatin C level was independently associated with MetS (OR 2.299, 95% CI 1.251–4.225, and P = 0.007). During a 12-month follow-up, the patients with high cystatin C level and MetS had higher incidence of MACEs (Log-rank = 24.586, P < 0.001) and cardiac death (Log-rank = 9.890, P = 0.020) compared to the others. Multivariate Cox analysis indicated that cystatin C level was an independent predictor of MACEs (HR 2.609, 95% CI 1.295–5.257, and P = 0.007). Conclusion Cystatin C may be an independent predictor of metabolic syndrome and therefore valuable for management of NSTE-ACS patients. Further multicenter, large-scale studies are required to assess the implication of these results.
Highlights
Cystatin C is an endogenous inhibitor of cathepsin cysteine proteases and is generally considered to be constantly secreted and be freely filtered by the glomerulus but be neither secreted by the renal tubule nor reabsorbed into circulation [1, 2]
The patients in the high cystatin C group had a higher incidence of diabetes (P = 0.036) and Metabolic syndrome (MetS) (P = 0.001), had more severe coronary artery lesion (P < 0.001), and had a higher Global Registry of Acute Coronary Events (GRACE) score (P < 0.001)
Our study focused on the link between non-glomerular filtration rate (GFR) determinants of cystatin C and cardiometabolic risk factors and highlighted the predictive role of non-GFR determinants in NSTE-acute coronary syndrome (ACS)
Summary
Cystatin C is an endogenous inhibitor of cathepsin cysteine proteases and is generally considered to be constantly secreted and be freely filtered by the glomerulus but be neither secreted by the renal tubule nor reabsorbed into circulation [1, 2]. Cystatin C is useful for estimation of glomerular filtration rate (GFR) and known as a marker of renal function [3, 4]. Recent studies have described cystatin C as a prominent predictor of cardiovascular diseases (CVD) that is significantly associated with high risk of cardiovascular outcomes in acute coronary syndrome (ACS) [5, 6]. The reasons by which cystatin C is associated with cardiovascular outcomes were mostly attributed to its higher sensitivity for identifying early renal impairment [7,8,9]. The Prospective Epidemiological Study of Myocardial Infarction (PRIME) showed that cystatin C was associated with coronary events independent of estimated GFR [13]. Tangri et al [14] reported that cystatin C remained associated with cardiovascular events even after adjustment for directly measured GFR.
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