Cystatin C was available in 2998 persons (mean age: 62.7?¡À?10.5 years; 30.3 % women). Of those 2346 suffered from coronary artery disease (CAD) and 652 (controls) did not. Creatinine (mean?¡À?SD: 83.1?¡À?47.8 vs. 74.1?¡À?24.7?¦Ìmol/L, p?=?0.036) but not Cystatin C (mean?¡À?SD: 1.02?¡À?0.44 vs. 0.92?¡À?0.26?mg/L, p?=?0.065) was significantly higher in patients with CAD. After a median follow-up of 9.9 years, in total 898 (30 % ) deaths occurred, 554 (18.5 % ) due to CV disease and 326 (10.9 % ) due to non-CV causes. Multivariable-adjusted Cox analysis (adjusting for eGFR and established cardiovascular risk factors, lipid lowering therapy, angiographic coronary artery disease, and C-reactive protein) revealed that patients in the highest cystatin C quartile were at an increased risk for all-cause (hazard ratio (HR) 1.93, 95 % CI 1.50-2.48) and CV mortality (HR 2.05 95 % CI 1.48-2.84) compared to those in the lowest quartile. The addition of cystatin C to a model consisting of established cardiovascular risk factors increased the area under the receiver-operating characteristic curve for CV and all-cause mortality, but the difference was statistically not significant. However, reclassification analysis revealed significant improvement by addition of cystatin C for CV and all-cause mortality (p?<?0.001), respectively.
The concentration of cystatin C is strongly associated with long-term all-cause and cardiovascular mortality in patients referred to coronary angiography, irrespective of creatinine-based renal function.