Circulating Cystatin C Is an Independent Risk Marker for Cardiovascular Outcomes, Development of Renal Impairment, and Long‐Term Mortality in Patients With Stable Coronary Heart Disease: The LIPID Study

Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

卷:11

David Hunt¹  Leonard Kritharides²  David Sullivan³  Malcolm West⁴  Edward Janus⁵  Ralph A. Stewart⁶  Harvey D. White⁶  John Simes⁷  Adrienne Kirby⁷  Ian Marschner⁷  Gerald F. Watts⁸  Andrew M. Tonkin⁹  Stefan Blankenberg¹⁰ 

[1] Cardiology Department Royal Melbourne Hospital Melbourne Australia;

[2] Department of Cardiology Concord Repatriation General HospitalSydney Local Health District Sydney Australia;

[3] Department of Chemical Pathology Royal Prince Alfred Hospital Sydney Australia;

[4] Department of Medicine University of Queensland Brisbane Australia;

[5] Department of Medicine Western Health Chronic Disease AllianceWestern HealthMelbourne Medical SchoolUniversity of Melbourne Melbourne Australia;

[6] Green Lane Cardiovascular Service Auckland City HospitalUniversity of Auckland Auckland New Zealand;

[7] National Health and Medical Research Council Clinical Trials CentreUniversity of Sydney Sydney Australia;

[8] School of Medicine Faculty of Health and Medical Sciences University of Western Australia Perth Australia;

[9] School of Public Health and Preventive Medicine Monash University Perth Australia;

[10] University Heart and Vascular Centre Hamburg Hamburg Germany;

关键词: biomarkers;    cardiovascular disease;    chronic kidney disease;    coronary disease;    cystatin C;    hydroxymethylglutaryl‐CoA reductase inhibitors;   

DOI  :  10.1161/JAHA.121.020745

来源: DOAJ

【 摘 要 】

Background Elevated plasma cystatin C levels reflect reduced renal function and increased cardiovascular risk. Less is known about whether the increased risk persists long‐term or is independent of renal function and other important biomarkers. Methods and Results Cystatin C and other biomarkers were measured at baseline (in 7863 patients) and 1 year later (in 6106 patients) in participants in the LIPID (Long‐Term Intervention with Pravastatin in Ischemic Disease) study, who had a previous acute coronary syndrome. Outcomes were ascertained during the study (median follow‐up, 6 years) and long‐term (median follow‐up, 16 years). Glomerular filtration rate (GFR) was estimated using Chronic Kidney Disease Epidemiology Collaboration equations (first GFR‐creatinine, then GFR‐creatinine‐cystatin C). Over 6 years, in fully adjusted multivariable time‐to‐event models, with respect to the primary end point of coronary heart disease mortality or nonfatal myocardial infarction, for comparison of Quartile 4 versus 1 of baseline cystatin C, the hazard ratio was 1.37 (95% CI, 1.07–1.74; P=0.01), and for major cardiovascular events was 1.47 (95% CI, 1.19–1.82; P<0.001). Over 16 years, the association of baseline cystatin C with coronary heart disease, cardiovascular, and all‐cause mortality persisted (each P<0.001) and remained significant after adjustment for estimated GFR‐creatinine‐cystatin C. Cystatin C also predicted the development of chronic kidney disease for 6 years (odds ratio, 6.61; 95% CI, 4.28–10.20) independently of estimated GFR‐creatinine and other risk factors. However, this association was no longer significant after adjustment for estimated GFR‐creatinine‐cystatin C. Conclusions Cystatin C independently predicted major cardiovascular events, development of chronic kidney disease, and cardiovascular and all‐cause mortality. Prediction of long‐term mortality was independent of improved estimation of GFR. Registration URL: https://anzctr.org.au; Unique identifier: ACTRN12616000535471.

【 授权许可】

Unknown