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

Standard

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. / West, Malcolm; Kirby, Adrienne; Stewart, Ralph A; Blankenberg, Stefan; Sullivan, David; White, Harvey D; Hunt, David; Marschner, Ian; Janus, Edward; Kritharides, Leonard; Watts, Gerald F; Simes, John; Tonkin, Andrew M; LIPID Study Investigators.

In: J AM HEART ASSOC, Vol. 11, No. 5, e020745, 03.2022.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

West, M, Kirby, A, Stewart, RA, Blankenberg, S, Sullivan, D, White, HD, Hunt, D, Marschner, I, Janus, E, Kritharides, L, Watts, GF, Simes, J, Tonkin, AM & LIPID Study Investigators 2022, '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', J AM HEART ASSOC, vol. 11, no. 5, e020745. https://doi.org/10.1161/JAHA.121.020745

APA

West, M., Kirby, A., Stewart, R. A., Blankenberg, S., Sullivan, D., White, H. D., Hunt, D., Marschner, I., Janus, E., Kritharides, L., Watts, G. F., Simes, J., Tonkin, A. M., & LIPID Study Investigators (2022). 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. J AM HEART ASSOC, 11(5), [e020745]. https://doi.org/10.1161/JAHA.121.020745

Vancouver

Bibtex

@article{b5bd9fdbd2de469388e7aca1f198a2d7,
title = "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",
abstract = "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.",
keywords = "Biomarkers/blood, Coronary Disease/blood, Creatinine/blood, Cystatin C/blood, Glomerular Filtration Rate, Humans, Lipids, Myocardial Infarction/blood, Renal Insufficiency/blood, Renal Insufficiency, Chronic/blood",
author = "Malcolm West and Adrienne Kirby and Stewart, {Ralph A} and Stefan Blankenberg and David Sullivan and White, {Harvey D} and David Hunt and Ian Marschner and Edward Janus and Leonard Kritharides and Watts, {Gerald F} and John Simes and Tonkin, {Andrew M} and {LIPID Study Investigators}",
year = "2022",
month = mar,
doi = "10.1161/JAHA.121.020745",
language = "English",
volume = "11",
journal = "J AM HEART ASSOC",
issn = "2047-9980",
publisher = "Wiley-Blackwell",
number = "5",

}

RIS

TY - JOUR

T1 - 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

AU - West, Malcolm

AU - Kirby, Adrienne

AU - Stewart, Ralph A

AU - Blankenberg, Stefan

AU - Sullivan, David

AU - White, Harvey D

AU - Hunt, David

AU - Marschner, Ian

AU - Janus, Edward

AU - Kritharides, Leonard

AU - Watts, Gerald F

AU - Simes, John

AU - Tonkin, Andrew M

AU - LIPID Study Investigators

PY - 2022/3

Y1 - 2022/3

N2 - 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.

AB - 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.

KW - Biomarkers/blood

KW - Coronary Disease/blood

KW - Creatinine/blood

KW - Cystatin C/blood

KW - Glomerular Filtration Rate

KW - Humans

KW - Lipids

KW - Myocardial Infarction/blood

KW - Renal Insufficiency/blood

KW - Renal Insufficiency, Chronic/blood

U2 - 10.1161/JAHA.121.020745

DO - 10.1161/JAHA.121.020745

M3 - SCORING: Journal article

C2 - 35179040

VL - 11

JO - J AM HEART ASSOC

JF - J AM HEART ASSOC

SN - 2047-9980

IS - 5

M1 - e020745

ER -