Association of Initial and Longitudinal Changes in C-reactive Protein With the Risk of Cardiovascular Disease, Cancer, and Mortality

Navin Suthahar*, Dongyu Wang, Joseph Pierre Aboumsallem, Canxia Shi, Sanne de Wit, Elizabeth E. Liu, Emily S. Lau, Stephan J.L. Bakker, Ron T. Gansevoort, Bert van der Vegt, Manol Jovani, Bernard E. Kreger, Greta Lee Splansky, Emelia J. Benjamin, Ramachandran S. Vasan, Martin G. Larson, Daniel Levy, Jennifer E. Ho, Rudolf A. de Boer*

*Corresponding author for this work

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Abstract

Objective: To evaluate the value of serial C-reactive protein (CRP) measurements in predicting the risk of cardiovascular disease (CVD), cancer, and mortality. Methods: The analysis was performed using data from two prospective, population-based observational cohorts: the Prevention of Renal and Vascular End-Stage Disease (PREVEND) study and the Framingham Heart Study (FHS). A total of 9253 participants had CRP measurements available at two examinations (PREVEND: 1997-1998 and 2001-2002; FHS Offspring cohort: 1995-1998 and 1998-2001). All CRP measurements were natural log-transformed before analyses. Cardiovascular disease included fatal and nonfatal cardiovascular, cerebrovascular and peripheral vascular events, and heart failure. Cancer included all malignancies except nonmelanoma skin cancers. Results: The mean age of the study population at baseline was 52.4±12.1 years and 51.2% (n=4733) were women. Advanced age, female sex, smoking, body mass index, and total cholesterol were associated with greater increases in CRP levels over time (Pall<.001 in the multivariable model). Baseline CRP, as well as increase in CRP over time (ΔCRP), were associated with incident CVD (hazard ratio [HR]: 1.29 per 1-SD increase; 95% confidence interval [CI]: 1.29 to 1.47, and HR per 1-SD increase: 1.19; 95% CI: 1.09 to 1.29 respectively). Similar findings were observed for incident cancer (baseline CRP, HR: 1.17; 95% CI: 1.09 to 1.26; ΔCRP, HR: 1.08; 95% CI: 1.01 to 1.15) and mortality (baseline CRP, HR: 1.29; 95% CI: 1.21 to 1.37; ΔCRP, HR: 1.10; 95% CI: 1.05 to 1.16). Conclusion: Initial as well as subsequent increases in CRP levels predict future CVD, cancer, and mortality in the general population.

Original languageEnglish
Pages (from-to)549-558
Number of pages10
JournalMayo Clinic Proceedings
Volume98
Issue number4
DOIs
Publication statusPublished - Apr 2023

Bibliographical note

Funding Information:
Dr. de Boer received speaker fees from Abbott, AstraZeneca, Bayer, Novartis, and Roche (outside the submitted work). Dr. Ho has received research grants from Gilead Sciences and Bayer; and has received research supplies from EcoNugenics. The remaining authors report no potential competing interests.

Funding Information:
Dr Suthahar and Mr Wang share first authorship. Drs Ho and de Boer share senior authorship. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services. Institutional Review Board approval was obtained from respective universities. Grant Support: The Prevention of Renal and Vascular End-Stage Disease study was supported by several grants, including grant E.013 from the Dutch Kidney Foundation. The Framingham Heart Study was supported by contracts from the National Heart, Lung, and Blood Institute (NO1-HC-25195, HHSN268201500001I, and 75N92019D00031). Drs Suthahar and de Boer are supported by the Netherlands Heart Foundation (CVON SHE-PREDICTS-HF, grant 2017-21; CVON RED-CVD, grant 2017-11; CVON PREDICT2, grant 2018-30; and CVON DOUBLE DOSE, grant 2020B005), and Drs de Boer, Aboumsallem, and Ms de Wit by a grant from the European Research Council (ERC CoG 818715, SECRETE-HF). Dr. Lau is supported by grants from the National Institutes of Health K23-HL159243 and the American Heart Association #853922. Dr Ho was supported by NIH grants R01 HL134893, R01 HL140224, and K24 HL153669. Ms. Shi is supported by a scholarship from the China Scholarship Council (CSC number: 201806170057). Dr. Benjamin was supported by NIH grants R01 HL092577; 5U54HL120163; 1RO1 HL64753; R01 HL076784; 1R01 AG028321

Funding Information:
Grant Support: The Prevention of Renal and Vascular End-Stage Disease study was supported by several grants, including grant E.013 from the Dutch Kidney Foundation. The Framingham Heart Study was supported by contracts from the National Heart, Lung, and Blood Institute (NO1-HC-25195, HHSN268201500001I, and 75N92019D00031). Drs Suthahar and de Boer are supported by the Netherlands Heart Foundation (CVON SHE-PREDICTS-HF, grant 2017-21; CVON RED-CVD, grant 2017-11; CVON PREDICT2, grant 2018-30; and CVON DOUBLE DOSE, grant 2020B005), and Drs de Boer, Aboumsallem, and Ms de Wit by a grant from the European Research Council (ERC CoG 818715, SECRETE-HF). Dr. Lau is supported by grants from the National Institutes of Health K23-HL159243 and the American Heart Association #853922. Dr Ho was supported by NIH grants R01 HL134893, R01 HL140224, and K24 HL153669. Ms. Shi is supported by a scholarship from the China Scholarship Council (CSC number: 201806170057). Dr. Benjamin was supported by NIH grants R01 HL092577; 5U54HL120163; 1RO1 HL64753; R01 HL076784; 1R01 AG028321

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