Sex-Specific Associations of Cardiovascular Risk Factors and Biomarkers With Incident Heart Failure

Navin Suthahar; Emily S. Lau; Michael J. Blaha; Samantha M. Paniagua; Martin G. Larson; Bruce M. Psaty; Emelia J. Benjamin; Matthew A. Allison; Traci M. Bartz; James L. Januzzi; Daniel Levy; Laura M.G. Meems; Stephan J.L. Bakker; Joao A.C. Lima; Mary Cushman; Douglas S. Lee; Thomas J. Wang; Christopher R. deFilippi; David M. Herrington; Matthew Nayor; Ramachandran S. Vasan; Julius M. Gardin; Jorge R. Kizer; Alain G. Bertoni; Norrina B. Allen; Ron T. Gansevoort; Sanjiv J. Shah; John S. Gottdiener; Jennifer E. Ho; Rudolf A. de Boer

doi:10.1016/j.jacc.2020.07.044

Sex-Specific Associations of Cardiovascular Risk Factors and Biomarkers With Incident Heart Failure

Navin Suthahar, Emily S. Lau, Michael J. Blaha, Samantha M. Paniagua, Martin G. Larson, Bruce M. Psaty, Emelia J. Benjamin, Matthew A. Allison, Traci M. Bartz, James L. Januzzi, Daniel Levy, Laura M.G. Meems, Stephan J.L. Bakker, Joao A.C. Lima, Mary Cushman, Douglas S. Lee, Thomas J. Wang, Christopher R. deFilippi, David M. Herrington, Matthew NayorRamachandran S. Vasan, Julius M. Gardin, Jorge R. Kizer, Alain G. Bertoni, Norrina B. Allen, Ron T. Gansevoort, Sanjiv J. Shah, John S. Gottdiener, Jennifer E. Ho^*, Rudolf A. de Boer^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

60 Scopus citations

Abstract

Background: Whether cardiovascular (CV) disease risk factors and biomarkers associate differentially with heart failure (HF) risk in men and women is unclear. Objectives: The purpose of this study was to evaluate sex-specific associations of CV risk factors and biomarkers with incident HF. Methods: The analysis was performed using data from 4 community-based cohorts with 12.5 years of follow-up. Participants (recruited between 1989 and 2002) were free of HF at baseline. Biomarker measurements included natriuretic peptides, cardiac troponins, plasminogen activator inhibitor-1, D-dimer, fibrinogen, C-reactive protein, sST2, galectin-3, cystatin-C, and urinary albumin-to-creatinine ratio. Results: Among 22,756 participants (mean age 60 ± 13 years, 53% women), HF occurred in 2,095 participants (47% women). Age, smoking, type 2 diabetes mellitus, hypertension, body mass index, atrial fibrillation, myocardial infarction, left ventricular hypertrophy, and left bundle branch block were strongly associated with HF in both sexes (p < 0.001), and the combined clinical model had good discrimination in men (C-statistic = 0.80) and in women (C-statistic = 0.83). The majority of biomarkers were strongly and similarly associated with HF in both sexes. The clinical model improved modestly after adding natriuretic peptides in men (ΔC-statistic = 0.006; likelihood ratio chi-square = 146; p < 0.001), and after adding cardiac troponins in women (ΔC-statistic = 0.003; likelihood ratio chi-square = 73; p < 0.001). Conclusions: CV risk factors are strongly and similarly associated with incident HF in both sexes, highlighting the similar importance of risk factor control in reducing HF risk in the community. There are subtle sex-related differences in the predictive value of individual biomarkers, but the overall improvement in HF risk estimation when included in a clinical HF risk prediction model is limited in both sexes.

Original language	English (US)
Pages (from-to)	1455-1465
Number of pages	11
Journal	Journal of the American College of Cardiology
Volume	76
Issue number	12
DOIs	https://doi.org/10.1016/j.jacc.2020.07.044
State	Published - Sep 22 2020

Funding

This work was partially supported by the National Heart, Lung, and Blood Institute (Framingham Heart Study, contract N01-HC25195 and HHSN268201500001I; Cardiovascular Health Study, contracts HHSN268201200036C, HHSN268200800007C, HHSN268201800001C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, and N01HC85086, and grants U01HL080295 and U01HL130114). The Multi-Ethnic Study of Atherosclerosis and the Multi-Ethnic Study of Atherosclerosis National Institutes of Health SNP Health Association Resource project are conducted and supported by the National Heart, Lung, and Blood Institute in collaboration with the Multi-Ethnic Study of Atherosclerosis investigators. Support for the Multi-Ethnic Study of Atherosclerosis is provided by contracts 75N92020D00001, HHSN268201500003I, N01-HC-95159, 75N92020D00005, N01-HC-95160, 75N92020D00002, N01-HC-95161, 75N92020D00003, N01-HC-95162, 75N92020D00006, N01-HC-95163, 75N92020D00004, N01-HC-95164, 75N92020D00007, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169 from the National Heart, Lung, and Blood Institute, and by grants UL1-TR-000040, UL1-TR-001079, and UL1-TR-001420 from the National Center for Advancing Translational Sciences (NCATS). Dr. Shah has been supported by grants from the National Institutes of Health (R01 HL107577, R01 HL127028, R01 HL140731, and R01 HL149423) and the American Heart Association (#16SFRN28780016). The Cardiovascular Health Study has received additional contributions from the National Institute of Neurological Disorders and Stroke and grant R01AG023629 from the National Institute on Aging. The Framingham Heart Study was supported by HHSN268201500001I; N01-HC 25195. Dr. Benjamin has been supported by grants from the National Institutes of Health R01 HL128914 and 2R01 HL092577, and grant 18SFRN34110082 from the American Heart Association. Dr. Nayor has been supported by grant K23-HL138260. Dr. Ho has been supported by grants R01 HL134893 and R01 HL140224. In Framingham Heart Study samples, measurement of sST2 was performed by Critical Diagnostics, Inc.; and measurement of high-sensitivity troponin I was performed by Singulex, Inc. The Prevention of Renal and Vascular End-Stage Disease study has been made possible by grants, including grant E.013 from the Dutch Kidney Foundation. Drs. de Boer and Suthahar are supported by the Netherlands Heart Foundation (CVON SHE-PREDICTS-HF, grant 2017-21). Dr. de Boer has been further supported by the Netherlands Heart Foundation (CVON-DOSIS, grant 2014-040; CVON RED-CVD, grant 2017-11; and CVON PREDICT2, grant 2018-30), and the European Research Council (ERC CoG 818715, SECRETE-HF). The funding sources had no role in the design and conduct of the study; collection, management, analysis and interpretation of the data; preparation, review or approval of the manuscript; and decision to submit the manuscript for publication. The views expressed in this paper 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. The UMCG, which employs Drs. Suthahar, Meems, Bakker, Gansevoort, and de Boer, has received research grants and/or fees from AstraZeneca, Abbott, Bristol-Myers Squibb, Novartis, Novo Nordisk, and Roche. Dr. Blaha has received grants and personal fees from Amgen and the U.S. Food and Drug Administration; has received grants from Aetna, the American Heart Association, and the National Institutes of Health; and has received personal fees from Sanofi, Regeneron, Novartis, and MedImmune. Dr. Psaty has served on a data and safety monitoring board for a clinical trial funded by the manufacturer (ZollLifeCor); and has served on the steering committee of the Yale Open Data Access Project funded by Johnson & Johnson. Dr. Benjamin has received grants from the National Institutes of Health and the American Heart Association/National Institutes of Health. Dr. Januzzi has received grants and personal fees from Roche, Abbott, Singulex, and Novartis; and has received personal fees from Critical Diagnostics, Janssen, Boehringer Ingelheim, Abbvie, Pfizer, General Electric, and Bayer. Dr. Cushman has received research funding in the form of assay costs from Sphingotec. Dr. Lee is supported by a Ted Rogers Chair in Heart Function Outcomes. Dr. DeFilippi has received research support from Roche Diagnostics; has received consulting fees from Roche, Siemens Healthcare Diagnostics, Alere, Metanomics, and Ortho Diagnostics; has served on the endpoint committee for Radiometer and Quintiles; and has received royalties from UpToDate. Dr. Herrington has received grants from the National Institutes of Health. Dr. Kizer has owned stock in Bristol-Myers Squibb, Johnson and Johnson, Medtronic, Merck, and Pfizer. Dr. Bertoni has received grants from the National Institutes of Health/National Heart, Lung, and Blood Institute. Dr. Shah has received research grants from Actelion, AstraZeneca, Corvia, Novartis, and Pfizer; and has received consulting fees from Abbott, Actelion, AstraZeneca, Amgen, Axon Therapeutics, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Cardiora, CVRx, Cytokinetics, Eisai, GlaxoSmithKline, Ionis, Ironwood, Merck, MyoKardia, Novartis, Pfizer, Sanofi, Shifamed, Tenax, and United Therapeutics. Dr. Ho has received grants from the National Institutes of Health and Gilead Sciences; and has received research support from Bayer and EcoNugenics. Dr. de Boer has received speaker fees from Abbott, AstraZeneca, Novartis, and Roche. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Javed Butler, MD, MPH, MBA, served as Guest Associate Editor for this paper. P.K. Shah, MD, served as Guest Editor-in-Chief for this paper. This work was partially supported by the National Heart, Lung, and Blood Institute (Framingham Heart Study, contract N01-HC25195 and HHSN268201500001I; Cardiovascular Health Study, contracts HHSN268201200036C, HHSN268200800007C, HHSN268201800001C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, and N01HC85086, and grants U01HL080295 and U01HL130114). The Multi-Ethnic Study of Atherosclerosis and the Multi-Ethnic Study of Atherosclerosis National Institutes of Health SNP Health Association Resource project are conducted and supported by the National Heart, Lung, and Blood Institute in collaboration with the Multi-Ethnic Study of Atherosclerosis investigators. Support for the Multi-Ethnic Study of Atherosclerosis is provided by contracts 75N92020D00001, HHSN268201500003I, N01-HC-95159, 75N92020D00005, N01-HC-95160, 75N92020D00002, N01-HC-95161, 75N92020D00003, N01-HC-95162, 75N92020D00006, N01-HC-95163, 75N92020D00004, N01-HC-95164, 75N92020D00007, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169 from the National Heart, Lung, and Blood Institute, and by grants UL1-TR-000040, UL1-TR-001079, and UL1-TR-001420 from the National Center for Advancing Translational Sciences (NCATS). Dr. Shah has been supported by grants from the National Institutes of Health (R01 HL107577, R01 HL127028, R01 HL140731, and R01 HL149423) and the American Heart Association (#16SFRN28780016). The Cardiovascular Health Study has received additional contributions from the National Institute of Neurological Disorders and Stroke and grant R01AG023629 from the National Institute on Aging. The Framingham Heart Study was supported by HHSN268201500001I; N01-HC 25195. Dr. Benjamin has been supported by grants from the National Institutes of Health R01 HL128914 and 2R01 HL092577, and grant 18SFRN34110082 from the American Heart Association. Dr. Nayor has been supported by grant K23-HL138260. Dr. Ho has been supported by grants R01 HL134893 and R01 HL140224. In Framingham Heart Study samples, measurement of sST2 was performed by Critical Diagnostics, Inc.; and measurement of high-sensitivity troponin I was performed by Singulex, Inc. The Prevention of Renal and Vascular End-Stage Disease study has been made possible by grants, including grant E.013 from the Dutch Kidney Foundation. Drs. de Boer and Suthahar are supported by the Netherlands Heart Foundation (CVON SHE-PREDICTS-HF, grant 2017-21). Dr. de Boer has been further supported by the Netherlands Heart Foundation (CVON-DOSIS, grant 2014-040; CVON RED-CVD, grant 2017-11; and CVON PREDICT2, grant 2018-30), and the European Research Council (ERC CoG 818715, SECRETE-HF). The funding sources had no role in the design and conduct of the study; collection, management, analysis and interpretation of the data; preparation, review or approval of the manuscript; and decision to submit the manuscript for publication. The views expressed in this paper 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. The UMCG, which employs Drs. Suthahar, Meems, Bakker, Gansevoort, and de Boer, has received research grants and/or fees from AstraZeneca, Abbott, Bristol-Myers Squibb, Novartis, Novo Nordisk, and Roche. Dr. Blaha has received grants and personal fees from Amgen and the U.S. Food and Drug Administration; has received grants from Aetna, the American Heart Association, and the National Institutes of Health; and has received personal fees from Sanofi, Regeneron, Novartis, and MedImmune. Dr. Psaty has served on a data and safety monitoring board for a clinical trial funded by the manufacturer (ZollLifeCor); and has served on the steering committee of the Yale Open Data Access Project funded by Johnson & Johnson. Dr. Benjamin has received grants from the National Institutes of Health and the American Heart Association/National Institutes of Health. Dr. Januzzi has received grants and personal fees from Roche, Abbott, Singulex, and Novartis; and has received personal fees from Critical Diagnostics, Janssen, Boehringer Ingelheim, Abbvie, Pfizer, General Electric, and Bayer. Dr. Cushman has received research funding in the form of assay costs from Sphingotec. Dr. Lee is supported by a Ted Rogers Chair in Heart Function Outcomes. Dr. DeFilippi has received research support from Roche Diagnostics; has received consulting fees from Roche, Siemens Healthcare Diagnostics, Alere, Metanomics, and Ortho Diagnostics; has served on the endpoint committee for Radiometer and Quintiles; and has received royalties from UpToDate. Dr. Herrington has received grants from the National Institutes of Health. Dr. Kizer has owned stock in Bristol-Myers Squibb, Johnson and Johnson, Medtronic, Merck, and Pfizer. Dr. Bertoni has received grants from the National Institutes of Health/National Heart, Lung, and Blood Institute. Dr. Shah has received research grants from Actelion, AstraZeneca, Corvia, Novartis, and Pfizer; and has received consulting fees from Abbott, Actelion, AstraZeneca, Amgen, Axon Therapeutics, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Cardiora, CVRx, Cytokinetics, Eisai, GlaxoSmithKline, Ionis, Ironwood, Merck, MyoKardia, Novartis, Pfizer, Sanofi, Shifamed, Tenax, and United Therapeutics. Dr. Ho has received grants from the National Institutes of Health and Gilead Sciences; and has received research support from Bayer and EcoNugenics. Dr. de Boer has received speaker fees from Abbott, AstraZeneca, Novartis, and Roche. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Javed Butler, MD, MPH, MBA, served as Guest Associate Editor for this paper. P.K. Shah, MD, served as Guest Editor-in-Chief for this paper.

Keywords

biomarkers
heart failure
predictive value
risk factors
sex differences

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.jacc.2020.07.044

Cite this

Suthahar, N., Lau, E. S., Blaha, M. J., Paniagua, S. M., Larson, M. G., Psaty, B. M., Benjamin, E. J., Allison, M. A., Bartz, T. M., Januzzi, J. L., Levy, D., Meems, L. M. G., Bakker, S. J. L., Lima, J. A. C., Cushman, M., Lee, D. S., Wang, T. J., deFilippi, C. R., Herrington, D. M., ... de Boer, R. A. (2020). Sex-Specific Associations of Cardiovascular Risk Factors and Biomarkers With Incident Heart Failure. Journal of the American College of Cardiology, 76(12), 1455-1465. https://doi.org/10.1016/j.jacc.2020.07.044

@article{5f607fc9c6394436b0aa93792ebf6875,

title = "Sex-Specific Associations of Cardiovascular Risk Factors and Biomarkers With Incident Heart Failure",

abstract = "Background: Whether cardiovascular (CV) disease risk factors and biomarkers associate differentially with heart failure (HF) risk in men and women is unclear. Objectives: The purpose of this study was to evaluate sex-specific associations of CV risk factors and biomarkers with incident HF. Methods: The analysis was performed using data from 4 community-based cohorts with 12.5 years of follow-up. Participants (recruited between 1989 and 2002) were free of HF at baseline. Biomarker measurements included natriuretic peptides, cardiac troponins, plasminogen activator inhibitor-1, D-dimer, fibrinogen, C-reactive protein, sST2, galectin-3, cystatin-C, and urinary albumin-to-creatinine ratio. Results: Among 22,756 participants (mean age 60 ± 13 years, 53% women), HF occurred in 2,095 participants (47% women). Age, smoking, type 2 diabetes mellitus, hypertension, body mass index, atrial fibrillation, myocardial infarction, left ventricular hypertrophy, and left bundle branch block were strongly associated with HF in both sexes (p < 0.001), and the combined clinical model had good discrimination in men (C-statistic = 0.80) and in women (C-statistic = 0.83). The majority of biomarkers were strongly and similarly associated with HF in both sexes. The clinical model improved modestly after adding natriuretic peptides in men (ΔC-statistic = 0.006; likelihood ratio chi-square = 146; p < 0.001), and after adding cardiac troponins in women (ΔC-statistic = 0.003; likelihood ratio chi-square = 73; p < 0.001). Conclusions: CV risk factors are strongly and similarly associated with incident HF in both sexes, highlighting the similar importance of risk factor control in reducing HF risk in the community. There are subtle sex-related differences in the predictive value of individual biomarkers, but the overall improvement in HF risk estimation when included in a clinical HF risk prediction model is limited in both sexes.",

keywords = "biomarkers, heart failure, predictive value, risk factors, sex differences",

author = "Navin Suthahar and Lau, {Emily S.} and Blaha, {Michael J.} and Paniagua, {Samantha M.} and Larson, {Martin G.} and Psaty, {Bruce M.} and Benjamin, {Emelia J.} and Allison, {Matthew A.} and Bartz, {Traci M.} and Januzzi, {James L.} and Daniel Levy and Meems, {Laura M.G.} and Bakker, {Stephan J.L.} and Lima, {Joao A.C.} and Mary Cushman and Lee, {Douglas S.} and Wang, {Thomas J.} and deFilippi, {Christopher R.} and Herrington, {David M.} and Matthew Nayor and Vasan, {Ramachandran S.} and Gardin, {Julius M.} and Kizer, {Jorge R.} and Bertoni, {Alain G.} and Allen, {Norrina B.} and Gansevoort, {Ron T.} and Shah, {Sanjiv J.} and Gottdiener, {John S.} and Ho, {Jennifer E.} and {de Boer}, {Rudolf A.}",

note = "Publisher Copyright: {\textcopyright} 2020 The Authors",

year = "2020",

month = sep,

day = "22",

doi = "10.1016/j.jacc.2020.07.044",

language = "English (US)",

volume = "76",

pages = "1455--1465",

journal = "Journal of the American College of Cardiology",

issn = "0735-1097",

publisher = "Elsevier USA",

number = "12",

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Suthahar, N, Lau, ES, Blaha, MJ, Paniagua, SM, Larson, MG, Psaty, BM, Benjamin, EJ, Allison, MA, Bartz, TM, Januzzi, JL, Levy, D, Meems, LMG, Bakker, SJL, Lima, JAC, Cushman, M, Lee, DS, Wang, TJ, deFilippi, CR, Herrington, DM, Nayor, M, Vasan, RS, Gardin, JM, Kizer, JR, Bertoni, AG, Allen, NB, Gansevoort, RT, Shah, SJ, Gottdiener, JS, Ho, JE & de Boer, RA 2020, 'Sex-Specific Associations of Cardiovascular Risk Factors and Biomarkers With Incident Heart Failure', Journal of the American College of Cardiology, vol. 76, no. 12, pp. 1455-1465. https://doi.org/10.1016/j.jacc.2020.07.044

TY - JOUR

T1 - Sex-Specific Associations of Cardiovascular Risk Factors and Biomarkers With Incident Heart Failure

AU - Suthahar, Navin

AU - Lau, Emily S.

AU - Blaha, Michael J.

AU - Paniagua, Samantha M.

AU - Larson, Martin G.

AU - Psaty, Bruce M.

AU - Benjamin, Emelia J.

AU - Allison, Matthew A.

AU - Bartz, Traci M.

AU - Januzzi, James L.

AU - Levy, Daniel

AU - Meems, Laura M.G.

AU - Bakker, Stephan J.L.

AU - Lima, Joao A.C.

AU - Cushman, Mary

AU - Lee, Douglas S.

AU - Wang, Thomas J.

AU - deFilippi, Christopher R.

AU - Herrington, David M.

AU - Nayor, Matthew

AU - Vasan, Ramachandran S.

AU - Gardin, Julius M.

AU - Kizer, Jorge R.

AU - Bertoni, Alain G.

AU - Allen, Norrina B.

AU - Gansevoort, Ron T.

AU - Shah, Sanjiv J.

AU - Gottdiener, John S.

AU - Ho, Jennifer E.

AU - de Boer, Rudolf A.

PY - 2020/9/22

Y1 - 2020/9/22

N2 - Background: Whether cardiovascular (CV) disease risk factors and biomarkers associate differentially with heart failure (HF) risk in men and women is unclear. Objectives: The purpose of this study was to evaluate sex-specific associations of CV risk factors and biomarkers with incident HF. Methods: The analysis was performed using data from 4 community-based cohorts with 12.5 years of follow-up. Participants (recruited between 1989 and 2002) were free of HF at baseline. Biomarker measurements included natriuretic peptides, cardiac troponins, plasminogen activator inhibitor-1, D-dimer, fibrinogen, C-reactive protein, sST2, galectin-3, cystatin-C, and urinary albumin-to-creatinine ratio. Results: Among 22,756 participants (mean age 60 ± 13 years, 53% women), HF occurred in 2,095 participants (47% women). Age, smoking, type 2 diabetes mellitus, hypertension, body mass index, atrial fibrillation, myocardial infarction, left ventricular hypertrophy, and left bundle branch block were strongly associated with HF in both sexes (p < 0.001), and the combined clinical model had good discrimination in men (C-statistic = 0.80) and in women (C-statistic = 0.83). The majority of biomarkers were strongly and similarly associated with HF in both sexes. The clinical model improved modestly after adding natriuretic peptides in men (ΔC-statistic = 0.006; likelihood ratio chi-square = 146; p < 0.001), and after adding cardiac troponins in women (ΔC-statistic = 0.003; likelihood ratio chi-square = 73; p < 0.001). Conclusions: CV risk factors are strongly and similarly associated with incident HF in both sexes, highlighting the similar importance of risk factor control in reducing HF risk in the community. There are subtle sex-related differences in the predictive value of individual biomarkers, but the overall improvement in HF risk estimation when included in a clinical HF risk prediction model is limited in both sexes.

AB - Background: Whether cardiovascular (CV) disease risk factors and biomarkers associate differentially with heart failure (HF) risk in men and women is unclear. Objectives: The purpose of this study was to evaluate sex-specific associations of CV risk factors and biomarkers with incident HF. Methods: The analysis was performed using data from 4 community-based cohorts with 12.5 years of follow-up. Participants (recruited between 1989 and 2002) were free of HF at baseline. Biomarker measurements included natriuretic peptides, cardiac troponins, plasminogen activator inhibitor-1, D-dimer, fibrinogen, C-reactive protein, sST2, galectin-3, cystatin-C, and urinary albumin-to-creatinine ratio. Results: Among 22,756 participants (mean age 60 ± 13 years, 53% women), HF occurred in 2,095 participants (47% women). Age, smoking, type 2 diabetes mellitus, hypertension, body mass index, atrial fibrillation, myocardial infarction, left ventricular hypertrophy, and left bundle branch block were strongly associated with HF in both sexes (p < 0.001), and the combined clinical model had good discrimination in men (C-statistic = 0.80) and in women (C-statistic = 0.83). The majority of biomarkers were strongly and similarly associated with HF in both sexes. The clinical model improved modestly after adding natriuretic peptides in men (ΔC-statistic = 0.006; likelihood ratio chi-square = 146; p < 0.001), and after adding cardiac troponins in women (ΔC-statistic = 0.003; likelihood ratio chi-square = 73; p < 0.001). Conclusions: CV risk factors are strongly and similarly associated with incident HF in both sexes, highlighting the similar importance of risk factor control in reducing HF risk in the community. There are subtle sex-related differences in the predictive value of individual biomarkers, but the overall improvement in HF risk estimation when included in a clinical HF risk prediction model is limited in both sexes.

KW - biomarkers

KW - heart failure

KW - predictive value

KW - risk factors

KW - sex differences

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DO - 10.1016/j.jacc.2020.07.044

M3 - Article

C2 - 32943164

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SN - 0735-1097

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JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

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ER -

Sex-Specific Associations of Cardiovascular Risk Factors and Biomarkers With Incident Heart Failure

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