Ultrasensitive Troponin I and Incident Cardiovascular Disease

Jean-Philippe Empana; Ivan Lerner; Marie-Cécile Perier; Catherine Guibout; Patricia Jabre; Karine Bailly; Muriel Andrieu; Rachel Climie; Thomas van Sloten; Benoit Vedie; Daniela Geromin; Eloi Marijon; Frederique Thomas; Nicolas Danchin; Pierre Boutouyrie; Xavier Jouven

doi:10.1161/atvbaha.122.317961

Ultrasensitive Troponin I and Incident Cardiovascular Disease

Jean-Philippe Empana^*, Ivan Lerner, Marie-Cécile Perier, Catherine Guibout, Patricia Jabre, Karine Bailly, Muriel Andrieu, Rachel Climie, Thomas van Sloten, Benoit Vedie, Daniela Geromin, Eloi Marijon, Frederique Thomas, Nicolas Danchin, Pierre Boutouyrie, Xavier Jouven

^*Corresponding author for this work

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

53 Downloads (Pure)

Abstract

BACKGROUND: To examine the association of ultrasensitive cTnI (cardiac troponin I) with incident cardiovascular disease events (CVDs) in the primary prevention setting.

METHODS: cTnI was analyzed in the baseline plasma (2008-2012) of CVD-free volunteers from the Paris Prospective Study III using a novel ultrasensitive immunoassay (Simoa Troponin-I 2.0 Kit, Quanterix, Lexington) with a limit of detection of 0.013 pg/mL. Incident CVD hospitalizations (coronary heart disease, stroke, cardiac arrhythmias, deep venous thrombosis or pulmonary embolism, heart failure, or arterial aneurysm) were validated by critical review of the hospital records. Hazard ratios were estimated per log-transformed SD increase of cTnI in Cox models using age as the time scale.

RESULTS: The study population includes 9503 participants (40% women) aged 59.6 (6.3) years. cTnI was detected in 99.6% of the participants (median value=0.63 pg/mL, interquartile range, 0.39-1.09). After a median follow-up of 8.34 years (interquartile range, 8.0-10.07), 516 participants suffered 612 events. In fully adjusted analysis, higher cTnI (per 1 SD increase of log cTnI) was significantly associated with CVD events combined (hazard ratio, 1.18 [1.08-1.30]). Among all single risk factors, cTnI had the highest discrimination capacity for incident CVD events (C index=0.6349). Adding log cTnI to the SCORE 2 (Systematic Coronary Risk Evaluation) risk improved moderately discriminatory capacity (C index 0.698 versus 0.685; bootstrapped C index difference: 0.0135 [95% CI, 0.0131-0.0138]), and reclassification of the participants (categorical net reclassification index, 0.0628 [95% CI, 0.023-0.102]). Findings were consistent using the US pooled cohort risk equation.

CONCLUSIONS: Ultrasensitive cTnI is an independent marker of CVD events in the primary prevention setting.

Original language	English
Pages (from-to)	1471-1481
Number of pages	11
Journal	Arteriosclerosis Thrombosis and Vascular Biology
Volume	42
Issue number	12
DOIs	https://doi.org/10.1161/atvbaha.122.317961
Publication status	Published - Dec 2022

Keywords

Female
Humans
Male
Biomarkers
Cardiovascular Diseases/diagnosis
Prognosis
Prospective Studies
Risk Factors
Troponin I
Middle Aged

Access to Document

10.1161/atvbaha.122.317961

Full TextFinal published version, 761 KBLicence: Taverne

Cite this

Empana, J.-P., Lerner, I., Perier, M.-C., Guibout, C., Jabre, P., Bailly, K., Andrieu, M., Climie, R., van Sloten, T., Vedie, B., Geromin, D., Marijon, E., Thomas, F., Danchin, N., Boutouyrie, P., & Jouven, X. (2022). Ultrasensitive Troponin I and Incident Cardiovascular Disease. Arteriosclerosis Thrombosis and Vascular Biology, 42(12), 1471-1481. https://doi.org/10.1161/atvbaha.122.317961

@article{6a033e2f95134933acfd44170be9303b,

title = "Ultrasensitive Troponin I and Incident Cardiovascular Disease",

abstract = "BACKGROUND: To examine the association of ultrasensitive cTnI (cardiac troponin I) with incident cardiovascular disease events (CVDs) in the primary prevention setting.METHODS: cTnI was analyzed in the baseline plasma (2008-2012) of CVD-free volunteers from the Paris Prospective Study III using a novel ultrasensitive immunoassay (Simoa Troponin-I 2.0 Kit, Quanterix, Lexington) with a limit of detection of 0.013 pg/mL. Incident CVD hospitalizations (coronary heart disease, stroke, cardiac arrhythmias, deep venous thrombosis or pulmonary embolism, heart failure, or arterial aneurysm) were validated by critical review of the hospital records. Hazard ratios were estimated per log-transformed SD increase of cTnI in Cox models using age as the time scale.RESULTS: The study population includes 9503 participants (40% women) aged 59.6 (6.3) years. cTnI was detected in 99.6% of the participants (median value=0.63 pg/mL, interquartile range, 0.39-1.09). After a median follow-up of 8.34 years (interquartile range, 8.0-10.07), 516 participants suffered 612 events. In fully adjusted analysis, higher cTnI (per 1 SD increase of log cTnI) was significantly associated with CVD events combined (hazard ratio, 1.18 [1.08-1.30]). Among all single risk factors, cTnI had the highest discrimination capacity for incident CVD events (C index=0.6349). Adding log cTnI to the SCORE 2 (Systematic Coronary Risk Evaluation) risk improved moderately discriminatory capacity (C index 0.698 versus 0.685; bootstrapped C index difference: 0.0135 [95% CI, 0.0131-0.0138]), and reclassification of the participants (categorical net reclassification index, 0.0628 [95% CI, 0.023-0.102]). Findings were consistent using the US pooled cohort risk equation.CONCLUSIONS: Ultrasensitive cTnI is an independent marker of CVD events in the primary prevention setting.",

keywords = "Female, Humans, Male, Biomarkers, Cardiovascular Diseases/diagnosis, Prognosis, Prospective Studies, Risk Factors, Troponin I, Middle Aged",

author = "Jean-Philippe Empana and Ivan Lerner and Marie-C{\'e}cile Perier and Catherine Guibout and Patricia Jabre and Karine Bailly and Muriel Andrieu and Rachel Climie and {van Sloten}, Thomas and Benoit Vedie and Daniela Geromin and Eloi Marijon and Frederique Thomas and Nicolas Danchin and Pierre Boutouyrie and Xavier Jouven",

note = "Funding Information: Acknowledgments We thank the assistant research team who has performed the study recruitment of PPS-3 (Paris Prospective Study III) participants, the medical, and technical staff of the Centre d'Investigations Pr{\'e}ventives et Cliniques (IPC), and the Platform for Biological Resources (PRB) of the H{\^o}pital Europ{\'e}en Georges Pompidou for the management of the biobank. We also thank the staff of the Cochin Cytometry and Immunobiology core facility (CYBIO) for the measurements of CRP (Creactive protein), IL (interleukin)-6, NT-proBNP (N-terminal pro-brain natriuretic peptide), and troponin I. We thank the assistant research team of PPS-3 including R. Bentaleb and M. Pernet for performing the follow-up of the participants. PPS- 3 is organized under an agreement between Institut National de la Sant{\'e} et de la Recherche M{\'e}dicale (INSERM) and the IPC Center and between INSERM and the Resources Biologiques de l'H{\^o}pital European Georges Pompidou, Paris, France. We also thank the Caisse Nationale d'Assurance Maladie des Travailleurs Salari{\'e}s (CNAM-TS, France) and the Caisse Primaire d'Assurance Maladie de Paris (CPAM-P, France) for helping make this study possible. Sources of Funding The PPS-3 (Paris Prospective Study III) was supported by grants from The National Research Agency (ANR), the Research Foundation for Hypertension (RFHTA), the Research Institute in Public Health (IRESP), the Region Ile de France (Domaine d'Int{\'e}r{\^e}t Majeur), and a European Horizon H2020 grant. Funding Information: The PPS-3 (Paris Prospective Study III) was supported by grants from The National Research Agency (ANR), the Research Foundation for Hypertension (RFHTA), the Research Institute in Public Health (IRESP), the Region Ile de France (Domaine d{\textquoteright}Int{\'e}r{\^e}t Majeur), and a European Horizon H2020 grant. Publisher Copyright: {\textcopyright} 2022 American Heart Association, Inc.",

year = "2022",

month = dec,

doi = "10.1161/atvbaha.122.317961",

language = "English",

volume = "42",

pages = "1471--1481",

journal = "Arteriosclerosis Thrombosis and Vascular Biology",

issn = "1079-5642",

publisher = "LIPPINCOTT WILLIAMS & WILKINS",

number = "12",

}

Empana, J-P, Lerner, I, Perier, M-C, Guibout, C, Jabre, P, Bailly, K, Andrieu, M, Climie, R, van Sloten, T, Vedie, B, Geromin, D, Marijon, E, Thomas, F, Danchin, N, Boutouyrie, P & Jouven, X 2022, 'Ultrasensitive Troponin I and Incident Cardiovascular Disease', Arteriosclerosis Thrombosis and Vascular Biology, vol. 42, no. 12, pp. 1471-1481. https://doi.org/10.1161/atvbaha.122.317961

TY - JOUR

T1 - Ultrasensitive Troponin I and Incident Cardiovascular Disease

AU - Empana, Jean-Philippe

AU - Lerner, Ivan

AU - Perier, Marie-Cécile

AU - Guibout, Catherine

AU - Jabre, Patricia

AU - Bailly, Karine

AU - Andrieu, Muriel

AU - Climie, Rachel

AU - van Sloten, Thomas

AU - Vedie, Benoit

AU - Geromin, Daniela

AU - Marijon, Eloi

AU - Thomas, Frederique

AU - Danchin, Nicolas

AU - Boutouyrie, Pierre

AU - Jouven, Xavier

N1 - Funding Information: Acknowledgments We thank the assistant research team who has performed the study recruitment of PPS-3 (Paris Prospective Study III) participants, the medical, and technical staff of the Centre d'Investigations Préventives et Cliniques (IPC), and the Platform for Biological Resources (PRB) of the Hôpital Européen Georges Pompidou for the management of the biobank. We also thank the staff of the Cochin Cytometry and Immunobiology core facility (CYBIO) for the measurements of CRP (Creactive protein), IL (interleukin)-6, NT-proBNP (N-terminal pro-brain natriuretic peptide), and troponin I. We thank the assistant research team of PPS-3 including R. Bentaleb and M. Pernet for performing the follow-up of the participants. PPS- 3 is organized under an agreement between Institut National de la Santé et de la Recherche Médicale (INSERM) and the IPC Center and between INSERM and the Resources Biologiques de l'Hôpital European Georges Pompidou, Paris, France. We also thank the Caisse Nationale d'Assurance Maladie des Travailleurs Salariés (CNAM-TS, France) and the Caisse Primaire d'Assurance Maladie de Paris (CPAM-P, France) for helping make this study possible. Sources of Funding The PPS-3 (Paris Prospective Study III) was supported by grants from The National Research Agency (ANR), the Research Foundation for Hypertension (RFHTA), the Research Institute in Public Health (IRESP), the Region Ile de France (Domaine d'Intérêt Majeur), and a European Horizon H2020 grant. Funding Information: The PPS-3 (Paris Prospective Study III) was supported by grants from The National Research Agency (ANR), the Research Foundation for Hypertension (RFHTA), the Research Institute in Public Health (IRESP), the Region Ile de France (Domaine d’Intérêt Majeur), and a European Horizon H2020 grant. Publisher Copyright: © 2022 American Heart Association, Inc.

PY - 2022/12

Y1 - 2022/12

N2 - BACKGROUND: To examine the association of ultrasensitive cTnI (cardiac troponin I) with incident cardiovascular disease events (CVDs) in the primary prevention setting.METHODS: cTnI was analyzed in the baseline plasma (2008-2012) of CVD-free volunteers from the Paris Prospective Study III using a novel ultrasensitive immunoassay (Simoa Troponin-I 2.0 Kit, Quanterix, Lexington) with a limit of detection of 0.013 pg/mL. Incident CVD hospitalizations (coronary heart disease, stroke, cardiac arrhythmias, deep venous thrombosis or pulmonary embolism, heart failure, or arterial aneurysm) were validated by critical review of the hospital records. Hazard ratios were estimated per log-transformed SD increase of cTnI in Cox models using age as the time scale.RESULTS: The study population includes 9503 participants (40% women) aged 59.6 (6.3) years. cTnI was detected in 99.6% of the participants (median value=0.63 pg/mL, interquartile range, 0.39-1.09). After a median follow-up of 8.34 years (interquartile range, 8.0-10.07), 516 participants suffered 612 events. In fully adjusted analysis, higher cTnI (per 1 SD increase of log cTnI) was significantly associated with CVD events combined (hazard ratio, 1.18 [1.08-1.30]). Among all single risk factors, cTnI had the highest discrimination capacity for incident CVD events (C index=0.6349). Adding log cTnI to the SCORE 2 (Systematic Coronary Risk Evaluation) risk improved moderately discriminatory capacity (C index 0.698 versus 0.685; bootstrapped C index difference: 0.0135 [95% CI, 0.0131-0.0138]), and reclassification of the participants (categorical net reclassification index, 0.0628 [95% CI, 0.023-0.102]). Findings were consistent using the US pooled cohort risk equation.CONCLUSIONS: Ultrasensitive cTnI is an independent marker of CVD events in the primary prevention setting.

AB - BACKGROUND: To examine the association of ultrasensitive cTnI (cardiac troponin I) with incident cardiovascular disease events (CVDs) in the primary prevention setting.METHODS: cTnI was analyzed in the baseline plasma (2008-2012) of CVD-free volunteers from the Paris Prospective Study III using a novel ultrasensitive immunoassay (Simoa Troponin-I 2.0 Kit, Quanterix, Lexington) with a limit of detection of 0.013 pg/mL. Incident CVD hospitalizations (coronary heart disease, stroke, cardiac arrhythmias, deep venous thrombosis or pulmonary embolism, heart failure, or arterial aneurysm) were validated by critical review of the hospital records. Hazard ratios were estimated per log-transformed SD increase of cTnI in Cox models using age as the time scale.RESULTS: The study population includes 9503 participants (40% women) aged 59.6 (6.3) years. cTnI was detected in 99.6% of the participants (median value=0.63 pg/mL, interquartile range, 0.39-1.09). After a median follow-up of 8.34 years (interquartile range, 8.0-10.07), 516 participants suffered 612 events. In fully adjusted analysis, higher cTnI (per 1 SD increase of log cTnI) was significantly associated with CVD events combined (hazard ratio, 1.18 [1.08-1.30]). Among all single risk factors, cTnI had the highest discrimination capacity for incident CVD events (C index=0.6349). Adding log cTnI to the SCORE 2 (Systematic Coronary Risk Evaluation) risk improved moderately discriminatory capacity (C index 0.698 versus 0.685; bootstrapped C index difference: 0.0135 [95% CI, 0.0131-0.0138]), and reclassification of the participants (categorical net reclassification index, 0.0628 [95% CI, 0.023-0.102]). Findings were consistent using the US pooled cohort risk equation.CONCLUSIONS: Ultrasensitive cTnI is an independent marker of CVD events in the primary prevention setting.

KW - Female

KW - Humans

KW - Male

KW - Biomarkers

KW - Cardiovascular Diseases/diagnosis

KW - Prognosis

KW - Prospective Studies

KW - Risk Factors

KW - Troponin I

KW - Middle Aged

U2 - 10.1161/atvbaha.122.317961

DO - 10.1161/atvbaha.122.317961

M3 - Article

C2 - 36325900

SN - 1079-5642

VL - 42

SP - 1471

EP - 1481

JO - Arteriosclerosis Thrombosis and Vascular Biology

JF - Arteriosclerosis Thrombosis and Vascular Biology

IS - 12

ER -

Ultrasensitive Troponin I and Incident Cardiovascular Disease

Abstract

Keywords

Access to Document

Fingerprint

Cite this