Longitudinal Changes in Cardiac Troponin and Risk of Heart Failure Among Black Adults.


Journal

Journal of cardiac failure
ISSN: 1532-8414
Titre abrégé: J Card Fail
Pays: United States
ID NLM: 9442138

Informations de publication

Date de publication:
01 2023
Historique:
received: 30 07 2021
revised: 17 05 2022
accepted: 18 05 2022
pubmed: 12 6 2022
medline: 17 1 2023
entrez: 11 6 2022
Statut: ppublish

Résumé

Among Black adults, high-sensitivity cardiac troponin I (hs-cTnI) is associated with heart failure (HF) risk. The association of longitudinal changes in hs-cTnI with risk of incident HF, HF with reduced and preserved ejection fraction (HFrEF and HFpEF, respectively), among Black adults is not well-established. This study included Black participants from the Jackson Heart Study with available hs-cTnI data at visits 1 (2000-2004) and 2 (2005-2008) and no history of cardiovascular disease. Cox models were used to evaluate associations of categories of longitudinal change in hs-cTnI with incident HF risk. Among 2423 participants, 11.6% had incident elevation in hs-cTnI at visit 2, and 16.9% had stable or improved elevation (≤50% increase in hs-cTnI), and 4.0% had worsened hs-cTnI elevation (>50% increase). Over a median follow-up of 12.0 years, there were 139 incident HF hospitalizations (64 HFrEF, 58 HFpEF). Compared with participants without an elevated hs-cTnI, those with incident, stable or improved, or worsened hs-cTnI elevation had higher HF risk (adjusted hazard ratio 3.20 [95% confidence interval, 1.92-5.33]; adjusted hazard ratio 2.40, [95% confidence interval, 1.47-3.92]; and adjusted hazard ratio 8.10, [95% confidence interval, 4.74-13.83], respectively). Similar patterns of association were observed for risk of HFrEF and HFpEF. Among Black adults, an increase in hs-cTnI levels on follow-up was associated with a higher HF risk. The present study included 2423 Black adults from the Jackson Heart Study with available biomarkers of cardiac injury and no history of cardiovascular disease at visits 1 and 2. The majority of participants did not have evidence of cardiac injury at both visits (67.5%), 11.6% had evidence of cardiac injury only on follow-up, 14.5% had stable elevations, 4.0% had worsened elevations, and 2.4% had improved elevations of cardiac injury biomarkers during follow-up. Compared with participants without evidence of cardiac injury, those with new, stable, and worsened levels of cardiac injury had a higher risk of developing heart failure. Among Black adults, persistent or worsening subclinical myocardial injury is associated with an elevated risk of HF.

Sections du résumé

BACKGROUND
Among Black adults, high-sensitivity cardiac troponin I (hs-cTnI) is associated with heart failure (HF) risk. The association of longitudinal changes in hs-cTnI with risk of incident HF, HF with reduced and preserved ejection fraction (HFrEF and HFpEF, respectively), among Black adults is not well-established.
METHODS AND RESULTS
This study included Black participants from the Jackson Heart Study with available hs-cTnI data at visits 1 (2000-2004) and 2 (2005-2008) and no history of cardiovascular disease. Cox models were used to evaluate associations of categories of longitudinal change in hs-cTnI with incident HF risk. Among 2423 participants, 11.6% had incident elevation in hs-cTnI at visit 2, and 16.9% had stable or improved elevation (≤50% increase in hs-cTnI), and 4.0% had worsened hs-cTnI elevation (>50% increase). Over a median follow-up of 12.0 years, there were 139 incident HF hospitalizations (64 HFrEF, 58 HFpEF). Compared with participants without an elevated hs-cTnI, those with incident, stable or improved, or worsened hs-cTnI elevation had higher HF risk (adjusted hazard ratio 3.20 [95% confidence interval, 1.92-5.33]; adjusted hazard ratio 2.40, [95% confidence interval, 1.47-3.92]; and adjusted hazard ratio 8.10, [95% confidence interval, 4.74-13.83], respectively). Similar patterns of association were observed for risk of HFrEF and HFpEF.
CONCLUSIONS
Among Black adults, an increase in hs-cTnI levels on follow-up was associated with a higher HF risk.
LAY SUMMARY
The present study included 2423 Black adults from the Jackson Heart Study with available biomarkers of cardiac injury and no history of cardiovascular disease at visits 1 and 2. The majority of participants did not have evidence of cardiac injury at both visits (67.5%), 11.6% had evidence of cardiac injury only on follow-up, 14.5% had stable elevations, 4.0% had worsened elevations, and 2.4% had improved elevations of cardiac injury biomarkers during follow-up. Compared with participants without evidence of cardiac injury, those with new, stable, and worsened levels of cardiac injury had a higher risk of developing heart failure.
TWEET
Among Black adults, persistent or worsening subclinical myocardial injury is associated with an elevated risk of HF.

Identifiants

pubmed: 35690315
pii: S1071-9164(22)00542-5
doi: 10.1016/j.cardfail.2022.05.013
pii:
doi:

Substances chimiques

Troponin I 0
Biomarkers 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

6-15

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 Elsevier Inc. All rights reserved.

Auteurs

Amit Saha (A)

Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.

Kershaw V Patel (KV)

Department of Cardiology, Houston Methodist DeBakey Heart & Vascular Center, Houston, Texas.

Colby Ayers (C)

Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.

Christie M Ballantyne (CM)

Department of Medicine, Baylor College of Medicine, Houston, Texas.

Adolfo Correa (A)

Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi.

Christopher Defilippi (C)

Inova Heart and Vascular Institute, Falls Church, Virginia.

Michael E Hall (ME)

Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi.

Robert J Mentz (RJ)

Division of Cardiology, Duke Clinical Research Institute, Durham, North Carolina.

Stephen L Seliger (SL)

Division of Nephrology, University of Maryland School of Medicine, Baltimore, Maryland.

Wondwosen Yimer (W)

Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi.

Javed Butler (J)

Baylor Scott and White Research Institute, Dallas, TX.

Jarett D Berry (JD)

Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.

James A De Lemos (JA)

Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.

Ambarish Pandey (A)

Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas. Electronic address: AMBARISH.PANDEY@utsouthwestern.edu.

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