Increased Prevalence of Myocardial Injury in Patients with SARS-CoV-2 Viremia.


Journal

The American journal of medicine
ISSN: 1555-7162
Titre abrégé: Am J Med
Pays: United States
ID NLM: 0267200

Informations de publication

Date de publication:
04 2021
Historique:
received: 15 09 2020
accepted: 16 09 2020
pubmed: 13 11 2020
medline: 4 5 2021
entrez: 12 11 2020
Statut: ppublish

Résumé

Patients with coronavirus disease 2019 (COVID-19) have a high prevalence of detectable troponin and myocardial injury. In addition, a subset of patients with COVID-19 has detectable severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral loads. The objective of this study was to understand the relationship among SARS-CoV-2 viremia, detectable troponin, and myocardial injury in hospitalized patients with COVID-19. SARS-CoV-2 plasma viral load was measured in plasma samples drawn from patients hospitalized for COVID-19 at 2 academic medical centers. Baseline characteristics and clinically obtained high-sensitivity cardiac troponin T (hs-cTnT) values were abstracted from the medical record. The main outcome was detectable hs-cTnT (≥6 ng/mL) and  myocardial injury (hs-cTnT ≥14 ng/mL; >99th percentile for assay). A total of 70 hospitalized patients with COVID-19 were included in this study, with 39% females and median age 58 ± 17 years; 21 patients (30%) were found to have detectable SARS-CoV-2 viral load and were classified in the viremia group. Patients with viremia were significantly older than those without viremia. All of the patients with viremia (100%) had detectable troponin during hospitalization compared with 59% of patients without viremia (P = 0.0003). Myocardial injury was seen in 76% of patients with viremia and 38% of those patients without viremia (P = 0.004). Hospitalized patients with COVID-19 with SARS-CoV-2 viremia have a significantly higher prevalence of detectable troponin and myocardial injury during their hospitalization compared with patients who did not. This first report of the relationship among SARS-CoV-2 viremia, detectable troponin, and myocardial injury in patients with COVID-19 points to additional mechanistic pathways that require deeper study to understand the complex interplay among these unique findings, cardiovascular outcomes, and mortality in COVID-19.

Sections du résumé

BACKGROUND
Patients with coronavirus disease 2019 (COVID-19) have a high prevalence of detectable troponin and myocardial injury. In addition, a subset of patients with COVID-19 has detectable severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral loads. The objective of this study was to understand the relationship among SARS-CoV-2 viremia, detectable troponin, and myocardial injury in hospitalized patients with COVID-19.
METHODS
SARS-CoV-2 plasma viral load was measured in plasma samples drawn from patients hospitalized for COVID-19 at 2 academic medical centers. Baseline characteristics and clinically obtained high-sensitivity cardiac troponin T (hs-cTnT) values were abstracted from the medical record. The main outcome was detectable hs-cTnT (≥6 ng/mL) and  myocardial injury (hs-cTnT ≥14 ng/mL; >99th percentile for assay).
RESULTS
A total of 70 hospitalized patients with COVID-19 were included in this study, with 39% females and median age 58 ± 17 years; 21 patients (30%) were found to have detectable SARS-CoV-2 viral load and were classified in the viremia group. Patients with viremia were significantly older than those without viremia. All of the patients with viremia (100%) had detectable troponin during hospitalization compared with 59% of patients without viremia (P = 0.0003). Myocardial injury was seen in 76% of patients with viremia and 38% of those patients without viremia (P = 0.004).
CONCLUSIONS
Hospitalized patients with COVID-19 with SARS-CoV-2 viremia have a significantly higher prevalence of detectable troponin and myocardial injury during their hospitalization compared with patients who did not. This first report of the relationship among SARS-CoV-2 viremia, detectable troponin, and myocardial injury in patients with COVID-19 points to additional mechanistic pathways that require deeper study to understand the complex interplay among these unique findings, cardiovascular outcomes, and mortality in COVID-19.

Identifiants

pubmed: 33181107
pii: S0002-9343(20)30933-5
doi: 10.1016/j.amjmed.2020.09.046
pmc: PMC7654293
pii:
doi:

Substances chimiques

Troponin 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

542-546

Subventions

Organisme : NHLBI NIH HHS
ID : T32 HL094301
Pays : United States

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Références

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Auteurs

Hasan K Siddiqi (HK)

Heart and Vascular Center, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.

Brittany Weber (B)

Heart and Vascular Center, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass; Cardiovascular Imaging Program, Departments of Medicine and Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.

Guohai Zhou (G)

Center for Clinical Investigation, Brigham and Women's Hospital, Boston, Mass.

James Regan (J)

Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.

Jesse Fajnzylber (J)

Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.

Kendyll Coxen (K)

Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.

Heather Corry (H)

Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.

Xu G Yu (XG)

Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass; Massachusetts General Hospital, Harvard Medical School, Boston, Mass; Ragon Institute of MGH, MIT and Harvard University, Boston, Mass.

Marcelo DiCarli (M)

Heart and Vascular Center, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass; Cardiovascular Imaging Program, Departments of Medicine and Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.

Jonathan Z Li (JZ)

Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.

Deepak L Bhatt (DL)

Heart and Vascular Center, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass. Electronic address: dlbhattmd@post.harvard.edu.

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