TY - JOUR
T1 - Atrial inflammation and microvascular thrombogenicity are increased in deceased COVID-19 patients
AU - Wu, Linghe
AU - Jiang, Zhu
AU - Meulendijks, Eva R.
AU - Baylan, Umit
AU - Waas, Ingeborg S. E.
AU - Bugiani, Marianna
AU - Tuinman, Pieter R.
AU - Fronczek, Judith
AU - Heunks, Leo M. A.
AU - de Groot, Joris R.
AU - van Rossum, Albert C.
AU - Niessen, Hans W. M.
AU - Krijnen, Paul A. J.
N1 - Funding Information: Funding: This work was supported by the China Scholarship Council (Beijing, China, Grant number: 201708260020 to LW, 202008320278 to JZ); Amsterdam UMC Corona Research Fund Publisher Copyright: © 2023 The Author(s)
PY - 2023/5/1
Y1 - 2023/5/1
N2 - Background: Histopathological studies have shown inflammation, cardiomyocyte injury, and microvascular thrombosis in the ventricular myocardium of patients with coronavirus disease 2019 (COVID-19). However, although atrial dysfunction is common in COVID-19, little is known about histopathological changes in the atria of the heart. We therefore analyzed inflammation, cardiomyocyte injury, and microvascular thrombogenicity in the atria of deceased patients with COVID-19. Methods: Atrial tissue was obtained from autopsied COVID-19 (n=16) patients and control patients (n=10) and analyzed using immunohistochemistry. The infiltration of CD45+ leukocytes, CD3+ T lymphocytes, CD68+ macrophages, MPO+ neutrophils, and Tryptase+ mast cells were quantified as well as cardiomyocyte damage and microvascular thrombosis. In addition, Tissue Factor (TF) and Factor XII (FXII) were quantified as markers of microvascular thrombogenicity. Results: The numbers of lymphocytes, macrophages, and neutrophils were significantly increased in the atrial myocardium and epicardial atrial adipose tissue of COVID-19 patients compared with the control group. This was accompanied by dispersed cardiomyocyte injury, the occasional presence of microvascular thrombosis, and an increased presence of TF and FXII in the microvascular endothelium. Conclusions: Severe COVID-19 induces inflammation, cardiomyocyte injury, and microvascular thrombosis in the atria of the heart.
AB - Background: Histopathological studies have shown inflammation, cardiomyocyte injury, and microvascular thrombosis in the ventricular myocardium of patients with coronavirus disease 2019 (COVID-19). However, although atrial dysfunction is common in COVID-19, little is known about histopathological changes in the atria of the heart. We therefore analyzed inflammation, cardiomyocyte injury, and microvascular thrombogenicity in the atria of deceased patients with COVID-19. Methods: Atrial tissue was obtained from autopsied COVID-19 (n=16) patients and control patients (n=10) and analyzed using immunohistochemistry. The infiltration of CD45+ leukocytes, CD3+ T lymphocytes, CD68+ macrophages, MPO+ neutrophils, and Tryptase+ mast cells were quantified as well as cardiomyocyte damage and microvascular thrombosis. In addition, Tissue Factor (TF) and Factor XII (FXII) were quantified as markers of microvascular thrombogenicity. Results: The numbers of lymphocytes, macrophages, and neutrophils were significantly increased in the atrial myocardium and epicardial atrial adipose tissue of COVID-19 patients compared with the control group. This was accompanied by dispersed cardiomyocyte injury, the occasional presence of microvascular thrombosis, and an increased presence of TF and FXII in the microvascular endothelium. Conclusions: Severe COVID-19 induces inflammation, cardiomyocyte injury, and microvascular thrombosis in the atria of the heart.
KW - Atria
KW - Coagulation factors
KW - First and second wave COVID-19
KW - Inflammation
KW - Thrombi
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85149720917&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/36649811
UR - http://www.scopus.com/inward/record.url?scp=85149720917&partnerID=8YFLogxK
U2 - https://doi.org/10.1016/j.carpath.2023.107524
DO - https://doi.org/10.1016/j.carpath.2023.107524
M3 - Article
C2 - 36649811
SN - 1054-8807
VL - 64
JO - Cardiovascular pathology
JF - Cardiovascular pathology
M1 - 107524
ER -