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Published on: November 21, 2023
Atrial inflammation and microvascular thrombogenicity are increased in deceased COVID-19 patients
Linghe Wu1, Zhu Jiang1, Eva R Meulendijks2
1Department of Pathology, Amsterdam University Medical Centre (AUMC), Location VUmc, Amsterdam, The Netherlands; Amsterdam Cardiovascular Sciences, AUMC, Location VUmc, Amsterdam, The Netherlands; Department of Pathology, AUMC, location AMC, Amsterdam, The Netherlands.
Insights
Severe COVID-19 causes inflammation, heart muscle cell damage, and blood clots in the atria. This study investigated these histopathological changes in deceased patients with coronavirus disease 2019 (COVID-19).
Area of Science:
- Cardiovascular Pathology
- Infectious Disease Research
- Histopathology
Background:
- Previous studies identified ventricular myocardial changes in COVID-19 patients, including inflammation, cardiomyocyte injury, and microvascular thrombosis.
- Atrial dysfunction is frequently observed in COVID-19, yet atrial histopathological alterations remain poorly understood.
- This study aimed to investigate inflammation, cardiomyocyte injury, and microvascular thrombogenicity in the atria of deceased COVID-19 patients.
Purpose of the Study:
- To analyze histopathological changes in the atria of patients who died from COVID-19.
- To compare atrial inflammation, cardiomyocyte injury, and microvascular thrombogenicity between COVID-19 patients and controls.
Main Methods:
- Atrial tissue samples were collected from autopsied COVID-19 (n=16) and control (n=10) patients.
- Immunohistochemistry was used to quantify leukocyte, lymphocyte, macrophage, neutrophil, and mast cell infiltration.
- Cardiomyocyte damage, microvascular thrombosis, Tissue Factor (TF), and Factor XII (FXII) were assessed.
Main Results:
- COVID-19 patients showed significantly increased numbers of lymphocytes, macrophages, and neutrophils in atrial myocardium and epicardial adipose tissue compared to controls.
- Dispersed cardiomyocyte injury and occasional microvascular thrombosis were observed in COVID-19 patients.
- An increased presence of TF and FXII was noted in the microvascular endothelium of COVID-19 patients.
Conclusions:
- Severe COVID-19 is associated with significant inflammation in the heart's atria.
- Cardiomyocyte injury and microvascular thrombosis are key histopathological findings in the atria of severe COVID-19 cases.
- These findings highlight the direct impact of COVID-19 on atrial cardiac tissue.
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.
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