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.
Abstract

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