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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Endothelialitis plays a central role in the pathophysiology of severe COVID-19 and its cardiovascular complications
Christiaan J M Vrints1,2, Konstantin A Krychtiuk3, Emeline M Van Craenenbroeck1,2
1Research Group Cardiovascular Diseases, Department GENCOR, University of Antwerp, Antwerp, Belgium.
Insights
Severe COVID-19 (coronavirus disease 2019) impacts the heart and lungs, causing endothelialitis and increasing risks for heart injury and blood clots. This review highlights critical cardiovascular care needs for severe cases.
Area of Science:
- Cardiology
- Infectious Diseases
- Pulmonology
Background:
- Severe COVID-19 (coronavirus disease 2019) disproportionately affects older individuals with comorbidities like obesity, diabetes, and hypertension.
- These comorbidities share pathophysiological pathways with severe SARS-CoV-2 infection, suggesting common underlying mechanisms.
- Endothelial dysfunction and impaired immunity are implicated in severe COVID-19 pathogenesis.
Purpose of the Study:
- To review the pathophysiology of pulmonary and cardiovascular manifestations in severe COVID-19.
- To discuss implications for acute cardiovascular care in intensive cardiac care units.
- To explore shared mechanisms between comorbidities and severe SARS-CoV-2 infection.
Main Methods:
- Literature review of clinical studies and reviews on COVID-19.
- Analysis of pathophysiological mechanisms linking SARS-CoV-2 infection to cardiovascular and pulmonary complications.
- Synthesis of information regarding acute cardiac care in severe COVID-19 patients.
Main Results:
- SARS-CoV-2 infection can cause acute endothelialitis in pulmonary and systemic circulation.
- Endothelialitis involves abnormal vasoconstriction, inflammatory cell plugging, and thrombosis.
- This can lead to acute myocardial injury, myocarditis, and thromboembolic events (arterial and venous).
Conclusions:
- Severe COVID-19 involves complex cardiovascular and pulmonary pathophysiology.
- Endothelial dysfunction is a key mechanism in severe SARS-CoV-2 infection.
- Urgent attention to acute cardiovascular care is crucial for patients with severe COVID-19.
Abstract:
This clinical review paper discusses the pathophysiology of the pulmonary and cardiovascular manifestations of a SARS-CoV-2 infection and the ensuing implications on acute cardiovascular care in patients presenting with a severe COVID-19 syndrome admitted to an intensive acute cardiac care unit. The high prevalence of old age, obesity, diabetes, hypertension, heart failure, and ischaemic heart disease in patients who develop a severe to critical COVID-19 syndrome suggests shared pathophysiological mechanisms. Pre-existing endothelial dysfunction and an impaired innate immune response promote the development by the viral infection of an acute endothelialitis in the pulmonary microcirculation complicated by abnormal vasoconstrictor responses, luminal plugging by inflammatory cells, and intravascular thrombosis. This endothelialitis extends into the systemic circulation what may lead to acute myocardial injury, myocarditis, and thromboembolic complications both in the arterial and venous circulation.
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