Endothelialitis plays a central role in the pathophysiology of severe COVID-19 and its cardiovascular complications.
Christiaan J M VrintsKonstantin A KrychtiukEmeline Van CraenenbroeckVincent F M SegersSusanna PriceHein HeidbuchelPublished in: Acta cardiologica (2020)
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.
Keyphrases
- liver failure
- drug induced
- immune response
- coronavirus disease
- sars cov
- respiratory failure
- heart failure
- healthcare
- pulmonary hypertension
- aortic dissection
- type diabetes
- palliative care
- blood pressure
- metabolic syndrome
- cardiovascular disease
- respiratory syndrome coronavirus
- hepatitis b virus
- case report
- weight loss
- coronary artery
- oxidative stress
- cell proliferation
- dendritic cells
- signaling pathway
- glycemic control
- body mass index
- inflammatory response
- acute respiratory distress syndrome
- cell death
- acute heart failure