COVID-19 precipitates an interstitial pneumonia that evolves through acute respiratory distress syndrome (ARDS). However, there is an increasing amount of evidence that COVID-19 not only causes lung damage, but is a thrombo-inflammatory disease with the endothelial cells as primary targets (1). Endothelial injury and dysfunction may be the result of direct infection by SARS-CoV-2 as well as due to the profound systemic inflammatory response. The endothelium is crucial for maintaining vascular tone and homeostasis – dysfunction is associated with vasoconstriction, inflammation, permeability, and coagulation. Therefore, increasingly more attention is turned to extrapulmonary COVID-19 complications related to endothelial dysfunction.

In severe COVID-19, evidence of acute myocardial injury (elevation of cardiac troponins) is common, and is associated with impaired prognosis. Puntmann et al. showed that the majority of patients who had recovered from COVID-19, had cardiac damage in the cardiac MRI (2). Acute kidney injury occurs in up to half of patients hospitalized with COVID-19. Recent evidence shows that in these patients the reduction may persist longterm (3). There is an increasing recognition of COVID-19 induced neurological manifestations, including loss of smell and taste, encephalitis, and acute cerebrovascular complications (4,5).

Accumulating evidence points toward an important role of endothelial dysfunction in the pathogenesis of COVID-19. Therapies aiming to improve endothelial dysfunction such as RAS inhibitors or statins may be particularly helpful to prevent and manage systemic complications of SARS-CoV-2 infection. These drugs should be prescribed or continued in patients with COVID-19 if indicated (6).

There is ongoing research in the area of cardiovascular complications of COVID-19. Major societies are gathering updates on this subject on their dedicated web pages and can be followed:

1. Nägele MP, Haubner B, Tanner FC, Ruschitzka F, Flammer AJ. Endothelial dysfunction in COVID-19: Current findings and therapeutic implications. Atherosclerosis. 2020 Dec;314:58-62.
2. Puntmann VO, Carerj ML, Wieters I, Fahim M, Arendt C, Hoffmann J, et al. Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. 2020;5:1265-1273.
3.Nugent J, Aklilu A, Yamamoto Y, Simonov M, Li F, Biswas A, Ghazi L, et al. Assessment of Acute Kidney Injury and Longitudinal Kidney Function After Hospital Discharge Among Patients With and Without COVID-19. JAMA Netw Open. 2021;4:e211095.
4. Ellul MA, Benjamin L, Singh B, Lant S, Michael BD, Easton A, Kneen R, Defres S, Sejvar J, Solomon T. Neurological associations of COVID-19. Lancet Neurol. 2020 Sep;19(9):767-783. doi: 10.1016/S1474-4422(20)30221-0. Epub 2020 Jul 2. PMID: 32622375; PMCID: PMC7332267.
5. Sashindranath M, Nandurkar HH. Endothelial Dysfunction in the Brain: Setting the Stage for Stroke and Other Cerebrovascular Complications of COVID-19. Stroke. 2021;52:1895-1904.
6. Morales DR, Conover MM, You SC, Pratt N, Kostka K, Duarte-Salles T, et al. Renin-angiotensin system blockers and susceptibility to COVID-19: an international, open science, cohort analysis. Lancet Digit Health. 2021;3:e98-e114.

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