Hyperinflammation as underlying mechanism predisposing patie
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It was already realized early in the COVID-19 pandemic that patients with cardiovascular disease, such as arterial hypertension, have a higher risk for an adverse course of COVID-19, raising the question of the underlying mechanisms. Furthermore, when it was described that the viral spike (S) glycoprotein mediates viral entry via binding to the angiotensin-converting enzyme 2 (ACE2), the question was raised whether therapies acting on the renin-angiotensin system, such as ACE inhibitors (ACEI) or angiotensin receptor blockers (ARBs), could affect the risk of infection or the clinical course of COVID-19. In a recent study, both aspects have been approached by using in-depth single-cell sequencing data of airway samples.

Notably, a distinct inflammatory predisposition of different immune cell subtypes relevant to COVID-19 was observed in patients with hypertension that correlated with critical disease progression but was already present before SARS-CoV-2 infection, i.e. in SARS-CoV-2-negative patients with hypertension.

Moreover, immune activation in hypertensive patients was largely augmented under COVID-19 providing a novel potential explanation for the adverse course of the disease related to a hyperinflammatory response in these patients with cardiovascular disease. Notably, in the RECOVERY trial treatment with dexamethasone reduced mortality among patients with COVID-19 who were receiving either oxygen alone or invasive mechanical ventilation, supporting the concept that immune dysregulation contributes to the critical clinical course of the disease.

In the single-cell sequencing study of airway samples, no difference in ACE2 expression and initial viral concentration was observed among patients with hypertension or cardiovascular disease. Furthermore, ACE2 expression was not altered in patients receiving ACEI/ARB treatment in both, SARS-CoV-2-positive and -negative patients.

These data are in line with observational studies that did not support an increased risk of infection with ACEI/ARB treatment and further support the ESC recommendation not to interrupt ACEI/ARB treatment in the COVID-19 pandemic. The impact of ACE inhibition or ARB treatment on the clinical course of COVID-19 is currently further examined in several randomized clinical studies.

Source: https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehab191/6209437?rss=1