COVID-19 could damage arteries, other organs as well as lungs

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In a new study, researchers found that COVID-19, the disease caused by SARS-CoV-2, not only may lead to severe pneumonia but also to thrombosis in the lungs and, subsequently, to multi-organ failure involving kidneys, liver, and pancreas.

The research was conducted by a team at the Hospital Graz II and elsewhere in Austria.

According to the team, COVID-19 is not purely a respiratory disease affecting the lungs.

They conducted autopsies on patients who had died from COVID-19 and analyzed the results of the first 11 cases.

The results showed that, although the disease started with lung damage, this was usually followed by thrombosis in the pulmonary arteries themselves and damage to other organs in those fatal cases.

As in a heart attack or stroke, thrombosis (occlusion of blood vessels by blood clots) can directly occlude blood vessels, leading to tissue death (infarction).

Although COVID-19 predominantly causes inflammation of the pulmonary alveoli, the accompanying reaction in the small arteries often seems to trigger blood clotting, which, especially in patients with pre-existing cardiovascular disease, can slow down pulmonary circulation, subsequently resulting in thrombosis in the lung arteries.

This results in rapidly progressing respiratory insufficiency and circulatory failure, which is the primary cause of death in COVID-19.

COVID-19 also affects a series of other organs such as the kidneys, liver, pancreas, adrenal glands, and lymphatic system.

It is not yet clear whether the disease causes long-term damage to the affected organs.

Other reports of COVID-19 patients who have suffered deep vein thrombosis with pulmonary embolism and strokes support the premise that an increased tendency to thrombosis has far-reaching implications in COVID-19.

The role of anticoagulant drugs in the prevention and treatment of these thromboses is not yet clear since hospital patients are routinely given blood-thinners as a precaution but these were unable to prevent the thromboses typical of COVID-19.

The study findings support the call from coagulation specialists for the need for thrombosis prophylaxis—even for non-hospitalized patients.

Further studies will need to investigate at what point and to what extent anticoagulant therapy is useful, based on laboratory results and imaging studies.

In order to develop new, effective treatments, follow-up studies are required to identify the systemic and local mechanisms in the pulmonary circulation that lead to these thrombotic tendencies.

One author of the study is Sigurd Lax, Professor of Pathology.

The study is published in the journal Annals of Internal Medicine.

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