As we learn more about coronavirus, it is becoming clear that it affects more than just the lungs. Phoebe Kitscha explores how and why Covid-19 affects the whole circulatory system and the research that is trying to tackle it.
Why coronavirus is a blood vessel problem
When the coronavirus that causes Covid-19 emerged at the end of 2019, it was initially thought that – like other coronaviruses affecting humans – it mainly caused lung problems.
But as the outbreak progressed, cases emerged suggesting that some of the most severe complications of the disease affect more than just the lungs. From reports of ‘sticky blood’ raising the risk of deep vein thrombosis, heart attack or stroke, to neurological effects, to painful red and swollen areas on the feet known as ‘Covid toe’ – many of these symptoms are thought to be linked to effects on our blood vessels.
In particular, these symptoms may be caused by the way that Covid-19 affects the lining of the blood vessels, called the endothelium. This layer of cells is not a solid barrier – it can allow or block certain substances through depending on conditions in the body. It also has a vital role in allowing our blood vessels to function normally.
A healthy, well-functioning endothelium helps to keep our blood vessels relaxed and open to the flow of blood. It also releases substances that help to prevent harmful blood clots and inflammation. But if the endothelium is damaged, these processes may not work effectively, known as endothelial dysfunction.
This is a key factor in the development of heart and circulatory conditions. For example, it is linked to the formation of fatty plaques in our arteries, which can rupture, leading to heart attacks and strokes.
In April 2020, a paper published in The Lancet gave the first evidence that the coronavirus that causes Covid-19 can infect endothelial cells. The molecule ACE2 (which the virus binds to in order to enter our cells and reproduce itself) can be found on the surface of endothelial cells.
In May, another study of the lungs of seven people who died from Covid-19 found higher ACE2 levels in lung endothelial cells, alongside evidence of severe injury to blood vessels. The researchers showed that the disease is linked to the formation of tiny clots within capillaries (our smallest blood vessels) in the lungs. There were nine times as many of these clots in people with Covid-19 as in the lungs of people who died from flu.
By damaging the endothelium, coronavirus infection has the potential to cause abnormal blood clotting, ‘leaky’ vessels and reduced blood flow. In the lungs, these effects cause clots and fluid to accumulate, which means the lungs are less able to get oxygen into the body. And these endothelial effects could have consequences from head to toe.
In the brain, damage to endothelial cells in the blood-brain barrier could lead to inflammation. In limbs, reduced blood flow could lead to ‘Covid toe’. Combined with the virus’s effects on the immune system, where overactivation of our inflammation systems can also make the blood more likely to clot, this could help to explain the range of symptoms people with Covid-19 can develop.
This may also help to explain why people with certain heart and circulatory conditions seem to be at a higher risk of developing severe complications of Covid-19. If another condition, such as diabetes or high blood pressure, has already damaged the endothelium, the virus’s impact is magnified.
While this sounds worrying, it raises the possibility that treatments already used to help limit blood clotting and improve the function of the circulatory system could be vital to saving lives.
Published by the BHF on 01/07/29