SARS-Cov-2, the virus that causes Covid-19, can directly infect coronary arteries and increase the risk of cardiovascular disease. Photo: Freepik
SARS-Cov-2, the virus that causes the covid-19can directly infect the coronary arteries and increase the risk of cardiovascular diseases, such as heart attacks or strokes, according to research in elderly patients with previous problems with atherosclerosis.
The study that publishes Nature Cardiovascular Research may help explain why certain people who contract Covid-19 are more likely to develop cardiovascular disease or, if they already have it, have more heart-related complications.
The research indicates that the virus can directly infect the arteries of the heart and also cause great inflammation of the fatty plaques inside them.
The authors caution, however, that the study was conducted with a small cohort of elderly individuals, who suffered from atherosclerosis and others medical conditions; Therefore, the results cannot be generalized to younger, healthier individuals.
“People with covid are at greater risk of suffering from cardiovascular disease or stroke up to a year after infection,” recalled Michelle Olive, from the American National Heart Institutelos Lungs and the Sangre (NHLBI), who considers that they have discovered “one of the reasons.”
Researchers knew that once the virus reaches the cellsthe immune system sends white blood cells known as macrophages to help remove the virus.
These macrophages also help eliminate cholesterol in the arteries and, when they become overloaded with that substance, they transform into a specialized type of cells called foam cells.
The team theorized that if the SARS-CoV-2 could directly infect arterial cells, macrophages that are normally loose could increase inflammation in existing plaque.
To test this idea, they took tissue from the coronary arteries and the plate of people who had died from covid-19 and confirmed that the virus was in those tissues.
Next, they took arterial and plaque cells, including macrophages and foam cellsfrom healthy patients and saw in a laboratory dish that the virus also infected them.
Cholesterol-laden foam cells were the most susceptible to infection and unable to easily clear the virus. Greater plaque accumulation, and therefore foam cells, could increase the severity or persistence of Covid-19.
The team also focused their attention on the inflammation they predicted could occur in the plaque after infecting it with the virus.
With tests, they found that molecules were released, known as cytokines, which are known to increase inflammation and promote the formation of even more plaque.
The cytokines were released by infected macrophages and foam cells, which the researchers said may help explain why people who have plaque buildup and contract Covid-19 can have cardiovascular complications long after contracting the infection.
Although the findings show conclusively that the SARS-CoV-2 can infect and replicate in plaque macrophages and arterial cells, are only relevant for the original strains of SARS-CoV-2 that circulated in New York City between May 2020 and May 2021, indicated the NHLBI. (I)
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