Scientists have noticed that serious cardiovascular problems can be triggered by COVID-19, especially among elderly people who have a build-up of fatty material in their blood vessels. But now a new study has revealed why and has shown that SARS-CoV-2, the virus that causes COVID-19, directly infects the arteries of the heart, according to an article in National Geographic.

Also, according to the study, it was found that the virus can survive and grow inside cells that form plaque – the accumulation of fat-filled cells that narrow and stiffen arteries, leading to atherosclerosis. If the plaque ruptures, it can block blood flow and cause a heart attack or stroke. Infection with SARS-CoV-2 worsens the situation by inflaming the plaque and increasing the chances that it will break.

This may explain the long-term cardiovascular effects seen in some, if not all, COVID-19 patients.

It has already been established that the SARS-CoV-2 virus infects many organs outside the respiratory system. But so far it has not been shown to attack the arteries.

“No one has really looked at whether there is a direct effect of the virus on the arterial wall,” says Chiara Giannarelli, a cardiologist at NYU Langone Health in New York, who led the study. Giannarelli said his team detected viral RNA – the genetic material of the virus – in the coronary arteries. “You wouldn’t expect to see (this) a few months after you’ve recovered from COVID.”

Increasing evidence now shows that SARS-CoV-2 is not only a respiratory virus, but can also affect the heart and many other organ systems, says Ziyad Al-Aly, a clinical epidemiologist at Washington University in St. Louis. Al-Aly’s research showed that the risk of developing heart and cardiovascular disease, including heart failure, stroke, irregular heart rhythm, cardiac arrest and blood clots, increases two to five times within a year of COVID-19, even when the person was not hospitalized.

“This important study directly links, for the first time, the SARS-CoV-2 virus to the inflammation of the atherosclerotic plaque,” says Charalambos Antoniades, head of the department of cardiovascular medicine at the University of Oxford, UK.

The virus triggers inflammation in the plaque

A recent study of more than 800,000 people, led by Fabio Angeli, a cardiologist at the University of Insubria in Varese, Italy, showed that patients with COVID-19 develop high blood pressure twice as often as others. Even more worrisome is the fact that the risk of heart disease may also increase in patients who have experienced only mild symptoms of COVID.

“I’ve seen a patient who now has a defibrillator, and she didn’t even have severe disease,” says Bernard Gersh, a cardiologist at the Mayo Clinic in Rochester, Minnesota.

“The original finding of this study is that the virus was convincingly found in plaque in the coronary artery,” says Juan Carlos Kaski, a cardiovascular specialist at St George’s, University of London, who was not involved in the study.

The NYU team found that in the arteries, the virus predominantly colonized white blood cells called macrophages. Macrophages are immune cells that are mobilized to fight an infection, but the same cells also absorb excess fat – including cholesterol – from the blood. When macrophages load with too much fat, they turn into foam cells, which can increase plaque formation.

To confirm that the virus was indeed infecting and growing in blood vessel cells, the scientists obtained arterial and plaque cells – including macrophages and foam cells – from healthy volunteers. They then cultured these cells in the laboratory in petri dishes and infected them with SARS-CoV-2.

Giannarelli found that although the virus infected macrophages at a higher rate than other arterial cells, it did not replicate in them to form new infectious particles. But when the macrophages were loaded with cholesterol and turned into foam cells, the virus was able to grow, reproduce and survive longer.

These results also confirm previous reports that measuring inflammation in the blood vessel wall can diagnose the extent of long-term cardiovascular complications after COVID-19, Antoniades says.

This study analyzed only 27 samples from eight deceased elderly patients, all of whom already had coronary heart disease and were infected with the original strains of the virus. Therefore, the results of this study do not necessarily apply to younger people without coronary disease; or to the new variants of the virus, which cause a slightly milder disease, says Angeli.

Experts recommend that patients with COVID watch for any new incidence of shortness of breath on exertion, chest discomfort, usually on exertion, palpitations, loss of consciousness; and talk to their doctor about possible heart disease.

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2023-11-08 06:31:00
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