Scientists have found that coronavirus infection can cause serious cardiovascular disease, especially among older people who have a buildup of fatty substances in their blood vessels. But now a new study reveals why, showing that SARS-CoV-2, the virus that causes COVID-19, directly infects the arteries of the heart.
The study also found that the virus can survive and reproduce. internal Cells that form plaques. It is a buildup of fat-filled cells that narrow and harden the arteries, causing atherosclerosis. When the plaque ruptures, it can block blood flow and cause a heart attack or stroke. SARS-CoV-2 infection worsens the situation by inflaming the plaques and increasing the likelihood of them being released.
This could explain the long-term cardiovascular effects seen in some, if not all, patients with COVID-19.
The SARS-CoV-2 virus is already known to infect many organs other than the respiratory system. But so far, it has not been shown to attack arteries.
“No one really thought about whether the virus had a direct effect on the arterial walls,” said Chiara Giannarelli, a cardiologist at New York University Langone Health who led the study. Giannarelli noted that her team detected viral RNA (the virus’ genetic material) in the coronary arteries. She said, ‘You wouldn’t expect to see [this] It’s been several months since I recovered from the coronavirus. ”
Ziyad Al Ali, a clinical epidemiologist at Washington University in St. Louis, said SARS-CoV-2 is not only a respiratory virus, but can also affect the heart and many other organ systems. He said there is growing evidence that this is the case. The risk of developing heart and circulatory diseases, such as heart failure, stroke, irregular heart rhythms, cardiac arrest, and blood clots, is lower even if you have had COVID-19, according to an Al Ahly study. It has been shown to increase by 2 to 5 times within a year. I’m not hospitalized.
“This important study provides the first direct link between the SARS-CoV-2 virus and atherosclerotic plaque inflammation,” said Charalambos Antoniades, head of the Department of Cardiology at the University of Oxford, UK.
Viruses cause plaque inflammation
A recent study of more than 800,000 people led by Fabio Angeli, a cardiologist at the University of Insubria in Varese, Italy, found that coronavirus patients were twice as likely to develop high blood pressure as other patients. It was shown that What’s even more concerning is that even patients with mild coronavirus symptoms may be at increased risk of heart disease.
“I saw a patient who is currently on a defibrillator and she didn’t even have severe symptoms.” [COVID] It’s a disease,” says Bernard Gersh, a cardiologist at the Mayo Clinic in Rochester, Minnesota.
Questioning whether the cardiovascular problems caused by the new coronavirus infection are due to the virus directly attacking blood vessels, a team from New York University investigated the anatomical tissue and plaques in the coronary arteries of elderly people who died from the new coronavirus infection. was analyzed. They found that the virus was present in the arteries, regardless of whether the fatty plaques were large or small.
“The first finding of this study is that the virus was found in plaques in coronary arteries,” says Juan Carlos Kaschi, a cardiovascular specialist at St. George’s, University of London, who was not involved in the study.
The New York University team found that within arteries, the virus primarily colonizes white blood cells called macrophages. Macrophages are immune cells that are recruited to fight infections, but these same cells also absorb excess fats, including cholesterol, from the blood. If microphages take up too much fat, they can turn into foam cells and increase plaque formation.
To confirm that the virus was actually infecting and multiplying in blood vessel cells, the scientists collected arterial and plaque cells, including macrophages and foam cells, from healthy volunteers. These cells were then grown in petri dishes in the lab and infected with SARS-CoV-2.
Giannarelli found that although the virus infects macrophages at a higher rate than other arterial cells, it does not replicate within the macrophages to form new infectious particles. But when the macrophages became loaded with cholesterol and turned into foam cells, the virus was able to grow, replicate, and survive longer.
“We found that the virus tends to persist longer in foam cells,” Giannarelli says. This suggests that foam cells may act as a reservoir for SARS-CoV-2. Because increased fat accumulation increases the number of foam cells, plaques can increase the survival time of the virus and the severity of COVID-19.
Scientists believe that when macrophages and foam cells are infected with SARS-CoV-2, they release large amounts of small proteins known as cytokines, which signal the immune system to mount a response against bacterial or viral infections. discovered. However, in the arteries, cytokines promote inflammation and promote the formation of more plaques.
“We found that there was some degree of inflammation.” [caused] It’s caused by a virus that can worsen atherosclerosis and cardiovascular events,” Giannarelli said.
These findings also support previous reports that measuring inflammation in blood vessel walls can help diagnose the extent of long-term cardiovascular complications following COVID-19 infection, Antoniades said.
“What we found in this study is that the presence of the virus can accelerate plaque breakdown and spread it,” Kaski said.
Understanding heart disease after COVID-19
This new study clearly shows that SARS-CoV-2 can infect, multiply, and persist in macrophages in plaques and arterial cells, but that SARS-CoV-2 has the potential to infect, multiply, and persist within macrophages in plaques and arterial cells. More research is needed to fully understand the different ways health can change.
“The New York University study identified one potential mechanism, specifically the source of the virus, to explain the possible effects,” says Gersh. “But that’s not the only mechanism.”
The study analyzed only 27 samples taken from eight elderly deceased patients, all of whom already had coronary artery disease and were infected with the original virus strain. Therefore, the results of this study do not necessarily apply to young people without coronary artery disease. Or they could be infected with a new variant of the virus that causes a milder illness, Angeli said.
“We don’t know if this will happen to vaccinated people,” Kaski said. “There are a lot of unknowns.”
Also, as shown in a new study, whether and how long the high inflammatory response observed in patients’ arteries within six months after infection lasts long enough to trigger new plaque formation. It is also unclear whether “New studies are needed to show the time course of resolution of vascular inflammation after infection,” Antoniades says.
Patients with coronavirus should be on the lookout for new onset of shortness of breath on exertion or chest discomfort (usually accompanied by exertion, palpitations, or loss of consciousness). And talk to your doctor about the possibility of heart disease.
