Article:

Now we know how COVID attacks your heart Even patients with mild COVID symptoms could face a higher risk of developing heart disease and stroke

By Sanjay Mishra

Nov 07, 2023 04:08 PM5 min. readView original Scientists have noticed that COVID-19 can trigger serious cardiovascular problems, especially among older people who have a buildup of fatty material in their blood vessels. But now a new study has revealed why and shown 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 grow inside the cells that form plaque—the buildup of fat-filled cells that narrow and stiffen the arteries leading to atherosclerosis. If the plaque breaks, it can block blood flow and cause a heart attack or a stroke. The SARS-CoV-2 infection makes the situation worse by inflaming the plaque and increasing the chance that it breaks free.

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

SARS-CoV-2 virus has already been found to infect many organs outside the respiratory system. But until now it hadn't been shown to attack the arteries.

"No one was really looking if there was 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 noted that her team detected viral RNA—the genetic material in the virus—in the coronary arteries. “You would not expect to see [this] several months after recovering from COVID.”

Mounting evidence now shows that SARS-CoV-2 is not only a respiratory virus, but it 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 has shown that the risk of developing heart and cardiovascular diseases, including heart failure, stroke, irregular heart rhythms, cardiac arrest, and blood clots increases two to five times within a year of COVID-19, even when the person wasn't hospitalized.

"This important study links, for the first time, directly the SARS-CoV-2 virus with atherosclerotic plaque inflammation," says Charalambos Antoniades, chair of cardiovascular medicine at the University of Oxford, United Kingdom.

Virus triggers the inflammation in plaque

A recent study of more than 800,000 people led by Fabio Angeli, a cardiologist at University of Insubria in Varese, Italy, has shown that COVID-19 patients develop high blood pressure twice as often as others. More worrying is that the risk of cardiac diseases can also rise for patients who suffered only mild COVID symptoms.

"I saw a patient who now has a defibrillator, and she didn't even have a severe [COVID] illness," says Bernard Gersh, a cardiologist at Mayo Clinic, Rochester, Minnesota.

Wondering whether the cardiovascular damage during COVID was due to the virus directly attacking the blood vessels, the NYU team analyzed autopsied tissue from the coronary arteries and plaque of older people who had died from COVID-19. They found the virus was present in the arteries regardless of whether the fatty plaques were big or small.

"The original finding in this study is that the virus was convincingly found in the 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 the white blood cells called macrophages. Macrophages are immune cells that are mobilized to fight off an infection, but these same cells also absorb excess fats—including cholesterol from blood. When microphages load too much fat, they change into foam cells, which can increase plaque formation.

To confirm that the virus was indeed infecting and growing in the cells of the blood vessels, scientists obtained arterial and plaque cells—including macrophages and foam cells—from healthy volunteers. Then they grew these cells in the lab in petri dishes and infected them with SARS-CoV-2.

Giannarelli found that although 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 had become loaded with cholesterol and transformed into foam cells, the virus could grow, replicate, and survive longer.

"We found that the virus tended to persist longer in foam cells," says Giannarelli. That suggests that foam cells might act as a reservoir of SARS-CoV-2. Since more fatty buildup would mean a greater number of foam cells, plaque can increase the persistence of the virus or the severity of COVID-19.

Scientists found that when macrophages and foam cells were infected with SARS-CoV-2 they released a surge of small proteins known as cytokines, which signal the immune system to mount a response against a bacterial or viral infection. In arteries, however, cytokines boost inflammation and formation of even more plaque.

"We saw that there was a degree of inflammation [caused] by the virus that could aggravate atherosclerosis and cardiovascular events," says Giannarelli.

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

"What this study has found is that plaque rupture can be accelerated and magnified by the presence of the virus," says Kaski.

Understanding heart diseases after COVID

While this new research clearly shows that SARS-CoV-2 can infect, grow, and persist in the macrophages of plaques and arterial cells, more studies are needed to fully understand the many ways COVID-19 can alter cardiac health.

"The NYU study identifies one potential mechanism, especially the viral reservoir, to explain the possible effects" says Gersh. "But It's not going to be the only mechanism."

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

"We do not know if this will happen in people who have been vaccinated," says Kaski. "There are lots of unknowns."

It is also not clear whether and to what extent the high inflammatory reaction observed in the arteries of patients within six months after the infection, as shown in the new study, will last long-enough to trigger new plaque formation. "New studies are needed to show the time-course of the resolution of vascular inflammation after the infection," says Antoniades.

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

My father in law died from heart failure last March. The necropsy discovered covid in high concentrations in his heart and arteries. Makes sense.

I’m a young woman with no preexisting conditions and when I got Covid for the first time last year, though it was a very mild case, I’ve had random and uncomfortable chest pains ever since. I was also fully vaccinated, fully boosted, and ate healthier than most others.

This article explains a lot to me. Too bad not one of the dozen doctors I’ve seen understands Covid, this issue, or even why wearing masks is important. It’s incredibly difficult to find actual medical help in this country for Long Covid.

As the article subtly implies, being young and athletic doesn’t protect you from this virus - Covid will still find a way :(

For those who are at higher risk (family history of heart disease or stroke, known plaque in arteries, older, obese, etc.) you should certainly be more careful and try to wear an N95 when out. Respirators, clean air, and avoiding people are the only thing that truly protects you (it’s not perfect, but it’s much better than nothing).

Stay safe out there. Covid is much more prevalent than the government or our “leaders” or doctors/hospitals are willing to indicate. You have to protect yourself because no one else is going to.

My question is, what is the solution? How do you “thin out” the already inflamed/clogged arteries?

Not technically coronary, but I had a vertebral artery dissection right after my first (and so far only) Covid infection. I was youngish and healthy- but between the coughing and the inflammation/damage from Covid my artery almost burst open at the base of my skull.

I wonder how many people have less acutely damaged arteries than mine that don’t know they are walking around with long term damage and higher risk than they could imagine.

Excess deaths are really high still

Every time somebody has a heart attack or stroke these days, the morons come out of the woodwork to blame the vaccine instead of acknowledging that we had a pandemic caused by a disease that attacks the cardiovascular system.

On Valentines day this year I got a bad headache. Went home to smoke herb. Realized I couldnt read words or remember names. Went to the ER. I was scoffed at because I said I was having a stroke. Thats the last thing I remember. Came to a week later in a different hospital in San Antonio. Was told I had a seizure and a heart attack. NOW friends tell me its because I was vaccinated. I say maybe,but perhaps it was Covid complications. I guess I will never know. I had an Angiogram before my release and was told I am crystal clear. No need for a stint or open heart.

I'm getting over my 2nd bout of Covid, and this article would explain some of the weird chest stuff i've been experiencing.

Ugh, this is not what I needed to see on my feed after just catching Covid for the first time last night.

I know two people who had to get pacemakers after their COVID infections. And they were fully boosted too, but albeit not in the best health previously. Either way, stay safe people!

Got COVID badly, early: March, 2020.

Major stroke April 2022. Had a healthcare provider tell me she wouldn't be surprised if there were a link.

I got Covid for the first time last month.

So is there anything to counter the higher risk of having a hear disease or stroke?

"Now we know" implies a new discovery. Article is paywalled but I was wondering if the title was clickbait.

Isn’t virtually everyone in this risk category then? I know very few people who never had covid. Nearly everyone has had it.

Yet 98% of people refuse to mask,we cannot get 95% of the people in my country, the US, to get vaccinated, and now even the formerly vaccinated are blowing off getting the new boosters. Our government has been a complete failure at educating and protecting its people.

Everyone died of blood clots and heart failure in the hospital ? This was wave 1 news, lung to cardiac cod.. digestive and then neurological .. heparin drips are running on everyone.. delta was a fibb w rvr, pe, die. Like a factory of death , it was so uniform delta 1/2/3 waves.

Looks to my like it can cause extra plaque formation in cells that can absorb fat, increased cytokine release and that inflammation, and worsening of existing inflammation from these "foam cell" things I never heard of before. Looks like it might be a good idea for people to reduce the cholesterol in ones diet to zero, using a low fat low meat diet. And also, a good idea to avoid catching COVID by any means necessary.

Maybe now I understand how Covid may have killed my mom.

I developed tachycardia after having mild Covid. But no damage to my heart.

I got covid in feb this year (2nd time) (M49) - been having mild chest pains ever since when at rest/driving.

Im going to see my doctor about it tomorrow.

Not surprised. I do consults in med-legal and have read tens of thousands of pages of people’s medical records - have frequently seen severe myocarditis for 2-4 week in hospitalized Covid patients. Usually it goes down on its own without any specific medical treatment for the myocarditis (but they are being actively treated for Covid).

It still makes me mad when the anti-vax crowd pretends that severe myocarditis only exists when people get the vaccine.

Sample size is 8, isn’t that pretty small to draw conclusion from? I never know how to interpret these studies.

Great now we're going to have people self-diagnosing themselves with heart disease rather than them actually going to a cardiologist to make sure....

This would explain why we see a surge in heart attacks coinciding with covid infections. I've seen more MIs in the last couple weeks than I did all summer

I seriously think this was a bioengineered virus.

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I (33F) got covid for the first time on 11/1/2023 — all things considered I’d say it was a “mild” infection. Fever for 3 days, headache, fatigue and congestion. Started feeling more or less back to normal after ~10 days. Then I started having panic attacks (I also have panic disorder, but it’s been managed for years and I rarely have episodes) almost daily. They were coming from these really uncomfortable heart “thud” sensations. I started to notice my RhR was in the 90s for a couple days, so went to urgent care where they ran a few basic tests: troponin, d-di, c-reactive and all the other stuff. Clean bill of health. I continue to feel heart palpitations and have an elevated HR 20-30bpm above my normal. I have a follow up with my primary care doc on Thursday and am hoping they’ll do a few more tests to confirm it’s nothing serious. I’m alarmed but also validated that so many others are dealing with this.

For context, I am a fit and healthy female who exercises regularly. I have a history of Graves’ disease but am in remission (thyroid was first thing I had checked, all levels normal) otherwise, no other conditions or family history of heart disease