One of the most widely known risks linked to the COVID-19 vaccine is myocarditis, especially in young males — and now a new Stanford study has shed some light on why this rare effect can occur.

Myocarditis, which is inflammation of the heart, occurs in about one in 140,000 people who receive the first dose of the vaccine and one in 32,000 after the second dose, according to a Stanford press release. Among males 30 and younger, that rises to one in 16,750.

Symptoms of the condition include chest pain, shortness of breath, fever and palpitations, which can occur just one to three days after vaccination. Another marker is heightened levels of cardiac troponin, which indicates that the heart muscle has been damaged.

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In most cases, people who experience myocarditis recover quickly and restore full heart function, according to study author Joseph Wu, MD, PhD, the director of the Stanford Cardiovascular Institute and a professor of medicine and radiology.

“It’s not a heart attack in the traditional sense,” Wu told Fox News Digital. “There’s no blockage of blood vessels as found in most common heart attacks. When symptoms are mild and the inflammation hasn’t caused structural damage to the heart, we just observe these patients to make sure they recover.”

In rare cases, however, severe heart inflammation can lead to hospitalizations, critical illness or death, Wu noted.

Finding the cause

The new Stanford study — conducted in collaboration with The Ohio State University — aimed to determine the reasons for the myocarditis. The research team analyzed blood samples from vaccinated people, some with myocarditis and some without. 

They found that those with myocarditis had two proteins in their blood, CXCL10 and IFN-gamma, which are released by immune cells. Those proteins then activate more inflammation.

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“We think these two are the major drivers of myocarditis,” said Wu. “Your body needs these cytokines to ward off viruses. It’s essential to immune response, but can become toxic in large amounts.”

In mouse and heart tissue models, high levels of these proteins led to signs of heart irritation, similar to mild myocarditis.

Prevention mechanism

“One of the most striking findings was how much we could reduce heart damage in our models by specifically blocking these two cytokines, without shutting down the entire (desired) immune response to the vaccine,” Wu told Fox News Digital, noting that a targeted, “fine‑tuning” immune approach might be enough to protect the heart.

“This points to a possible future way to prevent or treat myocarditis in people who are at the highest risk, while keeping the benefits of vaccination,” he added.

The team also found that genistein, an estrogen-like natural compound found in soybeans, reduced inflammation in lab tests, but this has not yet been tested in humans.

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The findings were published in the journal Science Translational Medicine.

“This is a very complex study,” Fox News senior medical analyst Dr. Marc Siegel told Fox News Digital. “Myocarditis is very rare, and the immune mechanism makes sense.”

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“Myocarditis is worse with COVID — much more common, and generally much more severe.” 

Wu agreed, adding that COVID infection is about 10 times more likely to cause myocarditis compared to mRNA-based vaccines.

‘Crucial tool’

The researchers emphasized that COVID-19 vaccines have been “heavily scrutinized” for safety and have been shown to have an “excellent safety record.”

“mRNA vaccines remain a crucial tool against COVID‑19, and this research helps explain a rare side effect and suggests ways to make future vaccines even safer, rather than a reason to avoid vaccination,” Wu said.

“The overall benefits of COVID‑19 vaccination still clearly outweigh the small risk of myocarditis for nearly all groups.”

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The study did have some limitations, primarily the fact that most of the data came from experimental systems (mice and human cells in the lab), which cannot fully capture how myocarditis develops and resolves in real patients, according to Wu.

“This points to a possible future way to prevent or treat myocarditis in people who are at the highest risk.”

“These findings do not change what people should do right now, because our work is still at the preclinical (mouse and human cells) stage,” he said. “Clinical studies will be needed to confirm whether targeted treatments are safe and effective.”

The researcher also added that myocarditis risk could rise with other types of vaccines.

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“Other vaccines can cause myocarditis and inflammatory problems, but the symptoms tend to be more diffuse,” he said in the release. “Plus, mRNA-based COVID-19 vaccines’ risks have received intense public scrutiny and media coverage. If you get chest pains from a COVID vaccine, you go to the hospital to get checked out, and if the serum troponin is positive, then you get diagnosed with myocarditis. If you get achy muscles or joints from a flu vaccine, you just blow it off.”

The study was funded by the National Institutes of Health and the Gootter-Jensen Foundation.