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Joseph Wu, MD, PhD, director of the Stanford Cardiovascular Institute and a senior author of the study, is quick to emphasize that the condition is usually manageable. “It’s not a heart attack in the traditional sense,” he said. “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.”
He is equally quick to note the broader context: a COVID-19 infection itself is approximately ten times more likely to cause myocarditis than the mRNA vaccine designed to prevent it — on top of all the other serious complications the illness can bring.
The Stanford team began their investigation by analyzing blood samples from people who had been vaccinated against COVID-19, comparing those who developed myocarditis with those who did not. Two proteins stood out prominently in the blood of those who experienced heart inflammation: CXCL10 and IFN-gamma.
Both belong to a category of molecules called cytokines — chemical messengers that immune cells use to communicate with one another. Wu described the pair as operating like a tag team, each playing a distinct but complementary role in driving the inflammatory process that ultimately harms the heart.
To understand how these proteins are produced, the researchers turned to laboratory experiments. They generated human immune cells called macrophages — aggressive frontline defenders of the immune system — and exposed them to mRNA vaccines in a controlled dish setting. The macrophages responded by releasing a variety of cytokines, with CXCL10 produced in particularly notable quantities.Continue reading…
