By Peter A. McCullough, MD, MPH
From the original Baric study demonstrating beta-coronavirus loading in laboratory models can cause myocarditis to the first year of the COVID-19 crisis there has been a concern that SARS-CoV-2 infection in humans could cause heart inflammation. Epidemiologic studies relying on ICD codes triggered by routine cardiac troponin testing and or results implied that hospitalized patients were developing myocarditis with the respiratory illness. None of these studies were confirmed with clinical adjudication or autopsy. In 2020 the NCAA Big Ten athletic conference, US Military, and many other organizations screened for myocarditis on clinical grounds—handful of cases were found without any reported hospitalizations or deaths. Tuvali, et al from Israel, demonstrated that myocarditis in 2020 was not any more common that the low levels of baseline myocarditis from parvovirus, giant cell, and other conditions.
Almamlouk et al performed a systematic review of 50 autopsy studies and 548 hearts of patients who died of or with COVID-19. Usual post-mortem findings of tissue edema and necrosis were reported commonly. About two thirds of hearts had SARS-CoV-2 found in the tissue. However, none of the hearts had extensive myocarditis as the cause of death.
In summary, this review should be the nail in the coffin in ruling out COVID-19 illness as a cause of fatal myocarditis. Despite the virus being found in heart tissue, it was not causing significant inflammation. The explosion of fatal myocarditis by report of unexplained cardiac arrest, adjudication, and at necropsy must have another explanation than SARS-CoV-2 infection. The only new proven cause of heart damage in human populations is COVID-19 vaccination. Vaccines used in America (Pfizer, Moderna, Janssen, Novavax) have been demonstrated to cause myocarditis as published in the peer-reviewed literature.
These observations call for immediate access to the CDC COVID-19 vaccine administration database for physicians and other providers who are managing the burgeoning caseload of myocarditis. This will be the only way the epidemiology of COVID-19 vaccine induced myocarditis can be studied and patient outcomes can be improved.
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