Myocarditis is an extremely concerning condition.
At five years post-diagnosis, myocarditis is correlated with a 72.4% mortality rate, and is therefore correlated with higher mortality than even Type 1 myocardial infarction (rupture of coronary artery plaque with thrombus) or Type 2 myocardial infarction (vasospasm generally), which have 36.7% and 62.5% five-year mortality rates respectively. [5] So myocarditis is likely even more concerning than myocardial infarction. This may be due to the generalized cytotoxic injury, due to external cause, throughout the heart in the myocarditis event, compared to the localized watershed damage affecting a portion of the heart, which is associated with myocardial infarction.
Heart function is mostly regulated by cardiomyocytes and vascular endothelial cells. Cardiomyocytes have no potential for self-renewal, as they are terminally differentiated cells. When they die, they necrose and are replaced by proliferating fibroblasts, which form fibrotic tissue. This tissue reduces systolic function, and is associated with a poor prognosis. [6]
Due to the generally much higher activity level of a young athlete than of the historical prototype myocarditis patient, are we simply noticing greater contrast in activity level before and after the COVID vaccines in the former, and missing this contrast, and hence the myocarditis diagnosis, in more sedentary individuals? This paper will examine the possible mechanisms of the mRNA COVID vaccine association with myocarditis, in order to assess how common this association might be.
When asked in June 2021 about the risk of myocarditis following the COVID vaccines, Dr. Roger Hodkinson, pathologist, replied:
“Myocarditis is never mild, particularly in young healthy males. It’s an inflammation of the heart muscle, the pump of the body. And we don’t know what percent of the heart muscle cells would have died in any one attack of myocarditis. The big thing about heart muscle, heart muscle fibers, is that they do not regenerate, . . . so you’re stuck with an unknown percentage of your heart muscle cells having died. We can’t estimate the number, and therefore the long-term results are utterly unpredictable. We do know . . . that myocarditis can present decades later, with premature onset of heart failure that would otherwise not have been expected. So it’s a terrible worry for these people to know what’s going to happen to them in the future. . . . It’s not trivial.”
In diagnosing myocarditis, cardiac magnetic resonance studies (CMR) have shown specific sites of inflammation or fibrosis, and help to evaluate functional impairment of heart muscle. Myocardial edema and late gadolinium enhancement are seen on CMR in cases of myocarditis. In all cases reporting chest pain post-COVID vaccine in one study these abnormal findings were present on CMR in each subject. Past or current COVID-19 disease had been excluded in all subjects. [7] However, the more widely accepted criterion of myocardial injury is a threshold of serum troponin levels at or above 99th percentile of upper reference range. [8] Elevated troponin is considered to be both sensitive and specific for myocardial damage. Troponin is a protein normally confined to the cytosol of cardiomyocytes, as well as other muscle cells, and is not normally found in the blood; however, it is released in the circulation when heart muscles become damaged.
| Is it possible to avoid heart damage from the COVID vaccine? Or do all COVID-vaccinated people have some myocarditis? - by ColleenHuberNMD - The Defeat Of COVID (substack.com) |
Excerpt: The spike protein in SARS-CoV-2 is a trimeric, or three-part protein, composed of two functional S1 subunits, as well as a structural S2 subunit. Each of those three units are, incidentally, bound and inactivated by the drug ivermectin. [28] In the absence of ivermectin or hydroxychloroquine, the two drugs most thoroughly studied and most widely used in early and late cases of COVID-19, [29] the spike protein remains in a conformation that enables it to attach to the ACE2 receptor on human cells, and to enter by that portal. Conversely, either of those drugs are able to change the conformation of the spike protein in such a way that prevents entry to the human cell. [30] |