The following peer-reviewed paper may be found at Primary Doctor Medical Journal.
Abstract
This paper addresses the question of prevalence of COVID vaccine-associated myocarditis, as well as known mechanisms of spike protein-induced myocarditis, considering the epidemiological consequences of mass vaccination with spike protein-generating COVID vaccines, such as are being deployed throughout the world at present. The cardiac impacts of spike protein distribution have risen to particular concern, due to the recent extraordinary increase in new cases of myocarditis and pericarditis, including among populations that typically have vanishingly rare incidence of this disease, especially young men, with particularly anomalous occurrence in young male athletes.Introduction
The US Centers for Disease Control and Prevention (CDC) finds increased reported cases of myocarditis and pericarditis following mRNA COVID-19 vaccination, most notably in adolescents and young adults, [1] including in the absence of COVID-19 infection. [2] Myocarditis was only rarely found post-vaccination prior to the COVID mRNA vaccines, and then mostly associated with the smallpox vaccine. [3] Typically and historically, myocarditis patients are older with high prevalence of diabetes, hypertension, atrial fibrillation, coronary artery disease and heart failure. [4] Myocarditis is an extremely concerning condition. At five years post-diagnosis, myocardial injury, which is a clinically indistinguishable condition from myocarditis, and often discussed interchangeably and synonymously, 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]
