by Sayer Ji, Green Med Info:
As an actively practicing clinical cardiologist for many years in three different communities, I knew about myocarditis. I just never saw it. Quite literally, I recall seeing ONE young woman who presented with a picture of acute congestive heart failure, and her echocardiogram study revealed a big and poorly contracting heart. Such a condition is diagnosed as an idiopathic congestive cardiomyopathy, which basically means the heart is enlarged and functioning very poorly, and you have no idea why. After treating her with traditional measures for congestive heart failure, she started getting better. To my great surprise, after six to nine months of follow-up, her echocardiogram had returned to normal.
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Retrospectively, it was then clear that she had likely contracted a virus that focused on her heart. The virus-induced inflammation in her heart muscle cells then decreased the strength of her heart contractions to the point of clinical heart failure with heart enlargement. Presumably, her young immune system eventually “kicked in” and eliminated the viral culprit. Even as a clinician who also received many patients in consultation from other doctors, she represented the entirety of my cases of myocarditis. And at that, the diagnosis was only a retrospective conclusion.
COVID and Myocarditis
Today, the active clinical cardiologist is seeing myocarditis patients on a regular basis. The scientific literature indicates that myocarditis is occurring quite frequently in patients harboring the chronic presence of the COVID-related spike protein. This is being seen in many individuals with persistent chronic COVID, many of whom have been vaccinated, as well as in a substantial number of individuals who have been vaccinated and have never contracted COVID. [1-4] A study in mice showed that the injection of the mRNA vaccine (which produces the spike protein) reliably induced myopericarditis. [5] Regardless of the initial source of exposure to spike protein, it appears to be the reason for the pathology and symptoms seen in chronic COVID. [6]
While not yet clearly documented by any well-designed studies in the medical literature, a great deal of anecdotal information indicates that vaccine mRNA shedding can occur. And once transmitted, the mRNA directly leads to spike protein production. [7] Such mRNA shedding means that the spike protein is indirectly, if not directly as well, transmissible from one individual to another via inhalation or various forms of skin contact. In fact, Pfizer’s own internal documents advise about the possibility of “environmental exposure” by “inhalation or skin contact” of the mRNA in the vaccine being transmitted from a vaccinated individual to another person. [8] Furthermore, while many try to dismiss such an “exposure” as too minimal to be of clinical consequence, such an assertion cannot be assumed to be true when dealing with an agent (spike protein) that appears capable of replication once it gains access to the body. The toxicity associated with spike protein would not be due to a one-time exposure, but one that could persist indefinitely because of this ability to replicate. A toxin that has such an ability is truly a clinical nightmare. It is never a good idea to overestimate the integrity of the pharmaceutical industry. [9]
The spike protein is the part of the COVID pathogen that facilitates its entry into various cells in the body. [10] This cellular entry occurs after the spike protein binds to ACE2 receptors present on the cell membranes found in a wide variety of tissues and organs. Spike protein binding to ACE2 receptors in the lungs, heart, and blood vessels has proven to be of particular importance in determining the severity of many COVID infections as well as the nature of the side effects seen following a spike protein vaccination. Deaths and severe complications have also resulted from vaccine-induced thrombosis occurring in the cerebrovascular circulation. [11,12] Autopsy evaluation of multiple vaccinated individuals who died shortly after receiving their vaccinations revealed acute myocarditis as the only logical cause of their deaths. [13]
Sufficient spike protein binding to ACE2 receptors on the endothelial cells lining the blood vessels has consistently resulted in increased blood clotting. Such clots are tiny in some people, which can then lead to various degrees of tissue and organ damage depending on how severely overall blood flow is impaired to those areas. [14,15] Other clots can rapidly increase in size and result in sudden death. [16] Spike protein can activate blood clotting by binding directly to the ACE2 receptors of platelets in the blood. [17,18] Also, circulating spike protein that has not yet been bound appears to stimulate hypercoagulation as well. [19] Of note, both Pfizer and Moderna appear quite proud to assert that their final formulations supply the “full-length” spike protein in the injections.
Myocarditis, which simply means inflammation of some or all of the muscle cells in the heart, can occur when the spike protein binds to the blood vessels in the heart, to the muscle cells themselves, or both. [20] Even when the myocardial blood vessels get more selectively targeted, inflammation of the heart muscle itself will still eventually ensue as the circulation of the heart gets progressively impaired by blood clotting and/or by an increased resistance to blood flow resulting from inflammation-induced vasoconstriction. Pre-pandemic myocarditis (cases not related to a spike protein presence) generally did not involve any predisposition to blood clotting in addition to the inflammation of the affected heart muscle cells.
Myocarditis presents no diagnostic challenge when it presents in its classical manner. Chest pain and rapid heart rate are often the earliest symptoms. If the myocardial inflammation is evolving rapidly, symptoms of congestive heart failure, including shortness of breath and swelling of the lower legs, can occur as well. Not uncommonly, an upper respiratory tract viral infection will be present or there will be a history of such an infection having recently resolved. Chest X-ray, electrocardiogram (ECG), and echocardiogram can all be used to help establish the diagnosis. An elevated troponin level on blood testing is extremely sensitive in picking up any ongoing heart muscle cell damage, and some elevation of this test will always be seen if any significant inflammation is present in those muscle cells.
Any continued elevation of troponin in the blood, however minimal, must be regarded with significant concern, even if there appears to be a complete clinical resolution of the myocarditis. Everyone should have this test done, even if they are feeling perfectly well, to both establish a baseline within the normal range or to detect any unsuspected low-grade myocardial inflammation.
The very high sensitivity of the troponin test has revealed that there are countless numbers of people post-COVID infection and/or post-vaccination that are continuing to have sustained subclinical degrees of myocardial inflammation. No matter how minimal the elevation of the test, any increase means that a gradual and continued loss of heart muscle function will occur over time. It also means that the heart is highly susceptible to an acute and potentially severe worsening of heart function when an additional exposure to more spike protein occurs, as is seen with the booster shots being vigorously promoted now. A heart with a minimal elevation of troponin is literally the perfect setting for a catastrophic clinical response when an additional spike protein-laden injection is given, much like what gasoline would do to smoldering coals. Not surprisingly, it has been shown that COVID patients with higher troponin levels were more likely to die than those with lower levels. [21]
Many abnormal troponin tests eventually resolve completely and many do not. The quality of nutrition, the strength of the immune system, and the quality of the nutrient/vitamin/mineral supplementation being taken are all critical factors in determining whether a minimal, subclinical degree of inflammation in the heart is capable of completely resolving with a return of the troponin level into the reference, or normal, range. With much of the world eating poorly and not supplementing at all, there is an ongoing presence of the spike protein in a very large number of people around the world. Clinical myocarditis is simply an advanced state of inflammation in the heart, with much higher levels of troponin being released into the blood. Cardiac injury was detected in 20% to 40% of patients hospitalized with COVID. [22,23] Any troponin elevation in hospitalized COVID patients was associated with an increased mortality. [24]
