Myocarditis: Once Rare, Now Common

Written by Thomas E. Levy, MD, JD Orthomolecular Medicine News Service on March 3, 2023. Posted in Current News

Following the startling revelation that the vaccine mRNA may be transmissible along with the spike protein, our consulting cardiologist Dr. Thomas Levy has recommended that ALL of us undergo a cardiac panel that includes very specific testing, whether jabbed or not

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.

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 percent of patients hospitalized with COVID. [22,23] Any troponin elevation in hospitalized COVID patients was associated with an increased mortality. [24]

Troponin testing is currently the most important and widely accepted way to determine whether a suspected heart attack has occurred, with the troponin being released into the circulation as the heart muscle cells die. [25]

Some degree of myocardial injury is felt to be present when any troponin level is detected beyond the 99th percentile upper reference limit, whether in the context of a suspected heart attack or the possible presence of any inflammation in the heart. [26,27]

Even an increase in baseline troponin levels that remains below the established upper limits of normal has been shown to be significantly associated with increased mortality after noncardiac surgery. [28]

Baseline troponin testing is a good idea for everyone, since normal ranges can vary from lab to lab, and because it appears myocardial injury can still be present when the troponin level rises significantly from a baseline point but remains short of the upper reference limit. [29]

The importance of the most minimal of troponin elevations has been established in several studies looking at the relationship of pre-operative troponin levels with long-term mortality following noncardiac surgery.

Compared to patients with no troponin elevation, a significant increase in 30-day mortality was seen in patients having minor troponin elevations following noncardiac surgery. [30,31] Another similar study found over a doubling of the mortality rate when the two patient groups were evaluated at three years following the noncardiac surgery. [32]

In a recent Swiss study yet to be published at the time of this writing, troponin levels were measured on 777 hospital employees who received a booster injection after having received two shots previously.

On the third day after the booster, troponin levels above the upper limits of normal were seen in 2.8% of those subjects. By the next day, half of the elevated troponin levels had come back into the normal range. [33] Longer-term follow-up data was not available.

This study raises more questions than it answers. What would the troponin levels have been at one day post-injection? Did the troponin levels still elevated at day four post-injection resolve completely? If so, how long did that take to occur?

Rather than be concerned that some myocardial damage was done by the vaccine, which is openly acknowledged in the study, it is dismissed as being of no importance since half of the elevated troponins resolved 24 hours later.

And, as with all of the current papers downplaying the significance of any vaccine side effect, however significant, the authors always conclude that the vaccine is doing much more good than harm without any further qualification as to why such a conclusion is valid.

Having even the most minimal elevation of troponin not only raises the concern of some collective long-term heart damage, or the ease of having a “re-flaring” of inflammation with new spike protein exposures, as from a booster shot, it also raises the concern of electrical instability in some of the inflamed myocardial cells.

There is always a possibility of electrical instability in any inflamed myocardial muscle cells, as it is their normal physiological nature to transmit electrical impulses from one cell to the next.

Because of this, stressful events that release surges of adrenalin and catecholamines in the circulation, as is seen with peak physical exertion, can readily provoke such electrically unstable cells into starting, and sustaining, an abnormal heart rhythm.

Literally hundreds of European soccer players have died or collapsed on the field of play in the last two years. Of note, they have not been seen to collapse while standing or sitting on the sidelines.

Similarly, any pilot with even a minimal but otherwise symptom-free elevation of troponin can potentially sustain such a life-threatening arrhythmia when a significant stress-provoking emergency arises in the cockpit.

However, regardless of any benefits a COVID vaccine might have on the overall morbidity and mortality on those receiving it, it completely ignores that MANY effective treatments have emerged that either prevent most cases of COVID or readily cure them when properly applied after the infection has been contracted. [34-38]

With the availability of effective treatments, no vaccine side effect, especially one that has already resulted in many deaths, should be tolerated, unless the vaccine candidate is fully aware of all possible side effects and chooses not be bothered with measures proven to prevent and/or treat the infection.

To date, every vaccine that has ever existed has a significant side effect profile. This information, along with a full disclosure of effective non-pharmaceutical therapies for the condition the vaccine is supposed to prevent, should always be afforded to both physicians and their patients.

It is important to realize that most of the tissues and organs of the body do not have reliable laboratory markers indicating the presence and degree of ongoing spike protein damage.

Tracking heart damage with troponin levels makes this organ relatively unique in this regard, and since ACE2 receptors are present in most organs and tissues, any continued elevation of troponin can also be considered a reliable indicator that spike protein damage is occurring in organs and tissues outside of the heart.

Spike protein would be expected to bind ACE2 receptors wherever it finds them, and such binding would always be expected to cause cellular inflammation and damage. Blood testing for natriuretic peptides also reflects myocardial damage, but the primary focus should remain on troponin testing and doing whatever is necessary to return that test into the normal range. [39-45]

COVID, Arrhythmias, Heart Block, and Pilots

As would be logically expected, any agent that can cause inflammation in the heart would also be expected to sometimes involve the cells in the heart that generate and conduct each electrical spark that initiates every contraction of the heart.

As myocarditis can be patchy and not affect all of the heart muscle cells uniformly, heart rhythm problems are not always part of the clinical presentation of myocarditis. However, various degrees of heart block have been reported because of the COVID-19 infection and/or because of the COVID-19 vaccination. [46-51]

A new condition known as multisystem inflammatory syndrome in children (MIS-C) has emerged since the onset of the COVID pandemic, appearing primarily in advanced COVID infections. [52,53] MIS-C, and MIS in adults, simply means the COVID infection has resulted in a widespread amount of inflammation in the body, often involving the heart and the lungs.

Minimal to advanced heartbeat conduction problems have occurred secondary to MIS-C, ranging from the often-innocuous prolonged PR interval (see below) on the ECG to advanced and potentially life-threatening degrees of AV block. [54,55]

When heart function is normal, the AV node allows a rapid conduction of the heartbeat throughout all of the heart muscle cells so that heart muscle contraction is synchronized and optimally efficient.

AV block results in an abnormal slowing of the heart rate and sometimes fatal secondary arrhythmias, including complete stoppage of the heartbeat (asystole). It appears likely that the spike protein can damage the heart at any age, and that the spike protein can be present because of the infection itself and/or the vaccination targeted at the infection.

The PR interval is the amount of time that the heartbeat takes to traverse the atrial chambers in the heart before reaching the conduction-accelerating AV node. The normal PR interval ranges from 0.12 to 0.2 seconds. In younger individuals, especially well-trained athletes, a PR interval greater than 0.2 is usually completely normal.

However, when PR interval measurements have always been 0.2 or less and then start to lengthen as an older adult, there should be significant concern that the aging conduction system might manifest more significant conduction abnormalities in the future.

In the setting of the pandemic, it is of particular concern when PR interval prolongation is seen for the first time following a bout of COVID and/or following a vaccination. This is a clear indicator of new inflammation in at least some of the heart cells, however minimal it may be.

Regardless, it should not just be assumed to be of no importance. All disease has a spectrum of pathology, and the earliest stages of pathology should never be trivialized. [56]

In a Harvard study that extended over a 30- to 40-year period, it was found that individuals with PR intervals greater than 0.2 seconds had twice the risk of atrial fibrillation, three times the risk of needing a pacemaker (meaning the presence of advanced degrees of heart block), and nearly a one and a half times increase in all-cause mortality. Furthermore, greater degrees of PR interval prolongation led to an even greater risk. [57]

However, ignoring the inherent pathology in a pandemic-induced prolonged PR interval is exactly what the Federal Aviation Administration (FAA) appears to have done.

Facing a shortage of pilots due to both the vaccine requirement it initiated during the pandemic for the pilots to fly, along with many early retirements that resulted, the FAA decided to change the rules, disregarding long-standing parameters of normalcy based on medical science and not convenience.

The FAA has now declared a PR interval of 0.3 seconds to be the “new normal” in the FAA Guide for Aviation Medical Examiners as of October, 2022. The October, 2021 standards asserted the PR interval was normal only at 0.2 seconds or less.

When the pilot has “no symptoms” he or she can now obtain clearance to fly with a PR interval of 0.3 or less. And when that interval is greater than 0.3, a “current Holter and cardiac evaluation” are then required.

Considering that the normal PR interval ranges between 0.12 and 0.20 seconds, an interval of 0.3 seconds represents a “permissible” increase in this interval by over 100 percent relative to the low normal interval of 0.12 seconds. This is not a nominal increase in PR interval, but a very large one.

Even now, a treadmill exercise stress test is not required to receive medical clearance to fly, even for commercial pilots.

This is simply not a safe policy by the FAA and arguably a shocking one, as many pilots are in the age range when heart attacks occur without any early symptoms but with a normal ECG, the ECG being the only mandatory heart-related test.

Roughly a third of all deaths around the world are due to cardiovascular disease. And in western countries sudden cardiac death occurs in about half of all coronary artery disease patients. [58,59]

Much more vigorous cardiac evaluations should be performed in prospective pilots, and repeated at appropriate intervals. A normal ECG means a heart attack has not occurred, nothing more.

It is irrelevant that the pilot might feel well, have a normal ECG, and have no clinical evidence of myocarditis.

This is taken from a long document. Read the rest here Orthomolecular Medicine News Service

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