the bongino report

Myocarditis: Once Rare, Now Common

I have been a practicing clinical cardiologist for over 30 years in three different cities.https://www.theepochtimes.com/t-myocarditis”>myocarditis. It’s just that I never saw it. I remember seeing one young woman with acute congestive heart disease. Her echocardiogram revealed that her heart was large and not contracting properly. Idiopathic congestive cardiacmyopathy is the diagnosis for such a condition. This basically means that her heart is large and is functioning poorly. Her condition improved after she was treated with traditional methods for congestive heart disease. After six to nine months of monitoring, my surprise was complete. Her echocardiogram was back to normal.

In retrospect, it became clear that she likely had a virus that was primarily focused on her heart. The virus-induced inflammation of her heart muscle cells led to decreased heart contraction strength, leading to her suffering from clinical heart failure. Her young immune system may have eventually failed. “kicked in” The virus culprit was removed. She represented all my myocarditis cases, even though she was a clinician and had many patients who were referred by other doctors. And the diagnosis was not final.

COVID and myocarditis

The active clinical cardiologist sees myocarditis patients regularly. Research has shown that myocarditis is very common in patients with chronic COVID-related protein spikes. This is happening in many people with chronic COVID, including many who have not been vaccinated. [1–4]. In mice, myocarditis was reliably inducible by injection of the mRNA vaccination (which makes the spike protein). [5]. It does not matter from where it was first exposed to spike protein. However, chronic COVID symptoms and pathology are likely to result. [6].

Although it is not yet documented in any scientific studies, there are many anecdotal evidences that vaccine mRNA loss can occur. Once transmitted, the mRNA can directly lead 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. Pfizer documents actually warn about the possibility. “environmental exposure” By “inhalation or skin contact” Transmission of the vaccine’s mRNA from one person to another [8]. Moreover, while many people try to ignore such an “exposure” As the impact of spike protein on human health is too small to warrant clinical concern, it cannot be assumed that such an assertion holds true for an agent (spike proteins) that can replicate once it has access to the body. Spike protein could cause toxicity that is not due to one-time exposure but can persist indefinitely as it has the ability to reproduce. Such a toxin is a clinical nightmare. It is not a good idea overestimate the integrity and professionalism of the pharmaceutical sector [9].

The spike protein is a component of COVID pathogens that allows the virus to enter various cells in the body. [10]. After the spike protein binds with ACE2 receptors on cell membranes in a variety of tissues and organs, this cellular entry takes place. In determining the severity of COVIDs, the binding of spike protein to ACE2 receptors in the lungs and heart has been a key factor. The cerebrovascular circulation has also been implicated in vaccine-induced thrombosis, which can lead to severe complications and death. [11,12]. Multiple vaccinated people who died soon after their shots were administered to autopsy showed that acute myocarditis was the cause of their deaths. [13].

Increased blood clotting has been consistent due to sufficient spike protein binding to ACE2 on the endothelial cell lining of the blood vessels. Some people may experience tiny clots, which can lead to organ and tissue damage. This is dependent on the extent of impaired blood flow in these areas. [14,15]. Other clots could rapidly multiply and cause sudden death. [16]. Spike protein can trigger blood clotting by binding directly with the ACE2 receptors on platelets in blood [17,18]. Hypercoagulation may also be stimulated by spike protein in circulation that has not been bound. [19]. Moderna and Pfizer are proud to claim that their final formulations supply the “full-length” Injections may cause an increase in protein.

Myocarditis simply refers to inflammation of any or all of the muscles cells in the heart. This can be caused by spike protein binding to either the blood vessels, the muscle cells, or both. [20]. Even though the myocardial blood vessels are more targeted, inflammation of heart muscle cells will continue to occur as blood clotting or increased resistance to blood flow due inflammation-induced vasoconstriction can cause the circulation to become less efficient. Prepandemic myocarditis cases that were not caused by a spike in protein generally didn’t involve any predispositions to blood clotting and/or inflammation of the affected heart muscles cells.

Myocarditis is not a difficult diagnosis when presented in its classic form. Rapid heart rate and chest pain are common symptoms. If myocardial inflammation is developing rapidly, congestive cardiac failure symptoms such as shortness or swelling of the legs and chest pain can also occur. A history of an infection in the upper respiratory tract or a previous infection may indicate that an upper respiratory infection is present. To diagnose the condition, a chest X-ray and an echocardiogram as well as an electrocardiogram (ECG) can be used. A high level of troponin in blood is very sensitive to detect any damage to the heart muscle cells. If there is significant inflammation, this will be seen.

It is important to monitor any elevated blood troponin, no matter how small, for at least 24 hours. Even if you feel fine, everyone should undergo this test to establish a baseline within the normal range, and detect any low-grade myocardial inflammation.

The high troponin test sensitivity has shown that many people have continued to suffer from subclinical myocardial inflammation after COVID infection or postvaccination. Whatever the level of the troponin test, any increase will cause a gradual and ongoing loss of heart muscle function over time. This means that the heart can be susceptible to an acute, potentially serious worsening in function if it is exposed to additional spike protein. As is evident with the booster shots currently being promoted. A heart that has a low level of troponin can be prone to severe clinical reactions when a spike protein-laden injection is administered. This is much like gasoline being injected into smoldering coals. It is no surprise that COVID patients who have higher troponin levels are more likely die than those with lower levels. [21].

Many abnormal troponin levels resolve completely, while others 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. Many people are experiencing spike protein due to poor diets and insufficient supplementation. Clinical myocarditis simply refers to an advanced stage of inflammation that causes the heart to release more troponin into the blood. In 20-40% of COVID patients, cardiac injury was found. [22,23]. Troponin elevations in COVID patients hospitalized were associated with higher mortality [24].

The most reliable and accepted method to test for a heart attack is troponin testing. This involves releasing troponin into the circulation when the heart muscle cells cease to function. [25]. If troponin levels are detected above the 99th percentile higher reference limit, it is considered to indicate that there is some degree of myocardial infarction. [26,27]. A significant association has been established between increased mortality following noncardiac surgery and an increase in baseline troponin levels, even if they are below the upper limits. [28]. Baseline troponin testing can be a good idea because normal ranges can differ from one lab to another. It also indicates that myocardial damage can still exist if the troponin level rises significantly above a baseline point, but is below the upper reference limit. [29].

Numerous studies have demonstrated the importance of the lowest possible troponin level. Patients who had minor troponin levels after noncardiac surgery experienced a significant increase of 30-day mortality compared to those with no elevation. [30,31]. Another similar study showed that there was a nearly doubling in mortality rates when patients were compared three years after noncardiac surgical procedures. [32].

Recent Swiss research has not yet published the troponin levels of 777 hospital staff who received a booster shot after receiving two shots. Troponin levels exceeding the normal limits were observed in 2.8 percent. The normal troponin levels had returned to half of their previous levels by the next morning. [33]. Unfortunately, there were no long-term follow-up data. This study raises many more questions than it answers. What were the troponin levels one day after injection? The troponin levels at day four were they still elevated? What time did this take? The vaccine did not cause any myocardial injury, as is clearly stated in the study. However, half of the elevated troponins disappeared within 24 hours. As with many other papers that minimize the importance of vaccine side effects, regardless of how significant they may be, the authors conclude that the vaccine does more good than harm and do not provide any explanation for why this conclusion is valid.

Even the smallest elevations of troponin can raise concerns about long-term cardiac damage or even cause a person to feel more comfortable. “re-flaring” An increase in inflammation due to new spike proteins, such as a booster shot, raises the possibility of electrical instability in some inflamed cells. Any inflamed muscle cells of the myocardium can experience electrical instability. It is normal for them to send electrical impulses from one to another. Stressful events such as high physical exertion can cause electrically instabilized cells to develop abnormal heart rhythms by releasing surges of adrenaline, catecholamines, and other chemicals. Literally hundreds have fallen or died on the soccer field in Europe over the past two decades. It is important to note that they are not seen to fall while sitting or standing. A pilot who has a slight but not severe elevation of troponin could also be susceptible to a potentially life-threatening arrhythmia if a serious stress-provoking emergency occurs in the cockpit.

Although a COVID vaccination may offer some health benefits, such as reducing mortality and morbidity, there are many other effective treatments available that can either cure or prevent COVID. [34–38].

If the side effects of the vaccine are not known and the candidate refuses to take any measures to treat or prevent them, there is no reason to tolerate them.

Every vaccine has had a significant side effect profile. Both physicians and patients should have access to this information as well as the disclosure of nonpharmaceutical treatments for the condition that the vaccine is meant to prevent.

It is important that you realize that not all tissues and organs have reliable laboratory markers to indicate the severity and extent of spike protein damage. This organ is unique because it tracks heart damage with troponin levels. Because ACE2 receptors can be found in almost all organs and tissues, any increase in troponin can also indicate that spike protein damage has occurred in other tissues and organs. It is expected that spike protein will bind ACE2 receptors where it finds them. This binding would cause cellular inflammation, and thus damage. While blood tests for natriuretic Peptides can also reflect myocardial injury, the main focus should be on troponin testing. This means that you do whatever it takes to get the test back to normal. [39–45].

COVID and Arrhythmias Heart Block and Pilots

It is natural to expect that any agent that causes inflammation in the heart will also affect the cells that conduct and generate every electrical spark that triggers each contraction. Myocarditis may not be present in all cases. Heart rhythm problems aren’t always a sign of myocarditis. However, different degrees of heart block have been reported due to the COVID-19 virus infection and/or the COVID-19 vaccine. [46–51].

Since the onset COVID pandemic, a new condition called multisystem inflammatory syndrome for children (MIS-C), has been emerging. It is primarily seen in those with advanced COVID infections. [52,53]. MIS-C in adults and MIS for children simply refers to a COVID infection that has led to a large amount of inflammation throughout the body, often in the heart and lungs. From the sometimes-innocuous PR interval (see below), to the more severe and potentially deadly AV block, MIS-C has caused heartbeat conduction problems secondary to a variety of conditions. [54,55]. Normal heart function allows the AV node to conduct the heartbeat quickly throughout all cells. This ensures that the heart muscle contractions are synchronized and efficient. An AV block causes an abnormally slowing of heart beat and can sometimes lead to fatal secondary arrhythmias. The spike protein may damage the heart at any age. It is possible that spike protein could also be caused by the infection or the vaccine.

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 PR interval is usually between 0.12 and 0.2 seconds. A PR interval greater than 0.02 is considered normal for younger people, especially athletes. If PR interval measurements are always 0.2 or lower and then begin to increase as an older adult, it is a sign that there may be more severe conduction abnormalities.

It is particularly concerning in the context of a pandemic if PR interval prolongation is first seen following a bout COVID or vaccination. This is a sign of inflammation, even if it’s minimal. It should not be dismissed as being of little importance. Every disease is characterized by a range of pathologies, so it’s important to not ignore the early stages. [56]. Harvard found that those with PR intervals longer than 0.2 seconds were twice as likely to develop atrial fibrillation and three times more likely to need a pacemaker. This is due to advanced levels of heart block and almost a one-and a half-time increase in all-cause death. Additionally, individuals with a prolonged PR interval were at greater risk. [57].

But, the Federal Aviation Administration (FAA), seems to have ignored the inherent disease in a pandemic-induced PR interval. Due to a shortage of pilots and due to the vaccine requirement that it introduced during the pandemic to pilots to fly, as well as the early retirements, the FAA changed the rules. They ignored long-standing norms of normalcy based upon medical science and not convenience. The FAA now declares a PR interval at 0.3 seconds as the official limit. “new normal” The FAA Guide for Aviation Medical Examiners, October 2022. According to the October 2021 standards, the PR interval was only 0.2 seconds. The pilot has “no symptoms,” A PR interval of 0.3 or lower will allow the pilot to obtain clearance to fly. A PR interval greater than 0.3 is considered unacceptable. “current Holter and cardiac evaluation” These are required. Given that the average PR interval ranges between 0.12 seconds and 0.20 seconds (the normal PR interval), a interval of 0.3 seconds is a reasonable interval. “permissible” increase in this interval by over 100 percent relative to the low normal interval of 0.12 seconds. This is a significant increase in PR interval.

To be cleared to fly medically, even commercial pilots, you do not need to pass a treadmill stress test. This policy is unsafe and shocking. It’s because many pilots are at the age when heart attacks can occur without early symptoms. They also need a normal ECG. The ECG is the only mandatory testing for heart health. One-third of all deaths in the world are related to cardiovascular disease. In Western countries, about half of patients with coronary artery disease die suddenly. [58,59]. Prospective pilots should have more thorough cardiac evaluations performed and be repeated at the appropriate times. A normal ECG means a heart attack has not occurred—nothing more. An extremely advanced case of coronary artery disease can cause a fatal heart attack within 10 minutes. A persistent elevation in troponin and/or D2-dimer levels should not be allowed to fly. It doesn’t matter if the pilot feels well, has a normal ECG and is not suffering from myocarditis.

COVID and Blood Clots.

D-dimer blood tests are used to determine if blood clots have broken up (lysis) or released the products. It does not indicate how likely the blood is to clot (increasedcoagulability). It is sensitive and will be elevated if there is increased blood clotting. This is because the clots must be removed to prevent circulation from shutting off. An elevated D-dimer test is very reliable and can indicate that there are bloodclots breaking down because too many new ones are being formed. In the absence of a high D-dimer, significant thrombosis is rare. [60].

A high D-dimer is a concern when there has been a history either of chronic or active COVID infection and a history that includes one or more vaccinations. There is strong evidence to show that there is an ongoing spike in protein presence binding ACE2 receptors within the inner lining of blood vessels (endothelium), causing platelet activation and subsequent blood clotting. [61]. Blood clots may range in size from tiny to large. Although not always the case, such clotting may be part of myocarditis. It is particularly alarming to have both elevated troponin and elevated D-dimer levels. This should be treated immediately in order for the pathology to be normalized.

Both the COVID vaccination and the COVID infection have been shown to increase blood clotting. [62,63]. In general, viral infections can cause abnormal bloodclotting. [64]. Elevated D-dimer levels in COVID patients who were critically ill were detected around 60% of the time [65]. Not surprising, the higher the D-dimer levels of COVID patients, both in terms of morbidity as well as mortality, the more severe they are. [66–68]. Similar to the above, higher D-dimer levels at COVID admissions increase the likelihood of in-hospital deaths [69].

D-dimer levels generally decrease if the underlying infection can be treated. D-dimer levels will usually return to normal after a thrombotic event is over. Many chronic COVID infections can cause blood clotting issues. A study showed that 25% of COVID patients recovering from the acute clinical phase had higher D-dimer levels. It is also important to note that blood clotting parameters were already returning to normal in almost 90 percent of patients. This demonstrates the sensitiveness of D-dimer tests for detecting bloodclotting pathology. Other tests include prothrombin, partial thromboplastin, fibrinogen and platelets. Even interleukin-6 (a test that tracks inflammation) and C-reactive proteins have typically returned to normal. [70].

The blood platelet levels tend to drop while D-dimer levels increase. This is because they are used in blood clot formation. [71]. This laboratory finding has been associated with a post-COVID syndrome, vaccine-induced prothrombotic immuno thrombocytopenia. [72–75].

D-dimer testing has been given greater attention during the pandemic than ever before. However, D-dimer elevations can also be caused by other conditions. [76]. Anyone who has a persistent spike in D-dimer levels, even if they are not experiencing acute illness, is most likely suffering from the effects of persistent spike protein presence within their vasculature. This could be due to COVID infection or lingering COVID vaccines. Even if an individual is not suffering from COVID or has had a vaccine, it is important to have a comprehensive medical evaluation. D-dimer levels that are elevated are not normal. The patient’s feeling well should not be considered a sign of a persistently elevated D2-dimer.

Therapeutic Recommendations

Simply put, the goal of treatment is to normalize D-dimer and troponin levels. For older patients with chronic medical conditions, this can be more challenging to achieve. These tests should be normalized with a coordinated effort from the start.

Most of the spikes in troponin and D dimers at this stage in the pandemic are secondary to persistent spike proteins in the body after COVID infection, one, two or more COVID vaccines, or both. Due to the possibility of spike protein transmission, there may be people who have elevated test levels even though they don’t know that they were infected. These tests should be done on all people at the same time. Any elevations should be treated immediately. If the results are not abnormal, it will still be a great baseline data point for dealing with any future medical conditions, or infections, COVID or not.

There is no standard protocol to deal with persistent spike protein syndrome with elevated levels of troponin and/or D dimer. Some people will quickly respond and return to normal after taking only minimal steps. Some will need more aggressive or prolonged treatment, while others may not respond to any of the measures taken. Younger patients should not experience inability to return to normal health, especially if a high-quality regimen of nutrients, vitamins and minerals is introduced.

These recommendations are applicable to individuals with elevated levels of troponin or D-dimer, or both. These tests require specific reference ranges (or normal ranges) from the laboratory performing them. There can be significant variation between testing sources. These recommendations can be applied to the clinically normal person as well as someone suffering from chronic COVID and other symptoms. This protocol and all variations thereof should be followed by a licensed medical professional.

  1. Intravenous vitamin A, infused for 60 to 120 minutes at a dose of 50 to 150 grams (1 gram/kilogram weight). Each IV should contain 25 mg hydrocortisone. Hydrocortisone can also be taken orally if it is not available. Take 50 mg approximately one hour before you start the infusion. Each IV bag should contain 500- 1,500 mg magnesium chloride. You can find more information on vitamin-C administration here. [77]​

Alternatively, take five packets of LivOn Labs liposome-encapsulated vitamin C orally three times daily [78]. Hydrocortisone can be taken orally, if available, with every dose.

You can also consume 2 to 4 g of sodium ascorbate with juice three times daily, along with 10-20 mg of hydrocortisone.

2. Infusions of vitamin C should be followed with an infusion of methyleneblue (a powerful anti-pathogen that has been shown to be extremely beneficial in advanced stages of COVID). [79–84]:

Infuse 50mg of MB in 250ml of 5 Percent Dextrose Solution for 30 to 45 minutes.

Alternately, 50mg of MB can also be taken orally every day after vitamin C administration. Drink 5 ml (1 percent) MB solution in a glass of juice (tomatoes are a good choice). Temporary teeth and tongue staining can be avoided by using a straw. Skin stains can be removed by quick administration of 3 percent hydrogen peroxide.

3. Hydrogen peroxide Nebulizations are tolerated to eliminate low grade colonizations by COVID or other pathogens in lower digestive tracts. [85].

Any, or all, of the following nutrient/vitamin/mineral supplements for general support of long-term health: [86]

  • Vitamin C
  • Magnesium chloride
  • Quercetin and zinc
  • Vitamin D
  • Vitamin K2
  • Olive leaf extract
  • Multivitamin and multimineral preparations that do not contain calcium, iron, or other minerals
  • For future blood clotting problems, serrapeptase (or lumbrokinase) can be used in addition to nattokinase.

The following steps can be added, at the discretion and approval of your health care professional.

  • Obzonated blood and saline infusions
  • Ultraviolet irradiation of the Blood
  • Hydrogen peroxide intravenous infusions
  • Hyperbaric oxygen treatments
  • Chlorine dioxide treatments
  • Hydroxychloroquine and chloroquine
  • Ivermectin

The patient must decide if they want to change the treatment or if they should continue for a longer time with the assistance of a health care professional.

Recap

Myocarditis used to be rare. Myocarditis has become more common due to COVID vaccines as well as COVID itself. A troponin test showed that many people still have low-grade myocardial swelling even after their clinical normalcy has returned. Such individuals are at risk of developing serious complications from their underlying disease if a booster shot is given or COVID or any variant is retracted. A persistent inflammation of the heart indicates that there is an inability to remove the spike protein from the organ. This could also be seen throughout the body. This creates the potential for dramatic health decline if spike protein is not increased or replicated in the body.

An elevated level of D-dimer indicates an active state of blood clotting. If these levels are high, long-term prognosis can be very poor.

Troponin levels can be elevated and cause heart rhythm problems or blockages. The FAA is currently changing their rules to allow pilots who have PR intervals greater then 0.3 seconds to fly. This development should concern everyone who flies. PR intervals that are longer in older people can indicate serious heart problems and early death. Politics should not replace science and the need for ever more money.

It is important to normalize any persistently elevated troponin or D-dimer test levels. This is crucial in pilot populations. These measures are discussed along with recommendations for long-term supplementation.

Thomas E. Levy, a cardiologist and attorney at law, is a contributing editor to the Orthomolecular Medicine News Service. Dr. Levy is a consultant for LivOn Labs. His email address is [email protected].

Refer to

1. Bozkurt B., Kamat I., Hotez P (2021). Myocarditis using COVID-19 mRNA vaccinations. Circulation 144.471-484. PMID: 34281357

2. Fazlollahi A, Zahmatyar M, Noori M et al. (2022) Cardiac complications after mRNA COVID-19 vaccinations: A systematic review of case reports, case series, and case reports. Reviews in Medical Virology 32.e2318. PMID: 34921468

3. Kyaw H, Shajahan S, Gulati A et al. (2022) COVID-19 mRNA vaccine-associated myocarditis. Cureus 14:e21009. PMID: 35154981

4. Lai F, Li X, Peng K et al. (2022) Carditis following COVID-19 vaccination using a messengerRNA vaccine and an inactivated vaccine vaccine: A case-control study. Annals of Internal Medicine 175(3), 362–370. PMID: 35073155

5. Li C, Chen Y, Zhao Y et al. (2022). Injecting intravenous coronavirus virus 2019 (COVID-19), the mRNA vaccine, can induce acute myopericarditis. Clinical Infectious Diseases. 74:1933-1950. PMID: 34406358

6. T. Theoharides (222) Could long-COVID syndrome be caused by the SARS-CoV-2-spike protein? Molecular Neurobiology 59.1850-1861. PMID: 35028901

7. Theoharides T, Conti PA (2021) SARS-CoV-2 spike protein is a serious problem. There are more details than you might think. Journal of Biological Regulators and Homeostatic Agents 35.833-838. PMID: 34100279

8. Pfizer (2021) Phase 1/2/3, placebo-controlled and randomized, observer blinded, dose-finding trial to evaluate safety, tolerability, and effectiveness of SARS CoV-2 RNA vaccine candidates for COVID-19.

9. Deruelle F (2022). The pharmaceutical industry poses a danger to your health. Additional evidence can be found with COVID-19. Surgical Neurology International 13 – 475. PMID: 36324959

10. Levy, T (2021) Striking visual evidence to cancel the spike protein http://orthomolecular.org/resources/omns/v17n24.shtml

11. Chakravarty A, Chatterjee A (2022). Neurological complications after COVID-19 vaccination. Current Neurology and Neuroscience Researchs Nov 29. Online before printing. PMID: 36445631

12. De Michele M, Kahan J, Berto I et al. (2022). Cerebrovascular complications due to COVID-19 or COVID-19 vaccination. Circulation Research 130, 1187-1203. PMID: 35420916

13. Schwab C, Domke L, Hartmann L et al. (2022) Autopsy-based histopathological characterization of myocarditis after anti-SARS-CoV-2-vaccination. Clinical Research in Cardiology Nov 27, Online ahead of printing. PMID: 36436002

14. Robles J, Zamora M, Adan-Castro E et al. (2022) The spike protein of SARS-CoV-2 induces endothelial inflammation through integrin α5β1 and NF-κB signaling. The Journal of Biological Chemistry 298.101695 PMID: 35143839

15. Rossouw, T., Anderson R. Manga P. Feldman C. (1922) The role of platelet-endothelium interactions and the pathogenesis severe SARS/CoV-2-associated myocardial infarction. Frontiers in Immunology 13 :776861. PMID: 35185878

16. Saei A, Sharifi S, Mahmoudi M (2020) COVID-19: nanomedicine uncovers blood-clot mystery. Journal of Proteome Research 19 (4364-4373). PMID: 32790309

17. Zhang S, Liu Y, Wang X et al. SARS-CoV-2 binds platelet ACE2 to improve thrombosis in COVID-19. Journal of Hematology & Oncology 13 – 120 PMID: 32887634

18. De Michele M, d’Amati G, Leopizzi M et al. (2022a). Evidence for a spike in SARS-CoV-2 protein on thrombi taken from COVID-19 sufferers. Journal of Hematology & Oncology 15, 108. PMID: 35974404

19. Grobbelaar L, Venter C, Vlok M et al. (2021). SARS-CoV-2 spike Protein S1 induces fibrin(ogen), resistant to fibrinolysis: Implications on microclot formation for COVID-19 Bioscience Reports 41.BSR20210611. PMID: 34328172

20. Imazio M, Klingel K, Kindermann I et al. (2020) COVID-19 pandemic, troponin and myocarditis: indirect myocardial damage, myocardial inflammation and myocarditis Heart 106, 1127-1131. PMID: 32499236

21. Chen T, Wu D, Chen H et al. (2020) Retrospective study of the clinical characteristics of 113 coronavirus-infected deceased patients. BMJ 368.m1091. PMID: 32217556

22. Shi S, Qin M, Shen B et al. (2020). Association of cardiac injury and mortality in hospitalized patients treated with COVID-19 in Wuhan China. JAMA Cardiology 5:802-810. PMID: 32211816

23. Chilazi M., Duffy E. Thakkar A., Michos E (2021). COVID and cardiovascular diseases: What we know in 2021. Current Atherosclerosis Reports 23.37 PMID: 33983522

24. Lala A, Johnson K, Januzzi J et al. 2020. Myocardial injury and its impact on patients with COVID-19 infection. Journal of the American College of Cardiology, 76:533-546. PMID: 32517963

25. Park K., Gaze D., Collinson P., Marber m (2017) Cardiac troponins – from myocardial damage to chronic diseases. Cardiovascular Research 113.1708-1718. PMID: 29016754

26. Thygesen K, Alpert J, Jaffe A et al. (2018) Fourth universal definition for myocardial injury (2018). Journal of the American College of Cardiology 72/2231-2264. PMID: 30153967

27. Sandoval J, Januzzi Jr J. Jaffe A (2020). Cardiac troponin in assessment of myocardial damage in COVID-19: JACC topic of the Week. Journal of the American College of Cardiology. 76:1244-1258. PMID: 32652195

28. Cho S (2020). Subclinical and small myocardial injuries within the upper limit of cardiac troponin should be treated after noncardiac surgery. Korean Circulation Journal 50:938-939. PMID: 32969209

29. Agirbasli MA (2019) Universal definition for MI: higher than 99 percentiles of the upper limit (URL) for Hs-cTn: “Yes, but which URL?” The American Journal of Emergency Medicine, 37:510. PMID: 30600186

30. Park J, Hyeon C, Lee S et al. (2020). Mildly elevated cardiac troponin after noncardiac surgical procedures. Korean Circulation Journal 50, 925-937. PMID: 32812403

31. Park J, Hyeon C, Lee S et al. (2020) Preoperative cardiac Troponin lower than the 99th percentile upper reference limit. Also, 30-day mortality following noncardiac surgery. Scientific Reports 10:17007 PMID: 33046756

32. Nagele P, Brown F, Gage B et al. (2013) The use of high-sensitivity cardiac troponin (T) in the diagnosis and prediction of myocardial injury and long-term mortality following noncardiac surgery. American Heart Journal 166.325-332. PMID: 23895816

33. Muller C et al. (2022). Not yet published https://www.unibas.ch/de/Aktuell/News/Uni-Research/Voruebergehende-milde-Herzmuskelzellschaeden-nach-Booster-Impfung.html

34. Saul A (2020). Vitamin C treatment of COVID-19. Case reports. http://orthomolecular.org/resources/omns/v16n47.shtml

35. Levy T (2020). COVID-19: What can I do to cure you? Let me count them. http://orthomolecular.org/resources/omns/v16n37.shtml

36. Levy T (2021). Hydrogen peroxide Nebulization and COVID Resolution: Impressive anecdotal Results http://orthomolecular.org/resources/omns/v16n37.shtml

37. Levy T (2021). Resolving “Long-Haul COVID” Also, vaccine toxicity. Neutralizing spike protein. http://orthomolecular.org/resources/omns/v17n15.shtml

38. Amaoh et al. (2022). Hospital study shows that hydrogen peroxide is effective in preventing COVID-19 http://orthomolecular.org/resources/omns/v18n18.shtml

39. Fish-Trotter H, Ferguson J, Patel N et al. (2020) Inflammation levels and circulating natriuretic Peptide levels. Circulation. Heart Failure 13 :e006570. PMID: 32507024

40. Liu P. Blet A. Smyth D. Li H (2020). The science behind COVID-19: Implications for the cardiovascular system. Circulation 142 :68-78. PMID: 32293910

41. Putschoegl, A, Auerbach S (2020). Diagnosis and treatment for myocarditis among children. Pediatric Clinics of North America, 67:855-874. PMID: 32888686

42. Kuwahara K (2021). Heart failure and the natriuretic-peptide system: diagnostic and therapeutic implications. Pharmacology & Therapeutics 227.107863. PMID: 33894277

43. Yu S, Zhang C, Xiong W et al. (2021) A hypothesis: Disproportional cardiac troponin levels and B-type Natriuretic Peptide levels-a high-risk biomarker and poor prognostic indicator in patients with fulminant Myocarditis. Heart, Lung & Circulation 30:837-842. PMID: 33582021

44. Moady, Perlmutter S and Atar S (2022). A retrospective study of the prognostic power of natriuretic Peptides in patients with suspected acute Myocarditis. Journal of Clinical Medicine 11/2472. PMID: 35566598

45. Zhao Y, Lyu N, Zhang W et al. (2022) The prognosis implications of the N-terminal proB-type Natriuretic Peptide in Adult Patients with Acute Myocarditis. Frontiers in Cardiovascular Medicine 9 :839763. PMID: 35433855

46. Mahdawi T, Wang H, Haddadin F et al. 2020. Heart block in coronavirus-infected patients: A case series of three patients infected by SARS-CoV-2. HeartRhythm Case Reports 6/652-656. PMID: 32837907

47. Chen J, Robinson B., Patel P, et al. (2021) A transient complete heart block in COVID-19 patients. Cureus 13:e15796. PMID: 34295600

48. Aryanti, R., Hermanto, D., Yuniadi, Y. (2022) Dynamic variations of atrioventricular Conduction during COVID-19 Infection: Does inflammation matter. International Journal of Arrhythmia 23.20. PMID: 35937564

49. Etienne H. Charles P. Pierre T (2022). A case report on a transient but persistent complete heart block following COVID-19 vaccination. Annals of Medicine and Surgery. 78:103694. PMID: 35530368

50. Lee K, Rahimi O. Gupta N. Ahsan C (2022). Complete AV block in COVID-19 vaccinated patient. Case Reports in Cardiology 2022. PMID: 35371571

51. Kimball E. Buchwalder K. Upchurch C. Kea B (2022). Intermittent total heart block with ventricular stoppage after Pfizer’s COVID-19 booster vaccination: Case report. Journal of the American College of Emergency Physicians open 3:e12723. PMID: 35475120

52. Nakra N. Blumberg D. Herrera-Guerra AA, Lakshminrusimha S. (2020) Multisystem inflammatory syndrome (MIS-C), in children following SARS-CoV-2 virus infection: Review of clinical presentation, hypotheses, and management. Children 7:69. PMID: 32630212

53. Radia T, Williams N, Agrawal P et al. (2021). Multi-system inflammation syndrome in children and teens (MIS-C: A systematic review. Paediatric Respiratory Journal 38:51-57. PMID: 32891582

54. Choi N, Fremed M, Starc T et al. (2020). MIS-C abnormalities and cardiac conduction abnormalities. Pediatrics 146.e2020009738. PMID: 33184170

55. Dionne A, Mah D, Son M et al. (2015) Atrioventricular block in multisystem inflammatory children. Pediatrics 146:e2020009704.

56. Holmqvist, F., and Daubert J. (2013) First-degree AVM block-an entirely benign condition or a potentially cureable cause of heart disease? Annals of Noninvasive Electrocardiology 18/221-224. PMID: 23714079

57. Cheng S, Keyes M, Larson M et al. (2009) Long-term outcomes for individuals with prolonged PR intervals or first-degree Atrioventricular Block. JAMA 301.2571-2577. PMID: 19549974

58. Sumner G. Mitchell L (2015) Sudden death from cardiac disease. Current Problems in Cardiology 40, 133-200. PMID: 25813838

59. Kumar A, Avishay D, Jones C et al. (2021). Sudden cardiac death: epidemiology. Review in Cardiovascular Medicine 22(2):147-158. PMID: 33792256

60. Carli G, Nichele I, Ruggeri M et al. (2021) Acute onset of deep vein thrombosis (DVT), shortly following the second dose mRNA SARS–CoV-2 vaccine. Internal and Emergency Medicine 16 :803-804. PMID: 33687691

61. Iba T., Connors J., Levy J. (2020) The coagulopathy and endotheliopathy of COVID-19. Inflammation Research 69:1181-1189. PMID: 32918567

62. Biswas S. Thakur V. Kaur P. and others. (2021) The mystery of blood clots in COVID-19 sufferers: simplifying it. Medical Hypotheses 146.110371. PMID: 33223324

63. Lundstrom K. Barh D. Uhal B et. (2021) COVID-19 vaccinations and thrombosis. Dead-end street or roadblock? Biomolecules 11:1020. PMID: 34356644

64. Subramaniam S. Scharrer, I (2018) Procoagulant activity in viral infections. Frontiers of Bioscience 23:1060-1081. PMID: 28930589

65. Iba T, Levy J, Levi M et al. (2020) Coagulopathy and coronavirus diseases. Critical Care Medicine 48.1358-1364. PMID: 32467443

66. Naymagon L. Zubizarreta Na, Feld J, et al. (2020). Admission D-dimer levels and D-dimer trends. COVID-19 results. Thrombosis research 196:99-105. PMID: 32853982

67. Paliogiannis P, Mangoni A, Dettori P et al. (2020) COVID-19 severity and D-dimer concentrations: A systematic review. Frontiers in Public Health 8 :432. PMID: 32903841

68. Rostami M., Mansouritorghabeh (2020) The D-dimer levels in COVID-19 infections: A systematic review. Expert Review of Haematology 13:1265-1275. PMID: 32997543

69. Zhang L, Yan X, Fan Q et al. 2020. D-dimer levels at admission can be used to predict in-hospital death in COVID-19 patients. Journal of Thrombosis and Hemostasis 18 (4): 1324-1329. PMID: 32306492

70. Townsend L, Fogarty H, Dyer A et al. (2021). The acute phase response does not affect the prolong elevation of D2-dimer levels in convalescent COVID-19-patients. Journal of Thrombosis and Haemostasis 19 :1064-1070. PMID: 33587810

71. Wool G, Miller JA (2021) The effect of COVID-19 illness on platelets and cocoagulation. Pathobiology 88:15-27. PMID: 33049751

72. Favaloro E (2021). Laboratory testing for COVID-19-immune thrombocytopenia. International Journal of Laboratory Hematology 43. 559-570. PMID: 34138513

73. Iba T., Levy J., Warkentin T. (2021) Recognizing vaccine induced immune thrombotic. Critical Care Medicine 50, e80-e86. PMID: 34259661

74. Scully M. Singh D., Lown R. et al. (2021) Platelet factor 4 pathologic antibodies after ChAdOx1 and nCoV-19 vaccine. The New England Journal of Medicine 384, 2202-2211. PMID: 33861525

75. Thaler J, Ay C, Gleixner K et al. (2021). Successful treatment of vaccine-induced thrombotic immune tuberculocytopenia. Journal of Thrombosis and Haemostasis 19 :1819-1822 PMID: 33877735

76. Lippi G., Bonfanti L., Saccenti C., Cervellin G. (2014). Causes of elevated D -dimer in urban patients admitted to large urban emergency departments. European Journal of Internal Medicine 25.45-48. PMID: 23948628

77. Levy, T. (2019) Magnesium and Reversing Disease. Henderson, NV: MedFox Publishing. Refer to Chapter 16. Download a free copy of the book in English or Spanish https://mag.medfoxpub.com/

78. https://www.peakenergy.com/articles/nh20140411/Exposing-the-truth-about-liposomal-nutrients/

79. Crossley K, Wainwright M. (2002) Methylene blue-a therapy dye for all seasons. Journal of Chemotherapy 14(4), 431-443. PMID: 12462423

80. Kwok E., Howes D. (2006) A systematic review of the use of methyleneblue for sepsis. Journal of Intensive Care Medicine 21. 359-363. PMID: 17095500

81. Oz M. Lorke D. Hasan M. Petroianu. (2011) Cellular, molecular, and cellular effects of methyleneblue on the nervous system. Medicinal Research Reviews, 31:93–117. PMID: 19760660

82. Hamidi-Alamdari D, Hafizi-Lotfabadi S, Bagheri-Moghaddam A et al. (2021) Methylene Blue for hospitalized COVID-19 Patients: A randomized controlled, open-label clinical study, phase 2. Revista de Investigacion Clinica 73:190-198. PMID: 34019535

83. Mahale N, Godavarthy P, Marreddy S et al. (2021). Intravenous injection of methyleneblue as a rescue treatment for refractory hypoxia among COVID-19 ARDS-patients: A case series. Indian Journal of Critical Care Medicine 25.934-938. PMID: 34733037

84. Xue H. Thaivalappil A. Cao K (2021). Potentials of methyleneblue as an anti-aging medication. Cells 10/3379. PMID: 34943887

85. LevyT (2021) Rapid Virus Recover: You don’t have to be afraid! Henderson, NV: MedFox Publishing. Refer to Chapter 3. Download a free copy of the book in English or Spanish https://rvr.medfoxpub.com/

86. Levy, T. (2019) Magnesium and Reversing Disease. Henderson, NV: MedFox Publishing. Refer to Chapter 17. Download a free copy of the book in English or Spanish https://mag.medfoxpub.com/

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