TRIBUNE – The vaccine against Covid-19 has been the subject of much controversy, mainly because of its mechanism of action (mRNA vaccine inducing the production of the spike protein by the cells of the host itself), and by the choice of this protein to establish immunity. This protein is indeed toxic, attacking the vascular endothelium, pro-inflammatory, not very immunizing mainly because of the variants (of which the Spike protein has undergone modifications during the mutations), and the quantity produced by the body is not precisely quantifiable, neither in terms of quantity nor in terms of duration. We will not return precisely to these questions, which have been the subject of passionate debate.
What about myocarditis induced by these vaccines? ?
The mechanism of action is still poorly understood. Here are the main assumptions made to date:
The vaccine used to try to prevent the disease has a unique feature compared to other conventional vaccines. This is not the inoculation of a viral protein, but its manufacture by the human cellular machinery via the injection of mRNA. The cells, as in the disease, can thus express the Spike protein on their surfaces, explaining the occurrence of myocarditis by a subsequent attack of the immune system. The mRNA could also intervene directly. Vaccine-induced cytokine changes could also favor the appearance of these myocarditis. We also recall the direct toxic effects of the spike protein produced against the vascular endothelium (wall) which strongly expresses ACE2, the target receptor of spike, causing inflammation, hypercoagulability and thrombosis. This is clinically expressed by myocardial infarctionof the cerebral thrombophlebitis and cerebrovascular accidents (CVA). It is crucial to note that myocarditis has already been described in the literature in the context of thrombotic thrombocytopenic purpura (TTP), a disease causing thrombosis, which can occur as a result of aggression and endothelial dysfunction (sources are in studies 1, 2, 3 and 4).
The incidence appears to predominate in young, male subjects. The scanner and especially the cardiac MRI can help in the diagnosis, specify the extent of the myocardial damage, and show dysfunctions of the contraction of the ventricles, and in certain cases have a prognostic value. Rarely, these myocarditis can present in an acute form with potentially fatal heart failure. Most often, clinical resolution is fortunately observed. to the whole (the patient no longer shows any signs: no pain or shortness of breath), having made it possible to conclude falsely in their benignity by unsophisticated scientists and doctors.
In reality, and we will demonstrate this below, no one can predict the evolution of these myocarditis and it is totally abnormal to put such a risk at young patients with an extremely low if not zero risk of serious covid.
Indeed, it is well reported in the published and peer-reviewed medical literature that the prognosis of these myocarditis cannot in any case be established early, because the most formidable complications are late, even very late. It is therefore yet another imposture to decree peremptorily that these damages linked to the Covid-19 vaccine, moreover abundantly reported in the literature, would not have potential serious implications. The “TV set doctors”, supporters of the Doxa according to which the vaccine would be risk-free, seem to ignore that dilated heart disease (heart disease where the ventricle expands and ends up no longer playing its role) can occur several years, sometimes more than 10 years after the acute episode (vaccinal myocarditis in this case). This has been well described in myocarditis in general, most often of viral origin (Coxsackie virus for example). Under these conditions, it is easy to understand that these late complications, which for the most part have not yet occurred, are not found in the registers for reporting adverse effects. We recall two things here: 1) few side effects are declared, because peremptorily and first considered unrelated to the vaccine 2) many myocarditis could be asymptomatic or paucisymptomatic and/or not be the subject of a cardiology consultation.
The law of large numbers thus intervenes because of mass vaccination. It is difficult to accurately estimate the number of patients with vaccinal myocarditis, a complication that is probably underestimated. Some prognostic factors are discussed; patients with ventricular contraction dysfunction at the time of diagnosis would present a greater risk of progressing to a severe form, which seems logical. However, some authors report benign forms evolving pejoratively. The Weiss study et al showed that clinical status during follow-up (based on scintigraphic assessment of left ventricular function) even after 12-15 months from disease onset, does not necessarily predict long-term prognosis in due to the potential recurrence of autoimmune inflammatory processes in initially benign-appearing forms.
Bear in mind that the RNA vaccine induces the expression of a foreign antigen on the cell surface (the viral spike protein), which promotes the occurrence of these autoimmune mechanisms!
The precise rate of evolution towards dilated heart disease therefore remains difficult to specify, because it would be necessary to follow cohorts of patients with such a diagnosis proven for many years by echocardiography or even MRI; it can nevertheless be estimated between 0 and 52%.
How could we estimate the number of patients who may in the future suffer from post-vaccination dilated heart disease? Let us propose the following equation: number of post-vaccination dilated heart disease = number of patients vaccinated with a double dose (the evaluation underestimates the number of cases, because many patients had a triple or even quadruple dose) x reported rate of vaccinal myocarditis x rate of late complications of myocarditis (dilated cardiomyopathy) x declared rate x weighting factor taking into account pauci or asymptomatic myocarditis. It should be noted that the number of vaccinated patients is underestimated due to a large number of false health passes, which are difficult to quantify. We find approximately 53 million patients doubly vaccinated in France. Among the latter, according to Pfizer data, 1/10,000 would present with myocarditis, which can be found on page 5 of this report. Young subjects would be the most affected with, according to certain studies (note 5 and note 6), much higher rates: 12-17 years: approximately 1/2700; 18-24 years old: approximately 1/1900.
We will therefore take according to these data, arbitrarily, the figure of 1/5000 vaccinated patients having had myocarditis. According to the studies reported below, we make a low estimate of 10% of patients progressing to a chronic form with the onset of dilated heart disease. Let us add a low rate of notification of these myocarditis and a diagnostic underestimation with a total weighting factor of 50%. The diagnostic underestimation for clinically minor forms is indeed published.
In total, 106,000 myocarditis would therefore have occurred, of which 10,600 (10%) progressed to heart failure without taking into account the diagnostic underestimation, which would bring this figure to 21,200 by taking an underestimation coefficient of 50%. This rate would be all the more outrageous given:
- that the patients were deprived of early care (treatments and oximetric monitoring whose effectiveness diminishes the alleged benefit of the vaccine)
- that these complications occur electively in young patients with mild forms of Covid in almost 100% of cases.
We thus perceive the falseness of the judgment of the “spectacle medicine” of social networks consisting in claiming that we have a decline of thousands of years concerning these vaccines, by multiplying the number of patients vaccinated by the two years of follow-up post-vaccination; on the contrary, it is necessary to follow each patient individually for several yearsmaybe more than 10 years, in order to have a clear idea of the consequences of the complications of the vaccine. Note that the evolution towards a serious and potentially fatal heart failure is quiet; the patient’s heart initially compensates for its damage by adapting and the latter does not notice anything. During the first clinical signs, the stage of the disease can be advanced, with all the implications that entails. Regular long-term cardiological follow-up would therefore be desirable for the vaccinated population, in particular for patients with myocarditis, with echocardiography or even MRI in certain cases.
As we finish this article, a new Swiss study has just been released and the results are even more alarming than previous studies, since it estimates the incidence of myocardial damage after the third dose at 2.8%, or 800 times higher than the usual incidence of myocarditis.
On time currently, no one can predict what the consequences of these vaccinal myocarditis will be, whether symptomatic or not. Let’s hope that the mass inoculation of such a totally innovative “vaccine”, disregarding the precautionary principleafter sending patients home without treatment and without supervision, does not lead to the occurrence of an epidemic of heart failure on dilated cardiomyopathy in the next 10 to 15 years.
Notes :
1. Siripanthong B, Nazarian S, Muser D, Deo R, Santangeli P, Khanji MY, Cooper LT Jr, Chahal CAA. Recognizing COVID-19-related myocarditis: The possible pathophysiology and proposed guideline for diagnosis and management. Heart Rhythm. 2020 Sep;17(9):1463-1471. doi: 10.1016/j.hrthm.2020.05.001. Epub 2020 May 5. PMID: 32387246; PMCID: PMC7199677.
2. Bozkurt B, Kamat I, Hotez PJ. Myocarditis With COVID-19 mRNA Vaccines. 2021 Aug 10;144(6):471-484. doi: 10.1161/CIRCULATIONAHA.121.056135. Epub 2021 Jul 20. PMID: 34281357; PMCID: PMC8340726.
3. Raghavan S, Kenchappa DB, Leo MD. SARS-CoV-2 Spike Protein Induces Degradation of Junctional Proteins That Maintain Endothelial Barrier Integrity. Front Cardiovasc Med. 2021 Jun 11;8:687783. doi: 10.3389/fcvm.2021.687783. PMID: 34179146; PMCID: PMC8225996.
4. Visagie GJ, Louw VJ. Myocardial injury in HIV-associated thrombotic thrombocytopenic purpura (TTP). Transfus Med. 2010 Aug 1;20(4):258-64. doi: 10.1111/j.1365-3148.2010.01006.x . Epub 2010 Apr 14. PMID: 20409074.
5. D’Ambrosio A, Patti G, Manzoli A, Sinagra G, Di Lenarda A, Silvestri F, Di Sciascio G. The fate of acute myocarditis between spontaneous improvement and evolution to dilated cardiomyopathy: a review. 2001 May;85(5):499-504. doi: 10.1136/heart.85.5.499. PMID: 11302994; PMCID: PMC1729727
6. Weiss MB, Marboe CC, Escala EL, et al. Natural history of untreated chronic myocarditis (active myocarditis with fibrosis). Eur Heart J 1987;8(suppl J):247–50. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9356639/