We request a doctor specializing in heart diseases to provide an opinion on the microbiological potentials in Nicholas's case, as the enemy will unfairly reference broad statistical data.
Only 0.5% of individuals develop bacterial endocarditis in a biological heart valve prosthesis over two years after surgery, and most of them are not children. Nicholas developed it two months after receiving the second injection of Moderna's COVID-19 vaccine, without informed consent.
https://www.msdmanuals.com/professional/cardiovascular-disorders/endocarditis/infective-endocarditis#Etiology_v939256
Healthcare failed to inform about the risk of myocarditis and pericarditis, despite WHO and the Medical Products Agency's directives about it more than a month before Nicholas was called for COVID-19 vaccination:
https://www.who.int/news/item/09-07-2021-gacvs-guidance-myocarditis-pericarditis-covid-19-mrna-vaccines
Additionally, they were obliged to inform about "significant risks of complications and side effects," according to the Patient Act 3:1:6.
Neither Nicholas's cardiologist nor his hepatologist were consulted before the vaccination (this is evident from the medical records), despite the Pediatric Association's recommendation for an individual assessment within his group "having undergone another organ transplant."
Nicholas did not have heart failure, so concerning his heart alone, he was not in a particular group recommended for the COVID-19 vaccine; it was due to the liver transplant he had at six months old that he received it. However, an individual assessment was not conducted.
Since Nicholas was clinically healthy and off medication, such an assessment would have shown he did not need the vaccine.
https://www.barnlakarforeningen.se/wp-content/uploads/2021/06/BLF-Rekommendationer-för-vaccination-mot-covid-19-för-särskilda-grupper-av-barn-och-ungdomar-från-12-år-HA210816.pdf
Nicholas developed a fever of 40 degrees Celsius the evening after the second shot. However, since we, as parents, were not aware of the risks of heart inflammation, we did not take Nicholas for an examination afterward.
A study shows that two doses of Moderna's COVID-19 vaccine increase the risk of myocarditis sixfold:
https://www.sciencedirect.com/science/article/pii/S0264410X24001270
The inflammation can be nearly asymptomatic and require more than a standard heart examination to detect.
https://www.hopkinsmedicine.org/heart-vascular-institute/cardiovascular-research/myocarditis
Myocarditis can occur up to a month after vaccination. The last month before Nicholas fell ill, he was tired and sluggish, which may indicate myocarditis.
https://www.heart.org/en/news/2021/12/06/post-vaccine-myocarditis-in-young-people-is-rare-and-usually-mild-study-confirms
Of course, there is no broad statistical basis for a 13-year-old boy developing an undetected myocarditis that weakens his heart and leads to a bacterial infection in it. How many boys with a biological heart valve prosthesis (homograft conduit in Nicholas's case) were even vaccinated against COVID-19?
But it is not new that vaccines can cause an immune-related inflammation that can weaken the heart and make it vulnerable to bacteria adhering to and colonizing the valves (Staphylococcus aureus in Nicholas's case).
This is related to the permeability of the vessels and that traces of inflammation can create attachment points (even on the inside of the heart) - and that the flow of blood can change.
And it has to do with the immune system's focus being on the inflammation, so it does not protect as well against the bacteria.
Inflammation in the heart, as in conditions such as endocarditis or myocarditis, can create an environment conducive to the growth and adherence of bacteria like Staphylococcus aureus on the heart valves. This can occur in the following ways:
1. Inflammation can lead to damage and changes in heart tissue, exposing underlying connective tissue and damaged valves. This exposed tissue provides bacteria with a surface to adhere to and form biofilms.
2. Inflammation can alter blood flow through the heart, especially at damaged or inflamed valves. Turbulent blood flow can increase the risk of bacteria adhering to the heart valves.
3. Inflammation can induce the expression of adhesion molecules on the surface of endothelial cells, promoting the binding of bacteria to the heart valves. Staphylococcus aureus has specific adhesions that can bind to these molecules and to damaged tissues.
4. Ongoing inflammation can lead to a locally weakened immune response, making it easier for bacteria to survive and grow in the heart. Inflammation can also cause the release of cytokines and other inflammatory mediators that can negatively affect the function of immune cells.
5. Inflammation can also lead to a procoagulant environment where blood clots form on damaged heart valves. These blood clots can capture bacteria circulating in the bloodstream and facilitate their colonization on the valves.
In summary, heart inflammation can facilitate the adhesion and growth of Staphylococcus aureus in multiple ways, increasing the risk of serious infections such as infectious endocarditis.