Is this coming disaster linked to the virus as much as to the mRNA vaccine? Directly linked to the spike protein, the deleterious portion of the virus and as such the deadly Malone mRNA LNP vaccine?
Is America going to face across time a heart failure epidemic, pandemic due to the mRNA vaccine? Silent heart damage e.g. myocardial lesions, scarring etc. myo-pericarditis that will manifest as heart failure?
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https://www.cell.com/iscience/fulltext/S2589-0042(23)02718-9
‘Highlights
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Persistent SARS-CoV-2 infection model of human cardiac tissue was established
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Hypoxic stress to the persistent infection model led to cardiac dysfunction
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ACE2 and SARS-CoV-2 S protein expression were elevated after the hypoxic stress
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This research may predict a “heart failure pandemic” in the post COVID-19 era
Summary
Patients with chronic cardiomyopathy may have persistent viral infections in their hearts, particularly with SARS-CoV-2, which targets the ACE2 receptor highly expressed in human hearts. This raises concerns about a potential global heart failure pandemic stemming from COVID-19, an SARS-CoV-2 pandemic in near future.
Although faced with this healthcare caveat, there is limited research on persistent viral heart infections, and no models have been established. In this study, we created an SARS-CoV-2 persistent infection model using human iPS cell-derived cardiac microtissues (CMTs). Mild infections sustained viral presence without significant dysfunction for a month, indicating persistent infection. However, when exposed to hypoxic conditions mimicking ischemic heart diseases, cardiac function deteriorated alongside intracellular SARS-CoV-2 reactivation in cardiomyocytes and disrupted vascular network formation.
This study demonstrates that SARS-CoV-2 persistently infects the heart opportunistically causing cardiac dysfunction triggered by detrimental stimuli such as ischemia, potentially predicting a post COVID-19 era heart failure pandemic.’
Start Naked here:
‘A new report from Japan’s Riken Institute warns of a pandemic of heart failures which may start soon due to people getting Covid.
The report published in Cell warns that people with long-term heart conditions (chronic cardiomyopathy) might be particularly vulnerable to Covid. This is because the virus targets a specific receptor (ACE2) which is found abundantly in human hearts. The authors fear that Covid could lead to a large number of heart failure cases worldwide because the virus can persist in the heart.
To better understand the situation, the researchers created a model using human heart tissues which was subsequently infected with SARS-CoV-2. They found that in cases of mild infection, the virus can stay in the heart tissue for a long time (a month) without causing immediate or severe damage. However, this suggested that the virus can persist in the heart for a long time.
When the infected heart tissues were placed under stressful conditions, like low oxygen levels (which mimic heart diseases), the situation worsened. The virus became more active and the heart tissues started to function poorly. The network of blood vessels in the heart were also affected.
Even though conclusive clinical evidence that persistent SARS-CoV-2 infection is associated with declined cardiac function has not been reported so far, the proof-of-concept study of the possibility of SARS-CoV-2 persistent infection of the heart and the potential risk of opportunistic progression of heart failure should be validated by a three-dimensional human cardiac tissue model which would serve as the alarm bell for a global healthcare risk.
Hidetoshi Masumoto, research leader, said “Some people infected with the coronavirus may have persistent viral infections in their hearts. A testing system and treatment methods must be established in preparation for a ‘heart failure pandemic,’ in which we will see a rapid increase in the number of heart failure patients.
The explosive increase in the number of virus-infected patients due to the COVID-19 pandemic may have led to an enormous increase in the number of patients at potential risk for future heart failure. These patients would be predicted to maintain cardiac function superficially despite being at marginal risk.”
Whilst I have no doubt that some people may end up with heart failure due to catching Covid, this has been shown to be rare. I have no doubt that some people may die because it is extremely likely that the virus contains a lab-created spike protein which has a particular affinity for human ACE2 receptors. The very ones that are in abundance in the heart.
However, as this study shows, mild or asymptomatic infections did not cause immediate or severe damage. This is probably because if the infection is mild or asymptomatic your respiratory tract has already dealt with the virus.
For the virus to affect an organ, such as your heart, it needs to enter your bloodstream through a process called viremia. Only if Covid reaches your bloodstream can it start to bind to the ACE2 receptors, which can make the heart vulnerable to direct viral infection.
So if viremia occurs and the virus ends up attaching to ACE2 receptors in your heart, this is likely to cause an inflammatory response and your chances of heart problems are quite high. But, fortunately, due to the excellent work our respiratory tract does, this is quite rare. Just look at the number of myocarditis cases in 2020 as proof of this.
As we all know, but the Japanese research failed to look at, there is another way for the Covid spike protein to bypass the respiratory tract and enter human heart cells – vaccination.
Even Pfizer’s own research showed that when their mRNA vaccines were encapsulated in lipid nanoparticles, they spread all around the body and accumulated in most of the organs.
So what happens when heart cells begin expressing the Covid spike protein? It triggers an immune response with the body recognising the spike as foreign and activating a response. But it doesn’t just neutralise the spike, it targets the whole cell. If you are unlucky enough for the mRNA to have reached your heart cells, suddenly your body begins to train itself that your heart cells are ‘foreign’ and that response causes inflammation.
Inflammation which causes myocarditis, pericarditis and a whole range of other heart-related problems.
Furthermore, if before your immune system neutralises that particular spike expressing cell, the spike breaks off and starts floating around, it will be attracted to the ACE2 receptors in other heart cells that weren’t ever producing the spike and start causing problems there.
If you were fortunate enough that the mRNA went to your heart, the cells began expressing the Covid spike but you didn’t suffer any problems, the story still isn’t over for you.
It has been shown that those who got jabbed at least twice start an IgG4 class switch, whereby the immune system starts to tolerate the virus. Instead of trying to clear it on detection, it tolerates it as it does pollen or a bee sting.
So now, not only will your body not try to clear SARS-CoV-2, it won’t try to clear any spike protein that your cells have been instructed to produce. Some cells continue to express the protein, whilst on others it will snap off and float around before attaching itself to an ACE2 receptor.
This could continue to happen and we have no idea for how long. But now, instead of an inflammatory response, your body just accepts the spike in your heart cells as normal.
That’s good, right? Now I won’t get myocarditis?
Of course it’s not good. As this recent Japanese study shows, the virus (or spike) staying in the heart tissue for a long time does not cause immediate or severe damage. It is only when the heart is placed under additional stress that the problems start to present themselves.
The study gives the example of low oxygen levels (which mimic heart diseases) as a stressful condition to worsen the situation. Suddenly, the virus becomes more active and the heart tissues start to function poorly, leading to heart damage and heart failure.
When I first saw the headlines about the Deadly Virus which could lead to a ‘Heart Failure Pandemic’, I though this was just click bait. But reading the study itself and connecting it with mRNA distribution to organs followed by an IgG4 switch, I’m beginning to think there is no smoke without fire.
Could this explain the number of sportsmen that we are seeing drop down mid match? Playing a hard match or doing a number of fast sprints could lead to low oxygen levels, suddenly activating a heart full of spike protein and causing it to fail.’
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