This will result in more need for the BSGM tech unfortunately. (I say unfortunately because I don't think people who were led to believe these shots were the 'safest' and 'most tested' drugs in history, and took them without really researching first, ever expected many of the ramifications would carry on years later with grave impact to too many.)
"The authors concluded that at the cellular level, the effects of the COVID-19 vaccines seemed to align closer with cardiomyopathy than with myocarditis. Cardiomyopathy is a condition where heart muscles become both structurally and functionally abnormal in the absence of other heart diseases."
"Myocarditis will present with a dilated heart and patients having trouble breathing and heart failure," Dr. McCullough said. "What we're seeing with vaccines is not heart failure. It's actually cardiac arrest, which is primarily an electrical [signaling] problem."
The heart abnormalities exhibited in the cells, likely caused by disruption to RyR2 and increased PKA protein levels, "are risk factors for sudden cardiac death, ventricular tachyarrhythmias, and contractile dysfunction," they added.
"It's very worrisome," particularly since disruptions to the RyR2 receptor
are directly linked to sudden cardiac death, Dr. McCullough said. "The pattern we're seeing is people take the vaccine, and they die during exercise, or they die between 3 a.m. and 6 a.m.—again, where there's a surge of catecholamines or stress in the body."
And this came out two weeks ago:
In the first 24 h after application, both mRNA-1273 and BNT162b2 caused neither functional disturbances nor morphological abnormalities. After 48 h, expression of the encoded spike protein was detected in ventricular cardiomyocytes for both mRNAs. At this point in time, mRNA-1273 induced arrhythmic as well as completely irregular contractions associated with irregular as well as localized calcium transients, which provide indications of significant dysfunction of the cardiac ryanodine receptor (RyR2). In contrast, BNT162b2 increased cardiomyocyte contraction via significantly increased protein kinase A (PKA) activity at the cellular level.
Conclusions and Implications
Here we demonstrated for the first time, that in isolated cardiomyocytes, both mRNA-1273 and BNT162b2 induce specific dysfunctions that correlate pathophysiologically to cardiomyopathy. Both RyR2 impairment and sustained PKA activation may significantly increase the risk of acute cardiac events.