I used to think that fibrosis was permanent and irreversible, until I was corrected by a cardiologist. If you leave it too long then it can be due to remodelling, but there are some drugs that, if given early, can mitigate some of the damage or inhibit the process:
Novel Therapies for the Treatment of Cardiac Fibrosis Following Myocardial Infarction (2022)
"4.4.1. ReninâAngiotensinâAldosterone System (RAAS) Inhibitors RAAS inhibitors are widely used to target cardiac fibrosis. Drugs such as lisinopril, losartan, amlodipine, and spironolactone have proven their anti-fibrotic effect on cardiomyocytes [23,99,100]. A recent study demonstrated that a new first-in-class angiotensin receptor inhibitor, sacubitril/valsartan, can suppress the effect of RAAS during cardiac remodeling by blocking angiotensin II type 1 receptors and activating vasoactive peptides through the inhibition of the neprilysin enzyme, which is responsible for their degradation [101]. Sacubitril/valsartan prevented maladaptive cardiac fibrosis and dysfunction by blocking cardiac fibroblast activation and proliferation in a mouse model of pressure overloadâinduced hypertrophy [102]."
It would be remiss of me not to bring magnesium into the discussion:
Magnesium enhances cardiomyocyte proliferation and suppresses cardiac fibrosis induced by chronic ACTH exposure in rats
Jelena PetroviÄ et al. Magnes Res. 2021.
"...Our results show, for the first time, that administration of Mg in rats was effective in ameliorating the development of ACTH-evoked cardiac fibrosis, while facilitating cardiomyocyte proliferation. Furthermore, we propose that Mg supplementation attenuates ACTH-induced HPA axis hyperactivity, as one of the underlying plausible mechanisms, which may contribute to its cardioprotective effects."
Two points I keep making about the myocarditis issue:
(1) it is likely that myocarditis is just the most visible and easily diagnosable manifestation of a process which - given what we know about distribution - is happening throughout the body.
(2) there is no reason to believe that cases which never required healthcare intervention (it is self-limiting in most cases, and complaining about side effects was most definitely NOT encouraged) are not at some risk as well. So we could be dealing with an even more massive problem than thought.
Notably, autopsies are finding microinflammation in the heart of people who died suddenly, after no diagnosis during life:
I used to think that fibrosis was permanent and irreversible, until I was corrected by a cardiologist. If you leave it too long then it can be due to remodelling, but there are some drugs that, if given early, can mitigate some of the damage or inhibit the process:
Novel Therapies for the Treatment of Cardiac Fibrosis Following Myocardial Infarction (2022)
"4.4.1. ReninâAngiotensinâAldosterone System (RAAS) Inhibitors RAAS inhibitors are widely used to target cardiac fibrosis. Drugs such as lisinopril, losartan, amlodipine, and spironolactone have proven their anti-fibrotic effect on cardiomyocytes [23,99,100]. A recent study demonstrated that a new first-in-class angiotensin receptor inhibitor, sacubitril/valsartan, can suppress the effect of RAAS during cardiac remodeling by blocking angiotensin II type 1 receptors and activating vasoactive peptides through the inhibition of the neprilysin enzyme, which is responsible for their degradation [101]. Sacubitril/valsartan prevented maladaptive cardiac fibrosis and dysfunction by blocking cardiac fibroblast activation and proliferation in a mouse model of pressure overloadâinduced hypertrophy [102]."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9496565/
It would be remiss of me not to bring magnesium into the discussion:
Magnesium enhances cardiomyocyte proliferation and suppresses cardiac fibrosis induced by chronic ACTH exposure in rats
Jelena PetroviÄ et al. Magnes Res. 2021.
"...Our results show, for the first time, that administration of Mg in rats was effective in ameliorating the development of ACTH-evoked cardiac fibrosis, while facilitating cardiomyocyte proliferation. Furthermore, we propose that Mg supplementation attenuates ACTH-induced HPA axis hyperactivity, as one of the underlying plausible mechanisms, which may contribute to its cardioprotective effects."
https://pubmed.ncbi.nlm.nih.gov/34463274/
Excellent
Cyprinus carpio - not good but an excellent and thorough examination. Your standard is the pinnacle others hope to acheive. Happy Easter.
Any idea which type of magnesium to take?
C-VAM only called that if damage occurs within 14 days of vax. But you aren't considered vaxxed until after 28 days. Clever/ diabolical!
Thank you for such a comprehensive piece.
Two points I keep making about the myocarditis issue:
(1) it is likely that myocarditis is just the most visible and easily diagnosable manifestation of a process which - given what we know about distribution - is happening throughout the body.
(2) there is no reason to believe that cases which never required healthcare intervention (it is self-limiting in most cases, and complaining about side effects was most definitely NOT encouraged) are not at some risk as well. So we could be dealing with an even more massive problem than thought.
Notably, autopsies are finding microinflammation in the heart of people who died suddenly, after no diagnosis during life:
https://hartuk.substack.com/p/new-autopsy-evidence-from-japan-myocarditis
;)
https://www.sciencedirect.com/science/article/pii/S0753332220302134
ânot final peer-reviewed papers (which unfortunately doesnât mean what it should)â
Multiple heavy sighs: so sad but true