This is perhaps the most important article in this Substack’s ongoing series exposing the Modified mRNA slow kill bioweapon, and the various associated “vaccine”-induced death and disease mitigation strategies incorporating inexpensive repurposed drugs that actually work.
…which establishes that adding Hydroxychloroquine to the Doxycycline and Ivermectin protocol may further treat, and even cure (post-C19 “vaccination”) myocarditis.
HCQ improved cardiac function in acute and chronic myocarditis. HCQ treatment reduced inflammation, fibrosis and immune cell infiltration in myocarditis models. Single-cell RNA sequencing revealed that HCQ lowered inflammatory cell proportions and suppressed macrophage chemotaxis. HCQ reduced YY1 levels, leading to the down-regulation of CXCL16 expression in macrophages and inhibition of CXCL16-mediated chemotaxis to Th17 and natural killer T (NKT) cells. CXCL16 neutralizing antibodies improved cardiac function and reduced inflammation in myocarditis.
We know that the reason a combination therapy of Doxycycline and Ivermectin significantly attenuates myocarditis is due to their anti-inflammatory and anti-matrix metalloproteinase (MMP) properties, but we also know that Hydroxychloroquine has been shown to modulate MMP levels, particularly MMP-2 and MMP-9, as well as tissue inhibitors of metalloproteinases (TIMPs), such as TIMP-1 and TIMP-2.
Knowing that these proteins play a significant role in tissue remodeling and inflammation, with elevated levels of TIMP-1, MMP-3, and MMP-7 associated with active disease and worsening renal function in ANCA-associated vasculitis (AAV), we may conclude that Hydroxychloroquine has a vital therapeutic role in the treatment of myocarditis.
Not only does Hydroxychloroquine stop all viruses like COVID-19 and seasonal flu dead in their tracks, has impressive anti-cancer properties…
…but it also has powerful anti-inflammatory properties, making this compound a vital treatment approach for VAIDS, not limited to turbo cancer, systemic inflammation and heart tissue damage.
In addition, during reperfusion after myocardial injury, an acute release of matrix metalloproteinases-2 (MMP-2) is noted14, and MMP inhibition after myocardial infarction yields preservation of left ventricular function15. DOXY reduces the adverse LV remodeling in patients with acute ST-segment elevation myocardial infarct (STEMI) and LV dysfunction, possibly via MMP inhibition pathway. These potential cardioprotective effects may have an additional implication in the COVID-19 patients with acute myocardial injury.
While the authors recognized the potential for Doxycycline's and Hydroxychloroquine’s myocardial infarction properties, they were primarily focused on COVID-19 long term care facility clinical outcomes, concluding:
DOXY and HCQ combination therapy is known to be anti-inflammatory, and immunomodulatory in both in-vitro and in-vivo studies. In addition, HCQ has anti-viral properties. Although this sample size is small (n=54), the results suggest that early intervention of DOXY-HCQ may improve the clinical outcome of high-risk COVID-19 patients suffering from moderate-severe symptoms in LTCF. These data is also associated with a reduction of hospitalization by 44% among moderate to high severity COVID-19 LTCF residents compared with previously reported data by similar populations from King county, Washington18.
Circling back to our more recent research study, the authors arrived at a more impressive conclusion regarding myocarditis:
HCQ improves cardiac function and reduces inflammation in myocarditis by inhibiting CXCL16 expression in macrophages, by suppressing its transcription factor YY1, which in turn reduced the chemotaxis of Th17 and NKT cells. HCQ is a promising therapeutic agent for myocarditis.
We may now confidently deduce that the combination therapy of DOXY-HCQ-IVM is the single most viable myocarditis treatment approach currently available, with significant tissue remodeling implications; in fact, any and all heart conditions would greatly benefit from this very same protocol.
With the following not only pertaining to myocarditis, but also representing the most comprehensive ‘holy grail’ cancer cure in plain sight that also heals asthma, prion-based diseases like Alzheimer’s, mood disorders, Parkinson’s, Lyme Disease, Lupus, skin conditions, and various other “incurable” ailments as well as the common cold and seasonal flu:
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Tocotrienol and Tocopherol forms (all 8) of Vitamin E (400-800mg per day, 7 days a week). A product called Gamma E by Life Extension or Perfect E are both great.
Bio-Available Curcumin (600mg per day, 2 pills per day 7 days a week). A product called Theracurmin HP by Integrative Therapeutics is bioavailable.
VIR-X immune support which also greatly increases the bioavailability of both FenbendazoleandHydroxychloroquine (2 capsules per day) —for prophylaxis 2 capsules per day
Removing sugars and carbohydrates (cancer food) from your diet and replacing table sugar with a zero glycemic index, zero calorie, keto friendly rare sugar like FLAV-X
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A vaxx-injury denier came down with a new inflammatory autoimmune condition. His mainstream female (!) Harvard (!) doc told him 1) don't take any more shots because we don't know what they are doing to your immune system; 2) do take HCQ. It's been working, but he'll never admit the truth.
Interesting mecahnism with the CXCL16-YY1 pathway. The MMP inhibition angle makes sense given the tissue remodeling challenges in myocarditis cases. I remember seeing similar inflammatory cascades in autoimmune contexts where innate immune suppresion helped reduce fibrosis progression. The chemotaxis reduction between macrophages and Th17/NKT cells is particularly relevant since its that cross-talk that amplifes the inflammatory damage in cardiac tissue.
A vaxx-injury denier came down with a new inflammatory autoimmune condition. His mainstream female (!) Harvard (!) doc told him 1) don't take any more shots because we don't know what they are doing to your immune system; 2) do take HCQ. It's been working, but he'll never admit the truth.
Interesting mecahnism with the CXCL16-YY1 pathway. The MMP inhibition angle makes sense given the tissue remodeling challenges in myocarditis cases. I remember seeing similar inflammatory cascades in autoimmune contexts where innate immune suppresion helped reduce fibrosis progression. The chemotaxis reduction between macrophages and Th17/NKT cells is particularly relevant since its that cross-talk that amplifes the inflammatory damage in cardiac tissue.