COVID Spike Protein: Persistent spike protein (PSP) syndrome is seen when the COVID pathogen-related spike protein stays in the body following a COVID vaccination and/or because it was never completely eliminated following an unresolved COVID infection (chronic or long-haul COVID). [80-82] While the spike protein has been found throughout the body in autopsy studies on COVID patients, it appears to have a particular predilection for attacking the heart and its blood vessels. [83-88]
The spike protein inflicts damage in the heart and elsewhere in the body by multiple mechanisms. These mechanisms include:
Myocarditis, often evolving heart enlargement and heart failure, can result from the spike protein exposure following COVID vaccine(s) and/or from its persistence presence in chronic COVID. However, many cases of spike protein myocarditis, probably a substantial majority, are chronic, smoldering conditions that remain undiagnosed except when there is clear clinical evidence indicating its presence.
PSP syndrome routinely involves the heart, even when not readily apparent clinically. In fact, the spike protein has such a preference for heart muscle that chronic COVID or post-vaccination patients are unlikely to ever have spike protein or its pathological impact elsewhere in the body while sparing the heart. In autopsies of patients who died of COVID-19, either COVID-related viral RNA or evidence of myocardial inflammation was seen more than 80% of the time. [101] Another autopsy study revealed spike protein presence over 60% of the time. [102]
Unlike the other toxic cardiomyopathies, spike protein only rarely involves the whole heart, and the amount of heart muscle involvement can be very minimal. Nevertheless, sudden cardiac death (not from a heart attack due to "traditional" coronary atherosclerosis) is no longer uncommon, and it appears a substantial number of individuals around the world can be symptom-free and still be liable to life-threatening arrhythmias under conditions of stress, including previously-healthy young athletes. [108]
As the number of people with undetected spike protein/COVID myocarditis is enormous already and steadily increasing, part of the therapy for anyone felt to have persistent spike protein should still involve the regular administration of one or more heavy metal chelation agents. As discussed above, heavy metals appear to "await" the microenvironment of myocardial inflammation of a previous viral infection to begin accumulating, if they have not already accumulated there prior to the COVID infection or the vaccine administration. As with all other toxins, heavy metals will always substantially worsen any inflammation and electrical instability already caused by the presence of the spike protein and the COVID pathogen. Most likely this worsening is synergistic in nature, and not just the additive effect of spike protein and heavy metals.
ATP Physiology and Cardiomyopathy
When cardiac ATP production can be restored to optimal levels with a normal increase capability for exercise, a healthy heart will result, unless irreversible damage has already taken place. [112] Of note, mitochondria are especially abundant in heart tissue, and more than 90% of the energy of the heart is generated by these mitochondria. As the heart completely renews its ATP content every 20 seconds or so, it can demonstrate clear mitochondrial insufficiency (heart failure) when other organs appear to be less affected or completely unaffected. [113,114] No organ consumes more energy per gram of tissue than the heart. [115]
As the mitochondria are the intracellular sites of ATP (energy) production, significant research has been directed at finding ways to reverse or lessen "mitochondrial dysfunction." [116] Most cases of mitochondrial dysfunction are due to the increased oxidative stress resulting from chronic infection and toxin accumulation, although rare genetic defects in mitochondrial function can result in the same clinical pictures of decreased energy production. [117]
Much of this mitochondrial research has focused on defects in the electron transport chain (ETC) embedded in the membranes of the mitochondria. The ETC directly fuels the ATP synthase enzyme vital to the production of ATP at the end of that chain. The ETC has four main complexes, or steps, that work to optimally shuttle electrons to the terminal ATP-producing enzyme. [118,119]
Defects in the ETC have been specifically identified in heart failure and are always present. [123] In even the most advanced cases of heart failure, most affected hearts still have inflamed but viable heart cells that can be positively impacted with improved ATP production. Aside from the chelation therapies noted above, bolstering mitochondrial function has been a major physiological goal in the treatment of heart failure. [124]
Traditional medicine has no drugs which directly work to normalize mitochondrial dysfunction in heart failure patients. Instead, all the current prescription drugs work only to basically mobilize excess fluid accumulations and/or to lessen the workload (peripheral resistance) faced by the failing heart muscle. This is not to say that there is no place for these drugs, only that they should not be the only agents given to the patient. As with most prescription drugs, the therapeutic goal appears limited to symptom improvement while letting the underlying pathology continue to evolve. Traditional medicine is much better at diagnosing and naming medical conditions than at reversing or resolving them.
Heart Failure or Therapy Failure? Toxins Cause Cardiomyopathy
Part 2.
by Dr. Thomas E. Levy, MD, JD