The Spike Protein, Takotsubo Cardiomyopathy and Macrophages

The Spike Protein’s ability to activate macrophages may help explain the occurrence of Takotsubo Cardiomyopathy post COVID disease/vaccination.

One of the many concerning epidemiological curiosities since the appearance of SARS-CoV-2 and its Spike Protein has been a dramatic increase in the occurrence of Takotsubo Cardiomyopathy (TTC). Takotsubo Cardiomyopathy is also colloquially known as “broken-heart syndrome.” I would like to discuss how macrophages, activated by the Spike Protein, are almost certainly a major contributing factor to this phenomenon. As readers of this Substack know, I am currently focusing on macrophage involvement in Long COVID and post Spike Protein exposure conditions.

First, a quick review of what Takotsubo Cardiomyopathy is:

Takotsubo cardiomyopathy is a temporary heart condition that develops in response to an intense emotional or physical experience. It’s also known as stress cardiomyopathy or broken heart syndrome.

In this condition, the heart’s main pumping chamber changes shape, affecting the heart’s ability to pump blood effectively

The heart’s chamber looks similar to a Tako -Tsubo pot, which is a Japanese fishing pot used to catch octopus.

Takotsubo Cardiomyopathy
https://www.svhhearthealth.com.au/conditions/takotsubo-cardiomyopathy

As noted earlier, there has been a very significant increase in the occurrence of this condition since the emergence of SARS-CoV-2 and its Spike Protein. Once again, we focus on the Spike Protein as TTC’s increased occurrence is related to both COVID infection and COVID vaccination.

The yearly rate of recurrence was seen to be 1.5% and the incidence of recurrence was increased by 1.2% at 6 months and 5% by 6 years.[13] Increasing anxiety and stress levels experienced in the Western populations resulted in a higher prevalence of TTS. During the coronavirus disease-19 (COVID-19) pandemic, the incidence of TTS has increased by 2 to 3 folds due to social isolation, stress, financial crisis, anxiety, and quarantine compared to before COVID-19.

Current Clinical Perspectives on Takotsubo Syndrome: Comprehensive analysis of Diagnosis, Management, and Pathophysiology
https://ijcva.org/articles/current-clinical-perspectives-on-takotsubo-syndrome-comprehensive-analysis-of-diagnosis-management-and-pathophysiology/doi/ijca.2024.63825

Ten studies, including 10 cases, participated in the current systematic review. The mean age was 61.8 years; 90 % were female, while 10 % were male. 80 % of the patients received the mRNA COVID-19 vaccine, while 20 % received other types. In addition, takotsubo cardiomyopathy (TCM) occurred in 50 % of patients receiving the first dose and another 40 % after the second dose of COVID-19 vaccines. Moreover, the mean number of days to the onset of symptoms was 2.62 days. All cases had an elevated troponin test and abnormal ECG findings. The left ventricular ejection fraction (LVEF) was lower than 50 % in 90 % of patients. In terms of the average length of hospital stay, 50 % stayed for 10.2 days, and all cases recovered from their symptoms. In conclusion, takotsubo (stress) cardiomyopathy (TCM) complications associated with COVID-19 vaccination are rare but can be life-threatening.

Global reports of takotsubo (stress) cardiomyopathy following COVID-19 vaccination: A systematic review and meta-analysis
https://pmc.ncbi.nlm.nih.gov/articles/PMC9381427/

Takotsubo Cardiomyopathy (TTC) is a cardiac condition that typically arises from emotional distress but, in an intriguing twist, has been identified in some COVID-19 patients, associated with physical stress [17]. The clinical presentation of COVID-19 patients with TTC included symptoms such as shortness of breath and chest pain. Electrocardiograms revealed a range of abnormalities, from ST-segment elevations to atrial fibrillation, T-wave inversion, and sinus tachycardia [18].

Cardiovascular disease and covid-19: A systematic review
https://www.sciencedirect.com/science/article/pii/S2352906724001489

What I find intriguing – and disturbing – is the cavalier dismissal of the manyfold increased occurrence of TTC by some of the authors due to “stress” caused by the pandemic. Indeed, there is far more concrete reason that can explain this increase – that is the infiltration of macrophages. This happens to be precisely what the Spike Protein does.

Peptides derived from recombinant S protein from SARS-CoV-2 were synthesized and validated by in silico, in vitro and in vivo methodologies.

Macrophages stimulated with one of the peptides showed increased production of NO, TNF-α and CXCL2. Inoculation of the peptides in zebrafish larvae triggered an inflammatory process marked by macrophage recruitment and increased mortality, as well as histopathological changes, similarly to what is observed in individuals with COVID-19.

A novel insight on SARS-CoV-2 S-derived fragments in the control of the host immunity
https://www.nature.com/articles/s41598-023-29588-8

Ultimately, the significance of this is that now we may have a better understanding of how any Spike Protein exposure is almost certainly destructive to all organs and tissues of the human body. The heart, of course, included. Let’s look at a study from a couple of years ago which shows that macrophage infiltration is what characterizes TTC.

We demonstrate for the first time that takotsubo cardiomyopathy is characterized by a myocardial macrophage inflammatory infiltrate, changes in the distribution of monocyte subsets, and an increase in systemic proinflammatory cytokines. Many of these changes persisted for at least 5 months, suggesting a low-grade chronic inflammatory state.

Myocardial and Systemic Inflammation in Acute Stress-Induced (Takotsubo) Cardiomyopathy
https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.118.037975

This further supports what I have seen from the beginning. The Spike Protein breaks down the walls protecting our organs (endothelium), then allows an army to invade. Except, that army is our own immune system.

Thank you, as always, for your readership, dialogue and support. I will continue to work on furthering our understanding and searching for therapeutics to prevent/treat this most malevolent of proteins.