How does COVID-19 destroy the heart? More and more is known about the harmful effects
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COVID-19 causes many symptoms and affects how various organs work in our body. Research shows that as much as 62 percent. patients hospitalized for COVID-19 suffer heart damage. Scientists investigated how SARS-CoV-2 affects heart muscle cells. Now they want to determine how the coronavirus causes inflammation in the heart.

  1. People who become infected with COVID-19, even if they have not been hospitalized, are at a higher risk of developing cardiovascular disease.
  2. Scientists conducted a series of experiments showing that the SARS-CoV-2 spike protein can damage the heart muscle through an inflammatory process.
  3. The data show that the spike protein from SARS-CoV-2 causes heart muscle damage. That’s why doctors say it’s important to get vaccinated and prevent COVID-19 and potential damage to the heart.
  4. More current information can be found on the Onet homepage.

Dr.Zhiqiang Lin, lead author of the study and assistant professor at the Masonic Institute of Medical Research in Utica, New York, noted that it is now known that COVID-19 infection can cause heart damage. «However, we do not know how. We suspect that the spike protein has an unknown pathological role. Our data show that the spike protein of SARS-CoV-2 causes damage to the heart muscle. That is why it is important to get vaccinated and prevent this disease »- he added.

The role of barbed protein. It is what damages the heart

SARS-CoV-2 enters healthy cells through the spike protein on its surface. This protein attaches to receptors known as angiotensin-converting enzyme 2 (ACE2) in healthy cells and so penetrates them. Scientists hypothesized that SARS-CoV-2 could damage the heart through an ACE2-independent immune response.

«The host’s natural immunity is the first line of defense against pathogen invasion, and myocardial cells have their own natural immune machinery. Activating the body’s immune response is essential to fighting viral infection. However, it can also disrupt the function of heart muscle cells and even lead to cell death and heart failure, »explained Dr Lin.

Researchers found that the SARS-CoV-2 protein led to heart dysfunction, hypertrophy, or enlargement of its cells, and organ inflammation.

Biopsy of a healthy heart and with myocarditis. This distinguished between healthy and diseased organs

The researchers used a biopsy to examine the heart of a deceased patient with COVID-19-related myocarditis, a patient who died from mRNA vaccine-related myocarditis, and the heart of a healthy person. Myocarditis occurs when the heart muscle becomes inflamed.

Prickly protein and other types of cells were detected in the heart muscle of a COVID-19 patient, while no protein was found in the healthy heart. The researchers found only a small fraction of the spike protein in the mRNA vaccine patient’s heart muscle cells and no clear signs of TLR4.

This means that mRNA vaccines are unlikely to cause inflammation of the heart muscle. The researchers concluded that SARS-CoV-2 spike protein could damage the heart via TLR4 inflammatory pathways, independent of ACE2.

«When the heart becomes infected with SARS-CoV-2, it activates TLR4 signaling. In addition to directly damaging the heart muscle cells, the spike protein itself is very inflammatory and can cause systemic inflammation that indirectly causes heart problems, »Dr. Lin noted.

How do coronavirus proteins cause myocarditis? There are two options

In further research, scientists set out to determine how SARS-CoV-2 peak proteins cause inflammation in the heart. So far, they have identified two potential ways in which this could happen.

The first possibility is that the spike protein directly activates inflammation in the heart muscle cells of those infected with the virus. The second possible way is to get spiny protein into the bloodstream and damage the heart while circulating it.

Research on the effects of SARS-CoV-2 on the heart could help develop new treatments to protect heart health. Researchers presented their findings at the American Heart Association’s Basic Cardiovascular Sciences 2022 Trusted Source scientific sessions.

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