SARS-CoV-2 Binds to Heart Cells

I have had a major relapse in symptoms since my reinfection with acute Covid-19 in November 2021. One of these has been the return of my crushing, squeezing chest pain. It's not occurring when I am gently exercising, or standing up, or in the middle of the night again thankfully, but it is when I am very angry, stressed or emotional (Probably thanks to all that circulating adrenaline - I am like a living cardiac stress test!)

Luckily I have worked SO hard on stress (body and mind) management that these attacks occur rarely.

Fortuitously I managed to have a follow-up appointment booked with my cardiologist so another cardiac MRI ( 3 and counting) has been booked in. I don't think it will reveal Myocarditis/Pericarditis. I am sure it is my old friend Microvascular Angina (MVA) which has been triggered with a new onslaught of inflammation. To diagnose MVA you ideally want a 3 -day ECG to show ischaemia (heart not getting enough oxygen) and a "stress" cardiac MRI.

Interestingly a new study has shown how SARS-CoV-2 may contribute to severe microvascular damage seen in severely-ill COVID-19 patients by transforming human heart vascular cells into inflammatory cells, without infecting them. Taken from the article "SARS-CoV-2 spike protein binds to heart's vascular cells, potentially contributing to severe microvascular damage"

Quick Summary

  • SARS-CoV-2 can damage the vascular cells of the heart (pericytes) without infecting them.

  • The virus' spike protein induces the vascular cells to secrete inflammatory cytokines.

  • Spike proteins are found in the blood of infected patients showing a way they can travel form the respiratory system to other organs such as the heart to cause damage.

  • Antibodies blocking CD147—a receptor for the spike protein—protected heart pericytes from damage and could possibly be used as a new treatment to alleviate cardiac complications.

For me the take home messages are that:

  1. Microvascular Angina (and other cardiac damage) can occur after an acute Covid-19 infection (only Alpha, Delta and original strain tested)

  2. A mechanism has been identified for this damage

  3. Spike proteins travelling in the blood circulation from their original point of entry (the respiratory system) could lead to damage in the heart and presumably elsewhere.

This last point is very satisfying to me as my first Respiratory Consultant said when I described my crushing chest pains - "you could not possibly have cardiac damage as I cannot identify any damage to your lungs and if your lungs aren't damaged then your heart isn't either"..... #medicalgaslighting at it's best. Thanks Queen Alexandra Hospital Portsmouth.

The article

In this new study, a multidisciplinary research team from the University's Bristol Heart Institute sought to investigate how SARS-CoV-2 interacts with heart cells causing the myocardial damage seen in COVID-19 patients. Until now, it remained unclear whether heart cells are infected by the virus or damaged because of an excess cytotoxic defense response. This response, also known as 'the cytokine storm', comes from our immune cells, whereby cytotoxic cells attack and kill the infected cells by releasing proteins, called cytokines. The team also sought to investigate whether heart cells contribute to producing excess cytokines.

A research team led by Bristol's Professor Paolo Madeddu exposed human heart pericytes, which are cells that wrap small blood vessels in the heart, to SARS-CoV-2 Alpha and Delta variants, along with the original virus. Surprisingly, they found the heart pericytes were not infected.

Intrigued by this finding, in a second test-tube experiment, the researchers challenged the cardiac pericytes with the spike protein alone, without the virus. The spike protein made pericytes unable to interact with their companion endothelial cells and induced them to secrete inflammatory cytokines, suggesting the spike protein is harmful to human cardiac cells. Interestingly, the team found that antibodies blocking CD147—a receptor for the spike protein—protected heart pericytes from damage.

Finally, the team identified the presence of the SARS-CoV-2 spike protein in blood samples obtained from COVID-19 patients, which opens the possibility that spike protein particles traveling through the circulation can reach a site distant from the respiratory system and cause systemic damage.

Dr. Elisa Avolio, the study's first author from the University's Bristol Medical School, said that "pericytes are essential cells of the heart, although their role in maintaining the structural integrity of the coronary vascular tree has emerged only recently. Our ongoing research on human cardiac pericytes indicates these cells co-operate with coronary endothelial cells during healing from a heart attack. This new study shows that the spike protein jeopardizes this interaction and transforms pericytes into inflammatory cells. Hopefully, CD147 blocking antibodies could represent a new treatment to alleviate cardiovascular complications in COVID-19 patients."


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