Peptide Drug May Help In The Treatment Of Covid-Related Heart Damage

Although vaccines are available to fight the coronavirus, scientists are working around the clock to find another way to halt the Covid-19 virus and its complications. They're looking at existing and experimental medicines as well as developing new ones to stop the virus from spreading from person to person. The coronavirus can also cause heart damage and affect heart function.

According to John Hopkins, Covid-19 binds to angiotensin-converting enzyme-2 (ACE-2) receptors on cardiac cells before entering them. High amounts of inflammation circulating in the body can potentially cause heart damage. The inflammatory process that occurs while the body's immune system battles the virus can harm certain healthy tissues, including the heart. Coronavirus infection affects the inner walls of veins and arteries, causing blood vessel inflammation, damage to extremely tiny capillaries, and blood clots, all of which can obstruct blood flow to the heart and other areas of the body.

Experimental Drug May Prevent Heart Damage Caused By Covid-19

A study conducted by researchers at the University of Cambridge has discovered a new medication that could help prevent heart damage caused by COVID-19. They used human embryonic stem cells to grow heart cells in the lab to better understand how the virus infects heart cells. Importantly, these model cardiac cells also had the critical components required for SARS-CoV-2 infection, including the ACE2 receptor.

The study published in Communications Biology discovered an experimental peptide medication named DX600 that can inhibit the virus from accessing the cardiac cells using the model. Dr Sanjay Sinha from the Wellcome-MRC Cambridge Stem Cell Institute says, "Using stem cells, we've managed to create a model which, in many ways, behaves just like a heart does, beating in rhythm. This has allowed us to look at how the coronavirus infects cells and, importantly, helps us screen possible drugs that might prevent damage to the heart."

How Does The Drug Work?

The researchers discovered that medicines that target proteins involved in SARS-CoV-2 viral entry lowered infection levels considerably. DX600 is an ACE2 peptide antagonist, a chemical that targets ACE2 and blocks the activity of peptides that help the virus break into the cell. When compared to the antibody, DX600 was roughly seven times more efficient at preventing infection, albeit the researchers believe this is due to the fact that it was used in higher quantities. The medicine had no effect on the number of cardiac cells, indicating that it was not harmful.

Professor Anthony Davenport from the Department of Medicine and a fellow at St Catharine's College, Cambridge says, "The spike protein is like a key that fits into the 'lock' on the surface of the cells -- the ACE-2 receptor -- allowing it entry. DX600 acts like gum, jamming the lock's mechanism, making it much more difficult for the key to turn and unlock the cell door."

"But it could provide us with a new treatment to help reduce harm to the heart in patients recently infected with the virus, particularly those who already have underlying heart conditions or who have not been vaccinated," he added, "but it could provide us with a new treatment to help reduce harm to the heart in patients recently infected with the virus, particularly those who already have underlying heart conditions or who have not been vaccinated." It may also "assist in the reduction of long-term Covid symptoms."

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Researchers identify cause and potential treatment for COVID-19-induced heart damage

Australian researchers at QIMR Berghofer Medical Research Institute have discovered some of the ways COVID-19 damages the heart and identified a class of drugs that could potentially protect or reverse this cardiac injury.

In severe cases of COVID-19, the immune system overreacts to the infection, releasing inflammatory molecules called cytokines into the bloodstream. This so-called "cytokine storm" can damage multiple organs, including the heart.

Canadian company Resverlogix has used the QIMR Berghofer research findings as the basis for expanding its clinical trial of the drug, apabetalone, in COVID-19 patients.

The head of QIMR Berghofer's Cardiac Bioengineering Research Group, Associate Professor James Hudson, said his team used thousands of lab-grown, miniature human heart organoids to understand how COVID-19 causes cardiac damage.

"We exposed the bioengineered, stem-cell-derived heart tissue to COVID-19 patient blood and found it caused dysfunction even when the virus didn't infect the tissue."

The President and CEO of Resverlogix, Donald McCaffrey, said it had been a pleasure to work with the QIMR Berghofer team.

"We are excited that we can finally share publicly some of the incredible early results of our collaborative COVID-19 research program," McCaffrey said.

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Is donating blood healthy for you?

Have you were donated blood? Do you know that a person should donate blood in every three months, not only for others, but also for the sake of his own health. Blood donation is a major problem in the world, especially in India. According to the data revealed by the Ministry of Health, India, in 2018, India had a shortage of supply of 1.9 million units of blood. According to this data, in India, every three second someone needs a blood transfusion. Apart from the issue of donation, another major problem in the system is collection. The collection of blood is not spread out throughout the year. Blood is collected in abundance at once, during blood donation camps. This collected blood goes to waste after some time, causing a shortage for future. We often hear that donating blood can save lives of three people, but what we don’t hear is that donating blood could also save the donor. Apart from helping another human, here are the health benefits you get from donating blood regularly.

Hemochromatosis refers to a condition where too much iron accumulates in the body. This condition is caused due to genetics or as a side effect of alcoholism. By donating blood, you are reducing the iron overload on the body.

According to a recent study published in the American Journal of Epidemiology, blood donors are 88 per cent less likely to suffer a heart attack and 33 percent less likely to suffer from cardiovascular diseases. Excess iron gets stored in the liver, pancreas, and heart, which increases the risk of developing cirrhosis, pancreatic damage, liver failure, and heart ailments. By donating blood, you keep your iron level under check and reduce the risk of liver and heart diseases.

According to the researchers at the University of California, San Diego, donating blood one time can burn up to 650 calories in the bodies. A lot more research is required in this field, but if it is true then it doesn’t look like a bad idea to lose weight while doing a good deed.

To replenish the lost blood, the body produces new blood cells which strengthens the bone marrow of an individual. Bone marrow is a tissue, where new blood cells are created. A weak bone marrow cannot produce white blood cells and red blood cells, which could impact the immune system.

According to a study published in the Journal of the National Cancer Institute, in 2017, removing excess iron from the blood can reduce the chances of cancer. The study says iron in the system gives strength to cancer causing free-radicals. Excess iron can also block anti-oxidants from tackling these free-radicals.

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Heart damage due to chemotherapy worse in diabetics

Heart damage caused by chemotherapy is worse in cancer patients who also have diabetes, a new study has warned. Researchers in the study investigate factors that could affect the likelihood of patients having heart damage after treatment with anthracyclines. “Cardiotoxicity induced by chemotherapy with anthracyclines is being increasingly reported, mainly because a smaller proportion of patients now die from cancer,” said Ana Catarina Gomes, from Hospital Garcia de Orta in Portugal. “In the coming years this cardiotoxicity looks set to increase the burden of heart failure in cancer survivors,” said Gomes.

 The good news is that cardiotoxicity can be reversible in the early stages before overt heart failure develops,” she said. 

“Surveillance programmes are hugely beneficial, particularly in the first year of treatment when up to 80 per cent of the systolic dysfunction develops,” she added.
 
The hospital has a surveillance programme to monitor cancer patients who receive anthracycline-based chemotherapy. Clinical and echocardiographic evaluation is conducted before, during and after chemotherapy, regardless of whether or not the patient has symptoms. The aim is to detect cardiotoxicity early so that heart failure can be prevented. The study included all 83 patients in the surveillance programme, of whom 54 had breast cancer, 20 had lymphoma and nine had gastric cancer.

For each patient, data was collected on demographics, cardiovascular risk factors (hypertension, diabetes mellitus, dyslipidaemia and smoking) previous cardiovascular and non-cardiovascular diseases and type and cumulative dose of anthracyclines. Echocardiographic evaluation included heart chamber dimensions, systolic and diastolic function, ejection fraction and global longitudinal strain.

Measurements were performed before chemotherapy was started, during treatment, and after the end of chemotherapy. Researchers tested the impact of each risk factor on changes in echocardiographic data from baseline to follow-up. 
Echocardiographic data were compared between patients with different types of cancer. A total of 39 patients were treated with doxorubicin and 44 received epirubicin. Cumulative doses were within recommended ranges. Patients were 52 years old on average (range 39 to 65 years) and 78 per cent were female.

Some 31 per cent had hypertension, seven per cent had diabetes, 16 per cent had dyslipidaemia, and 16 per cent were smokers. Patients with hypertension showed a trend towards greater reductions in ejection fraction. Patients with diabetes had a significantly greater decrease in global longitudinal strain during treatment, despite having baseline levels similar to non-diabetics.

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