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Treatment shows promise for heart damage from COVID-19

COVID-19 viral particles have been detected in the heart muscles of people with COVID-19 as well as in autopsy samples. Heart damage is also thought to contribute to the symptoms of “long haul” COVID-19.

As of August 2021, there were 201.75 million cases of COVID-19 worldwide and 4.28 million deaths associated with the virus (1). When someone with a pre-existing condition contracts COVID-19, their risk for death often increases. For people with cardiovascular disease, the risk increases from 2.3% to 10.5% (2).

Why does COVID-19 cause heart damage, and what treatment can help to prevent it?

First, it is helpful to understand how a healthy heart works. The heart is a big muscle made up of four chambers. The upper chambers are atrium, and the lower chambers are ventricles. Blood is pumped into the chambers through four heart valves.

Blood flows from the body, through the right atrium and ventricle and into the lungs to be oxygenated. The oxygenated blood flows back through the left atrium and ventricle and then out to the rest of the body (3).

With each heartbeat, pressure is created as the heart pumps blood. Blood pressure readings measure the pressure of the blood as it is pumped out of the heart, known as the systolic blood pressure and measure the pressure between beats, known as the diastolic blood pressure (4).

As one ages the blood vessels can become damaged. Sedentary lifestyles also cause a buildup of plaque inside blood vessel walls, causing them to narrow (atherosclerosis). The damaged, narrower blood vessels cause blood pressure to increase.

The body makes various hormones, proteins, and enzymes to regulate blood pressure and fluid balance in the body (5). When blood pressure increases, the body produces more of these chemicals, such as angiotensin converting enzyme 2 (ACE2). ACE2 is produced by the lungs, and researchers have determined ACE2 receptors are how someone becomes infected with COVID-19 (6).

From there, the spike protein from COVID-19 binds to the cell surface of ACE2 receptors, including those ACE2 receptors in cardiac muscle. This allows COVID-19 to spread throughout the body (2) and potentially cause heart damage.

How COVID-19 affects the heart

To better understand how COVID-19 damages the heart and potential treatments for it, scientists from the University of Cambridge completed a study of heart cells grown from human embryonic stem cells. Their study was published in the journal, Communications Biology.

Initially the researchers grew the heart cells to mimic the functions of human hearts. The heart cells were then infected with a modified synthetic virus that had the COVID-19 spike protein attached (2).

When the heart cells were fully infected with COVID-19, different drug treatments were administered to the infected heart cells. The researchers treated the cells with small molecule inhibitors, an ACE2 peptide antagonist, and an ACE2 antibody targeting protein. Uninfected heart cells were treated with the same drugs for comparison (2).

The researchers found promising results when infected cells were treated with benztropine and DX600 to prevent cells from being infected with COVID-19. Additionally, COVID-19 infection was inhibited when the cells were treated with camostat, E64d, and ACE2 antibody. DX600 was more effective at preventing infection than the antibody, but additional research is needed to determine if it is actually more effective (2).

Explaining how DX600 works in a press release, study author Dr. Anthony Davenport stated, “The spike protein is like a key that fits into the ‘lock’ on the surface of the cells – the ACE2 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. We need to do further research on this drug, 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. We believe it may also help reduce the symptoms of long COVID.”


  1. Ritchie H, Ortiz-Ospina E, Beltekian D, et al. Coronavirus Pandemic (COVID-19). Our World in Data. Published online March 5, 2020.
  2. Williams TL, Colzani MT, Macrae RGC, et al. Human embryonic stem cell-derived cardiomyocyte platform screens inhibitors of SARS-CoV-2 infection. Communications Biology. 2021;4(1). doi:10.1038/s42003-021-02453-y
  3. How the Healthy Heart Works. Published 2019. Accessed August 10, 2021.
  4. American Heart Association. What is High Blood Pressure? Published 2016. Accessed August 10, 2021.
  5. Speller J. The Renin-Angiotensin-Aldosterone-System – Renin Release – Angiotensin II Production – TeachMePhysiology. TeachMePhysiology. Published April 28, 2020. Accessed August 10, 2021.
  6. Ni W, Yang X, Yang D, et al. Role of angiotensin-converting enzyme 2 (ACE2) in COVID-19. Critical Care. 2020;24(1). doi:10.1186/s13054-020-03120-0

Image by Gerd Altmann from Pixabay 

Rebecca Blankenship BSc
Rebecca Blankenship BSc
Rebecca Blankenship is a freelance technical writer. She reviews, edits, and authors internal quality documentation required for regulatory compliance. She has twenty years experience in industrial pharma/medical device quality management systems and an honors BSc in chemistry. She is a natural born rule follower and enjoys applying this strength to help others be audit ready to meet regulatory requirements. She also loves learning about the latest scientific discoveries while writing for Medical News Bulletin. Her free time is spent as a full-time mom, encouraging can-do attitudes and cooperation in her three children.


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