For months, scientists have been expressing concern about the increase in cardiovascular diseases among COVID-19 patients, even after the SARS-CoV-2 virus has long since cleared their bodies. These heart issues have long been part of the larger conversation about the long-term aftermath of COVID-19, with a June study by the Department of Veterans Affairs even finding that those reinfected with COVID-19 were twice as likely to either die or have a heart attack as people who were only infected once.
“The two respiratory viruses (COVID and flu) look very different in the hearts of these patients.”
Now, a new study in the scientific journal Immunology uses a technique known as spatial transcriptomics — which allows scientists to directly map how genes are expressed on tissues — to reveal the SARS-CoV-2 virus’ unique effects on human organs. The study compared SARS-CoV-2 to the influenza virus H1N1, which caused the 2009 pandemic.
Unfortunately, the evidence also suggests that the SARS-CoV-2 virus is more damaging to human organs, and for a longer period of time, compared to H1N1.
In the study, the scientists examined and compared heart tissue from individuals who had died from both diseases, as well as a group of control patients. While the COVID-19 patients did not have the SARS-CoV-2 virus itself present in their heart tissue, the cardiac muscles showed signs of DNA damage that was unique to them — and which was utterly distinct from the inflammatory signal from influenza patients. By contrast, COVID-19 patients had a suppressed inflammatory signal.
“The two respiratory viruses (COVID and flu) look very different in the hearts of these patients,” corresponding author Dr. Arutha Kulasinghe from the University of Queensland told Salon by email. “DNA damage is a marker of genomic instability — we’ve known about it in chronic conditions such as cancer, neurodegenerative disease and diabetes — however its role in COVID was not known and the clinical implications for this aren’t clear at this stage. “
Kulasinghe expressed concern that their findings may be “the ‘canary in the coal mine,'” revealing that there are fundamental biological differences between how influenza and COVID-19 affect the human heart.
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dr Monica Gandhi, an infectious disease doctor and professor of medicine at the University of California-San Francisco who was not involved in the study, observed to Salon by email that the study was small, as it only included four autopsies from older COVID-19 patients , all of whom had either underlying heart disease or risk factors for heart disease. As such, “this study likely indicates that severe COVID-19 in patients with underlying cardiac disease can lead to further cardiac inflammation but does not yet make any conclusions about the effects of COVID-19 on the heart in mild disease, nor in patients without underlying cardiac conditions,” Gandhi explained. “This is a ‘hypothesis’ generating study and should trigger us to both study the inflammatory response in COVID-19 further and to continue to minimize severe disease from SARS-CoV-2 with vaccines and therapeutics.”
Placing the study in a larger context, Dr. Georges Benjamin — executive director of the American Public Health Association — told Salon by email that “we know very little about the long term implications of COVID related heart disease. We also know even less about how protective vaccines are for specific organ damage. So this is another important area of research.”
The list of heart-released symptoms linked to initial COVID-19 infections includes myocarditis, palpitations, heart failure and arrhythmias.
For their part, the scientists behind the Immunology study were modest when describing the breadth of their findings.
“It tells us that COVID and flu are very different in how they affect the heart, with COVID-19 potentially being more damaging (and potentially longer term),” Kulasinghe told Salon. “More work needs to be done to determine the utility of this DNA damage signal (was identified in severe/ICU patients who then died), so what does this mean for living patients post-infection is not known.”
One possible approach is for scientists to search for the same DNA damage signal found in the cardiac tissue in nasal swabs and blood samples. If the same DNA damage is detected there, doctors may be able to help determine potential cardiac complications long in advance.
The concerns about heart disease and long COVID are part of a broader conversation about the long-term effects of COVID-19. While there are signs that COVID-19 may cause long-term damage to the brain, lungs and other vital organs, the SARS-CoV-2 virus is so new to the scene that scientists cannot assess for sure its long-term impact. The Immunology study notes that the list of heart-released symptoms linked to initial COVID-19 infections includes myocarditis, palpitations, heart failure and arrhythmias.
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