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Published On: September 21st, 2020By Categories: Fundamental Science

Editor-in-Chief: Fatima Tokhmafshan

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Although COVID-19 is a respiratory illness, a new review1 of COVID-19 studies published in the journal PLoS One shows that cardiovascular complications are common in COVID-19 patients, which might increase the risk of death.

The meta-analysis examined data from 21 studies that included over 77,000 patients hospitalized for COVID-19.

The authors found that close to 13% of study participants had been diagnosed with a cardiovascular condition including hypertension, coronary artery disease, and heart failure before being admitted for COVID-19. Risk factors for developing cardiovascular disease including diabetes, obesity, and smoking were also commonly reported among those hospitalized. COVID-19 increased the risk for cardiac events in hospitalized patients. After admission, over 10% of patients had a documented cardiac injury, including arrhythmia, angina, or heart attack.

Patients who had cardiovascular disease before developing COVID-19, or who suffered cardiovascular complications while hospitalized for COVID-19, had higher rates of in-hospital death. It is clear from this meta-analysis that heart health is critical in determining outcomes in COVID-19 patients.

The Path to Injury

How does a virus that primarily targets the respiratory system cause damage to the heart? Cardiac muscle cells express proteins that may allow the virus to directly infect them. There is some evidence that SARS-CoV2 can infect the hearts of COVID-19 patients2, but whether infection damages or kills the cells is unknown.

Viruses like SARS-CoV2 can also damage the cardiovascular system through “cytokine storms’— excessive amounts of molecules that normally help to coordinate the immune system’s response but that can cause an exaggerated reaction. This hyperactivity of the immune system can cause native cells in the body to be attacked, including those of the heart and vasculature, causing them to become damaged or even die.

Heart muscle cells are normally not replaced with new cells, meaning the loss of muscle is permanent. If enough muscle is killed, the heart cannot contract properly, and it begins to fail.

Some Perspective

The link between cardiovascular disease and viral infection is not unique to COVID-19. Studies have reported cardiac injuries in individuals hospitalized for influenza. In the 2009 influenza pandemic, one study reported that 5% of hospitalized patients exhibited signs of cardiac damage 3. Of the influenza patients admitted to the ICU, almost half suffered some form of cardiac injury4. Patients with cardiovascular disease are more likely to be re-admitted within 1 year of hospitalization for influenza5. Together these studies show that cardiac damage is a known risk of viral infections, and that pre-existing cardiovascular disease worsens outcomes.

What is concerning about COVID-19 is its high rate of infection and relatively high rate of hospitalization compared to influenza. In the United States it is estimated that approximately 1% of individuals with influenza require hospitalization6. By contrast, 12-20% of patients that test positive for SARS-CoV2 infection are hospitalized7. More severe viral illnesses are associated with higher rates of cardiac injury, which suggests that the long-term consequences of COVID-19 on the heart may be substantial.

The Long Run

One area of growing concern regarding COVID-19 patients and cardiovascular disease is myocarditis.

Myocarditis is an inflammation of the heart muscle that is often associated with bacterial or viral infections. Most patients with myocarditis are successfully treated in hospital and experience few long-term complications. However, up to 25% suffer permanent damage to the heart8. Heart failure from myocarditis is the most common reason for heart transplantation9.

The preferred treatments for myocarditis are drugs that eliminate the infectious agent. However, without any effective therapies to kill SARS-CoV2, COVID-19 patients who develop myocarditis can only be treated with therapies that support heart function.

Early data suggest that SARS-CoV2 may have higher rates of cardiac infection than many other viruses10. Equally concerning is the fact that myocarditis is typically found in young (<35 years old), healthy adults11. This demographic group has a much lower mortality rate from COVID-19 than those with pre-existing health conditions or older patients. The low rate of death in younger, otherwise healthy individuals has led to this cohort being classified as of little concern. But the potential for long-term, serious consequences of COVID-19 is alarming.

One area in which cardiac damage is emerging as a significant problem is the pediatric population. A series of studies at medical centers across the globe have reported increasing numbers of pediatric cases of COVID-19 in which the heart experiences damage, even after patients have cleared the virus12. These reports suggest that even if COVID-19 appears to be a relatively uneventful illness for most children, there may be long-term consequences resulting from heart damage. As with many issues related to COVID-19, only time will tell whether these fears are warranted or not.

The novelty of COVID-19 presents a number of uncertainties. One area that has remained consistently concerning since the earliest studies of SARS-CoV2 infected patients is the strong link between outcomes and the cardiovascular system. The global epidemic of cardiovascular disease provides fertile ground for SARS-CoV2 to grow and wreak havoc. At the same time, the COVID-19 pandemic increases cardiovascular disease by attacking the heart and blood vessels, leaving behind lasting damage.

Where the long-term effects of COVID-19 may lead no one really knows, but one thing is certain: unless we take this pandemic to heart, the consequences will be heartbreaking.


About the Author: Glen Pyle

Glen Pyle, PhD is a Professor of Molecular Cardiology at the University of Guelph and an Associate Member of the IMPART Team Canada Investigator Network at Dalhousie Medicine.