APR 03, 2020 6:52 AM PDT

How Cardiovascular Disease Increases Mortality Risk of COVID-19

WRITTEN BY: Annie Lennon

Although initial reports focused mostly on COVID 19’s respiratory effects, including pneumonia and difficulty breathing, more recent studies have found that between 10% and 20% of hospitalized patients experience severe cardiovascular complications. But how? 

Although exactly why this happens is unknown, several theories exist, some of which at least may be able to explain certain cases of severe cardiovascular complications. For example, someone with pre-existing cardiovascular conditions may be more likely to suffer from a heart attack or congestive heart failure when the body is under stress. These may occur due to increasing demands on the heart (such as an increased heart rate from a fever), low oxygen levels from pneumonia and a higher likelihood to have blood clots. 

Moreover, patients suffering from myocarditis, marked by significant inflammation to the heart, are also more likely to die from COVID-19. This comes as inflammation weakens the ability of the heart to function, meaning that dangerous rhythms unable to properly regulate the circulatory system are more likely to occur. Although observed as a compounding factor towards a negative outcome from the disease however, doctors are still unsure whether myocarditis is a direct effect of the virus, or rather due to an overactive immune response, meaning treatment options are still limited. 

Next, increased risk of death from the virus has been observed among people with high blood pressure (hypertension) and coronary artery disease. Although clinicians don’t understand how exactly this happens, some suggest that blood pressure medications angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) may be responsible. 

Some of the most commonly prescribed medications to treat high blood pressure, both ACE inhibitors and ARBs work by increasing the number of ACE2 receptors in the body, found in heart and lung tissue. Their mechanisms have thus led some clinicians to suspect their ability to enable the spread of COVID-19 throughout the heart and lungs, as the virus has been observed to attach itself to these receptors. However, although suspected, as there is insufficient evidence to ascertain this theory, it can not be taken as a direct explanation for the negative outcomes patients taking these medications may face upon contracting COVID-19. 


Sources: Harvard Health, JAMA

About the Author
  • Science writer with keen interests in technology and behavioral biology. Her current focus is on the interplay between these fields to create meaningful interactions, applications and environments.
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