Dr. Sandra El Hajj -MSc, N-MD, DHSc
While it is known that COVID-19 causes mainly damage to the lungs, recently, health professionals have found that the virus is also damaging other major organs.
Most people infected with COVID-19 develop heart-related problems as a complication of a preexisting cardiac disease. Cardiac injury was reported among 41 patients hospitalized with COVID-19 in Wuhan, China. Among them, 12 percent had signs of cardiovascular damage(1). These patients showed both elevated levels of proteins released by the injured heart muscle as well as abnormalities shown on electrocardiograms and heart ultrasounds.
COVID-19-related heart injuries could occur in several ways. People who are currently diagnosed with heart disease are at a greater risk for severe cardiovascular and respiratory complications from COVID-19. Also, people with previously undiagnosed heart diseases may show cardiac symptoms which can be worsened by the viral infection. Some people may even experience heart damage that may look similar to heart attack injury. This can occur when the heart muscle does not receive enough oxygen. COVID-19 may trigger such a decreased oxygen supply.
Fever and inflammation can accelerate your heart rate and increase the metabolic demands of many organs, including the heart itself. That stress can be very impactful if the lungs are infected and incapable of exchanging oxygen and carbon dioxide optimally. Such an impaired gas exchange can diminish further the oxygen supply to the heart muscle. In some cases, there are people with COVID-19, who were previously healthy with no underlying cardiac problems, but still developed fulminant inflammation of the heart muscle as a result of the virus directly infecting the heart. This type of inflammation could lead to heart rhythm disturbances and cardiac muscle damage. It can also interfere with the heart’s ability to pump blood optimally. Such a severe reaction can be life-threatening and can happen even to those who don't have any preexisting risk factors.
Inflammation is a normal defensive response of the body triggered by an infection. This is how the body prepares to get rid of the agent causing the infection. However, such a protective response can also cause damage to the tissues. During inflammation, the body releases inflammatory proteins known as “cytokines” that recruit white blood cells and other messenger molecules to fight off the infective agent. In an effort to fight the infection, some normal processes could get disrupted. Cytokines can boost the local inflammatory response and eventually trigger a heart attack.
During inflammatory processes, the liver also increases the production of important proteins aimed at defending the body from infection. But, these proteins can also make the blood more prone to clotting, while reducing the secretion of natural clot-dissolving substances. These tiny clots can clog small blood vessels in the heart and other organs, such as the kidneys, depriving them of oxygen and nutrients. This clogging may lead to serious damages causing organ failure.
Therefore, immune-mediated injuries to the heart and other organs could be the result of the body’s heightened response, commonly known as the cytokine storm. It is marked by the widespread release of cytokines that can cause cellular damage, tissue injury as well as organ damage.
SARS-CoV-2, the causative agent of COVID-19, invades our human cells by using the spike-like proteins. These specifically interact with the ACE2 receptors found on cells in airways, lungs, heart, kidneys and blood vessels. To clarify, ACE2 Receptors are proteins that are found on the surface of specific cells. They are enzymes that form small proteins from large ones by cutting them. The large proteins are the angiotensinogens. In healthy individuals, the small proteins resulting from angiotensions help keep our blood pressure stable.
When the COVID-19’s protein-like spike binds to the ACE2 receptor (from the cells), it creates a channel to the virus. This allows the entry of the virus into the cells.
The ACE2 protein also plays an important role in the regulation of blood vessel dilation and of course blood pressure(2). Two classes of drugs, widely used to treat high blood pressure and heart disease, interact with the ACE2 receptor. It is important to note that these blood pressure medications could increase the number of ACE2 receptors expressed on cells, and hence possibly create more opportunities for the virus to enter. Experts are still investigating whether the use of such drugs could render people who take them more susceptible to infection. A recent review and a study published by the British Medical Journal(3) in February 2020 suggests that these medicines may play a dual role in COVID-19. On one hand, they can increase the chance of infection by helping to incorporate the virus inside our cells. On the other, they protect the heart and improving lung damage from the disease. Up until now, further studies are needed to assert how problematic these medications can be and the extend of their caused damages.
For a novel infection, COVID-19 surely made its impact on the world. While preliminary studies showed the direct link between this infection and our lungs, evidence showed that one out of every five infected patients ended up suffering from heart injury, regardless of the other exacerbated symptoms. No clear-cut explanation was discovered that could clarify such a causative effect. As a preliminary finding, heart inflammation was noticed in COVID-19 positive individuals; however, it was not clear whether it is the direct impact of the virus or a secondary side effect of the adopted experimental medications.