The novel coronavirus mainly attacks the lungs. But doctors have been increasingly reporting cases of another battlefield raging within the body: the heart.
More than 1 in 5 patients develop heart damage as a result of COVID-19 in Wuhan, China, one small study published March 27 in the journal JAMA Cardiology suggested. While some of these patients have a history of heart conditions, others do not. So what’s going on?
Cardiologists say several scenarios could be unfolding: The heart may struggle to pump blood in the absence of enough oxygen; the virus may directly invade heart cells; or the body, in its attempt to eradicate the virus, may mobilize a storm of immune cells that attack the heart.
“We know that this is not the only virus that affects the heart,” said Dr. Mohammad Madjid, an assistant professor at McGovern Medical School at The University of Texas Health Science Center at Houston (UTHealth). The risk of developing heart attacks, for example, is thought to increase about sixfold when a person is infected with the flu virus, according to a study published in 2018 in the New England Journal of Medicine.
What’s more, during most influenza epidemics, more patients die from heart complications than from pneumonia, according to a review published March 27 in the journal JAMA Cardiology. Viral infections can disrupt blood flow to the heart, cause irregular heartbeats and heart failure, according to the review.
So while it doesn’t “come as a surprise,” that novel coronavirus called SARS-CoV-2 can lead to heart damage, it may be occurring more frequently in these patients than it does in people infected with other viruses, Madjid, the lead author of the review, told Live Science.
The double-edged sword
The virus might be directly attacking the heart.
“We’re seeing cases of people who don’t have an underlying heart disease,” who are getting heart damage, said Dr. Erin Michos, the associate director of preventive cardiology at Johns Hopkins School of Medicine. Heart damage isn’t typical in mild cases of COVID-19, and tends to occur more often in patients who have severe symptoms and are hospitalized, she said.
Though the virus predominantly affects the lungs, it is circulating in the bloodstream; that means the virus could directly invade and attack other organs, including the heart, Michos told Live Science.
Both heart cells and lung cells are covered with surface proteins known as angiotensin-converting enzyme 2 (ACE2) — these molecules serve as “doorways” for the virus to enter cells. But this enzyme is a “double-edged sword,” she said. On one hand, the ACE2 molecule acts as a gateway for the virus to enter the cell and replicate, but on the other hand, it normally serves a “protective” function, Michos said.
When tissues in the body are damaged — either by an invading virus such as SARS-CoV-2 or by other means, the body’s natural healing response involves releasing inflammatory molecules, such as small proteins called cytokines, into the bloodstream. But paradoxically, too much inflammation can actually make things worse. The ACE2 enzyme acts as an anti-inflammatory, keeping immune cells from inflicting more damage on the body’s own cells.
But when the virus latches onto ACE2 proteins, these proteins get knocked out of commission, possibly reducing the anti-inflammatory protection that they give. So the virus may be acting as a double-whammy by damaging cells directly and preventing the body from protecting tissues from inflammatory damage.
“If the heart muscle is inflamed and damaged by the virus, the heart can’t function,” she said.
The novel coronavirus might also indirectly damage the heart. In this scenario, the patient’s immune system winds up “going haywire,” Michos said. This scenario has played out in some really sick patients who have highly elevated inflammatory markers — or proteins that signal high levels of inflammation in the body.
This is called a “cytokine storm,” Michos said. Cytokine storms damage organs throughout the body, including the heart and liver, she added. It’s not clear why some people have such an elevated response compared with others, but some people could be genetically prone to it, she added.
And then you have patients who have underlying heart disease who are at higher risk of developing severe symptoms of COVID-19 — and higher risk of mortality. “You can imagine, if their heart already has difficulty working … they don’t have the capacity to meet this challenge” of not having enough oxygen because their lungs aren’t working as well.
So COVID-19 can “exacerbate” underlying heart disease, Michos said. A new study, published April 3 in the journal Circulation, described four cases of heart damage among COVID-19 patients in New York, some with underlying conditions. (Michos is on the editorial board for the journal Circulation.)
Treatments and complications
Cardiologists identify heart damage using a blood test for a protein called troponin. When heart cells are injured, they leak troponin into the bloodstream. But “it’s sometimes not that easy,” to figure out what kind of heart damage a patient is having, Michos said.
“We are really seeing different cardiac involvement,” Michos said. So it matters “what’s causing the heart damage because you would treat it differently.”
For example, if the virus is directly invading the heart, the patient may need antiviral medications. If instead the immune system is causing heart damage, the patient might need immunosuppressants. Right now, no direct treatments target COVID-19, and most of the treatment being used currently involves supportive care such as providing more oxygen.
What’s more, people who have high blood pressure or other underlying heart conditions commonly take ACE inhibitors or angiotensin receptor blockers (ARBs) — medications that widen blood vessels, therefore increasing the amount of blood the heart pumps and lowering blood pressure.
Cardiologists are hotly debating whether people should stop or start taking those medications if they’re at high risk for COVID-19. (One paper suggested the drugs could be harmful, while some clinical trials are assessing the use of ARBs to reduce the severity of COVID-19, Live Science previously reported.)
It’s really hard to tease out whether having more ACE2 is helpful or harmful, as these proteins are how the virus enters the cells, but also known to protect the cells against injury, Michos said.
The current consensus is that if patients are already taking these medications, they should stay on them, she said. “Patients taking ACE-[inhibitors] and ARBs who contract COVID-19 should continue treatment, unless otherwise advised by their physician,” according to a statement from the American Heart Association, the Heart Failure Society of America and the American College of Cardiology.
Experts from Australia and New Zealand similarly said they strongly recommend patients with hypertension, heart failure and cardiovascular disease who are already on these medications keep using them, according to a study preprint published on April 3 in The Medical Journal of Australia.
Complicating matters, certain drugs that are currently under investigation for treating COVID-19, including hydroxychloroquine — the drug that President Trump has said is a game-changer — could cause heart damage, those experts said. Now, the goal is to figure out if there’s a genetic or biochemical reason some people are more prone to heart damage from COVID-19 — and to figure out what drugs work best “to protect the heart from injury,” Michos said.
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Originally published on Live Science.
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