Cardiac Patients and Covid - 19
As researchers examine deaths from COVID-19, heart patients appear especially vulnerable.
In Italy, where the number of deaths has now surpassed those in China, public health officials reported on March 17 that among 355 people who died, a whopping 76 percent had hypertension and 33 percent had heart disease. And among more than 44,000 confirmed cases of COVID-19 in China, the case fatality rate for people with underlying conditions was highest for those with cardiovascular disease, at 10.5 percent compared with the overall fatality rate of 2.3 percent.
Researchers know generally that infections can take a toll on people who have other health problems. But SARS-CoV-2, the virus that causes COVID-19, may pose particular danger to the heart because of how the virus gets into cells, researchers speculate.
To invade a cell, SARS-CoV-2 latches onto a protein called angiotensin-converting enzyme 2, or ACE2. This protein is found on cells in the lungs, allowing the virus to invade these cells and cause respiratory symptoms. But ACE2 also is on heart muscle cells and cells that line the blood vessels.
Considering the involvement of ACE2, COVID-19 may damage the heart directly, researchers write in a commentary in Nature Reviews Cardiology March 5. According to studies out of Wuhan, China, where the outbreak started, some people with COVID-19 have developed myocardial injury, the death of heart cells for reasons other than a heart attack.
But ACE2 does more than offer an entry point for SARS-CoV-2. The protein is also part of a wide-ranging system of hormones, called the renin angiotensin aldosterone system, that regulates blood pressure and cardiovascular and kidney function. Drugs that target other parts of this system are widely prescribed to lower blood pressure in people with hypertension and cardiovascular disease.
Two classes of these drugs — ACE inhibitors and angiotensin II receptor blockers — are getting some scrutiny during the COVID-19 pandemic. ACE inhibitors block ACE proteins, which are different than ACE2 proteins. The aim is to prevent ACE from helping to make a protein called angiotensin II, which increases blood pressure in the arteries. Angiotensin II receptor blockers, or ARBs, stop angiotensin II from functioning.
There is some evidence in animals that use of these drugs can lead to more ACE2 protein on cells in the heart. But there haven’t been studies showing this in people, or studies in the context of COVID-19. Nor have there been reports describing the types of medications that patients who’ve had severe COVID-19 or have died from the infection were taking.
But the animal evidence has led some to wonder if the use of ACE inhibitors and ARBs can increase the risk of severe disease. “If you look at the mechanistic rationale for concern … it’s there,” although at this point it’s “an extrapolation,” Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health in Bethesda, Md., said during a webcast interview with the editor in chief of JAMA on March 18. “We really need to get data, and we need to get data fast.”
Until there’s more research, the American College of Cardiology, the American Heart Association and the Heart Failure Society of America are advising people with hypertension, cardiovascular disease or heart failure to continue taking these medications. For those who develop COVID-19, the condition of the individual patient should be considered to determine whether it’s necessary to stop the drugs, the groups recommended in a statement released March 17.
Besides the possibility that SARS-CoV-2 targets the heart itself, researchers have evidence that the body’s response to infections can put the heart in danger, especially for those with underlying medical conditions. For example, having the flu can increase the risk of a heart attack, a 2018 study in the New England Journal of Medicine found.
Infections can place an undue burden on a heart that’s already struggling with cardiovascular disease. “Respiratory infections in general have the potential to increase the workload that the heart is under,” says cardiologist Scott Solomon of Brigham and Women’s Hospital and Harvard Medical School in Boston. “That means that your heart’s going to need more oxygen.” As influenza and COVID-19 can interfere with the lungs ability to deliver oxygen, “that can put an additional strain on the heart,” he says.
An infection also stresses other parts of the cardiovascular system, notably where arteries are narrowed by plaques. As the body’s immune system fights the virus, “inflammation can cause a plaque rupture,” says preventive cardiologist Erin Michos of the Johns Hopkins University School of Medicine. That rupture induces blood clotting that can block an artery and lead to a heart attack.
“The question is, why is the heart getting weak” during a COVID-19 infection, says Michos. For now, she recommends that her patients take seriously the recommendations to wash hands and to practice social distancing. “I am telling them to stay home if they can,” she says. “I’m very concerned for everybody, but particularly for my cardiac patients.”
courtesy of sciencenews.org