Drugs for high blood pressure don’t appear to make COVID-19 worse

Two observational studies provide some reassurance for patients taking the drugs

ACE inhibitors

Two new studies suggest drugs called angiotensin converting enzyme inhibitors, or ACE inhibitors (like the one shown), and angiotensin receptor blockers don’t make COVID-19 more severe in hospitalized patients.

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Drugs widely used to treat high blood pressure do not appear to make COVID-19 dangerously worse.

Two new studies from China offer the first observational evidence that the drugs do not increase the risk that hospitalized patients with COVID-19 will develop severe complications or die. One study looked at 362 patients with high blood pressure treated at Central Hospital of Wuhan, the city where the initial outbreak occurred. It found no difference between those on the drugs and those not in terms of the severity of the disease and whether a patient survived or died, researchers from the hospital report online April 23 in JAMA Cardiology.

The other study followed 1,128 COVID-19 patients with hypertension from nine hospitals in Hubei Provence, where Wuhan is located. It found that the mortality rate was lower for the 188 on the drugs, an international research team reports online April 17 in Circulation Research.

The new studies provide reassurance that the drugs “are not associated with harm in patients with COVID-19, as some had suspected,” says cardiologist Scott Solomon of Brigham and Women’s Hospital and Harvard Medical School in Boston. But without randomized controlled trials, in which patients are randomly chosen to take a drug or a placebo, “it will be very difficult to get at the truth” of exactly what impact the drugs have, he says.

The drugs — angiotensin converting enzyme inhibitors, or ACE inhibitors, and angiotensin receptor blockers, or ARBs — have been in the spotlight since data emerged that COVID-19 takes a harder toll on people with hypertension, cardiovascular disease and diabetes (SN: 3/20/20). Many with these conditions take the drugs, which work to stop a hormone called angiotensin II from increasing blood pressure in the arteries.

Some researchers wondered if the drugs themselves helped to explain why these patients are more likely to have severe complications or die from COVID-19. Animal data show that the drugs can increase the amount of a protein called angiotensin converting enzyme 2, or ACE2. That’s the protein that SARS-CoV-2, the virus that causes COVID-19, grabs onto to enter a cell (SN: 2/3/20).

In response to the speculation, the major heart health organizations have recommended that patients on the drugs continue to take them, until there’s evidence of harm.

And there’s more to the story than just the potential for unwanted effects. “ACE2 is sort of a double-edged sword,” says Erin Michos, a preventive cardiologist at Johns Hopkins University School of Medicine. Although it’s the entry point for the coronavirus, “it’s thought to be potentially protective in the lungs,” she says.

ACE2 inactivates angiotensin II, regulating the hormone. A study published in the aftermath of the SARS epidemic reported that ACE2, which is found on lung cells, protected mice from an acute lung injury similar to acute respiratory distress syndrome — a severe complication of SARS and COVID-19. In contrast, angiotensin II led to excess fluid in the lungs and impaired their function, researchers reported in Nature in 2005.

So in theory, it’s plausible that the drugs might help patients with COVID-19, Michos says. Blocking angiotensin II might mean it can’t contribute to fluid buildup in the lungs. Along with clinical trials to investigate this, it will be useful to learn whether the drugs “make a difference in whether you need hospitalization or not,” she says, since the new studies looked at people who were already hospitalized with COVID-19.

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