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

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

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:
). 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

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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