NEW YORK, May 1, 2020 /PRNewswire/ -- Despite concerns
expressed by some experts, common high blood pressure drugs did not
increase the risk of contracting COVID-19 – or of developing severe
disease – in a study of 12,594 patients.
Published online May 1 in the
New England Journal of Medicine, the study was launched in
response to a March 17 joint
statement issued by the American Heart Association, the American
College of Cardiology, and the Heart Failure Society of America. It
urgently called for research to answer a question raised by past
studies: do high blood pressure (antihypertensive) drugs worsen
COVID-19 patient outcomes?
Led by researchers from NYU Grossman School of Medicine, the
study found no links between treatment with four drug classes –
angiotensin-converting enzyme (ACE) inhibitors, angiotensin
receptor blockers (ARBs), beta blockers, or calcium channel
blockers — and increased likelihood of a positive test for
COVID-19.
Further, the study found no substantial increase in risk for
more severe illness (intensive care, use of a ventilator, or death)
with any of the treatments in patients with the pandemic virus.
"With nearly half of American adults having high blood pressure,
and heart disease patients more vulnerable to COVID-19,
understanding the relationship between these commonly used
medications and COVID-19 was a critical public health concern,"
says lead investigator Harmony
Reynolds, MD, associate director of the Cardiovascular
Clinical Research Center at NYU Langone Health. "Our findings
should reassure the medical community and patients about the
continued use of these commonly prescribed medications, which
prevent potentially severe heart events in their own right."
For the study, the researchers identified patients in the NYU
Langone Health electronic health record with COVID-19 test results.
For each identified patient with COVID-19 test results, the team
discretely extracted medical history needed for the analysis, which
compared treated and untreated patients.
"Before our study, there were no experimental or clinical data
demonstrating the consequences of using these medications one way
or the other in people at risk for COVID-19," says senior study
author Judith Hochman, MD, the
Harold Snyder Family Professor of Medicine and Senior Associate
Dean for Clinical Sciences at NYU Langone Health. "In terms of next
steps, our plan is to use similar approaches to investigate other
medications and their relationship to COVID-19 illness."
Cause for Concern
The study revolves around drugs that act on the
renin-angiotensin-aldosterone hormonal system, which influences
blood pressure. Central to this system is the signaling protein
angiotensin II, levels of which are controlled
by angiotensin-converting enzyme (ACE), say the
authors. Angiotensin II narrows blood vessels to increase
blood pressure, and the study drugs counter that, either by
blocking ACE-induced increases in angiotensin II, or the ability of
ACE to interact with its receptor signaling partners on cells.
According to the researchers, one version of ACE, angiotensin
converting enzyme 2 (ACE2), is present in the outer membrane
of lung cells. SARS-CoV-2, the current pandemic virus, has been
shown to connect to ACE2 on lung cells, a first step toward viral
infection. This led to concern in the field that ACE inhibitors and
ARBs might increase or worsen COVID-19 infection. Past studies in
animal models had suggested that ACE inhibitors and ARBs increase
ACE2 production in other organs, but how they related to ACE2
levels in the lungs was not known.
On the other hand, ACE inhibitors and ARBs had been shown
elsewhere to reduce lung injury in certain viral pneumonias,
creating speculation that they might be helpful. The new study was
designed to address these contradictions.
Along with Reynolds and Hochman, authors of the study from NYU
Grossman School of Medicine were Andrea
Troxel, director of the Division of Biostatistics;
Samrachana Adhikari, Claudia
Pulgarin, Eduardo Iturrate,
Stephen Johnson, Anais Hausvater, Jonathan Newman, Jeffrey
Berger, Sripal Bangalore, Stuart
Katz, Glenn Fishman, Dennis
Kunichoff, Yu Chen, and Gbenga Ogedegbe.
Media Contact:
Robert Magyar
robert.magyar@nyumc.org
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SOURCE NYU Grossman School of Medicine