Blood pressure medicines lower risk of COVID-19 death, study says
Bad outcomes cut by one-third
We pooled data from 19 relevant COVID-19 studies that included patients taking two particular types of blood pressure medication: angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs). This allowed us to look at the outcomes of more than 28,000 COVID-19 patients to assess the effects of these drugs.
[Read:Are EVs too expensive? Here are 5 common myths, debunked]
ACEIs and ARBs work by acting on the renin-angiotensin-aldosterone system (RAAS), which is essential for regulating blood pressure and the balance of fluids and electrolytes. These drugs were also thought to potentially increase the expression of a protein found on the surface of cells called angiotensin-converting enzyme 2 (ACE2).
Apart from helping regulate blood pressure, theACE2 proteinis also what allows the coronavirus to enter the body’s cells. This is why there were concerns about patients using these drugs. If the medications increased the amount of ACE2 present on cells, it was suspected they would make it easier for the virus to infect them,worsening a patient’s condition.
But when we looked at the outcomes of patients taking ACEIs and ARBs compared with those not on these medications, this wasn’t the case.
We found no evidence that these medications might increase the severity of COVID-19 or the risk of death. On the contrary, among patients taking ACEIs and ARBs that had been prescribed to treat high blood pressure, there was actually a significantly lower risk of death, being admitted to intensive care or being put on ventilation. We observed a reduction of such events by one-third in this group.
It may be that these medications actually have a protective role – particularly in patients with high blood pressure.
What’s behind this effect?
It’s not clear why patients taking ACEIs and ARBs experienced less severe disease, but there are a couple of points to consider.
The first is that while theoretically these drugs were thought to increase ACE2 levels, there’sno convincing evidencethat this actually happens. We don’t have anyclinical dataon the effects of these drugs on ACE2 expression in human tissue.
And even if these drugs do increase ACE2 levels in cells, not all of it is surface-bound. Additional ACE2 that appears elsewhere in the cell might not function as an entry point for SARS-CoV-2.
There’s also a second potentially relevant piece of information. Infection with SARS-CoV-2 may also lead to anoverreaction of the RAAS pathway– which is what these blood pressure drugs target – and inflammation. This increased inflammatory process is thought to be the culprit for acute lung injury and can lead to worsening pneumonia andacute respiratory distress syndrome. Hence, it might be that taking medications that inhibit the RAAS system prevents such a sequence of events and improves clinical outcomes in COVID-19.
What we do know is that our study provides substantial evidence that patients should continue using these medications during the pandemic, as they are safe. We haven’t investigated whether starting these tablets in acutely ill COVID-19 patients will improve their outcomes, but this is now the subject of a randomized controlled trial.
This article is republished fromThe ConversationbyVassilios Vassiliou, Senior Clinical Lecturer in Cardiovascular Medicine,University of East AngliaandRanu Baral, Visiting Researcher (Academic Foundation Doctor FY2), University of East Anglia under a Creative Commons license. Read theoriginal article.
Story byThe Conversation
An independent news and commentary website produced by academics and journalists.An independent news and commentary website produced by academics and journalists.
Get the TNW newsletter
Get the most important tech news in your inbox each week.
