Previously, I wrote a detailed post on concerns that have been raised about certain blood pressure medications potentially increasing the risk of contracting SARS-CoV-2 or increasing the likelihood of death and serious disease related to the virus.
Millions of patients worldwide with heart failure and hypertension are taking drugs that inhibit pathways in the renal angiotensin aldosterone system termed angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs.)
Lisinopril and ramipril are common ACE inhibitors whereas valsartan, losartan, and irbesartan are common ARBs.
Speculation that these drugs might be contributing to mortality associated with COVID-19 was initiated by a “Rapid Response” published online March 3 by the British Medical Journal in response to an editorial on “preventing a COVID-19 pandemic.” and “Correspondence” to the Lancet published March 7.
Since then I’ve been following this topic closely but nothing has emerged from any new data or new expert analysis to suggest that patients should stop taking ACE inhibitors or ARBs.
Yesterday, an excellent summary of the topic from some of the world’s leading authorities was published in the New England Journal of Medicine entitled “Renin–Angiotensin–Aldosterone System Inhibitors in Patients with Covid-19″
It begins with this wonderful sentence: “The renin–angiotensin–aldosterone system (RAAS) is an elegant cascade of vasoactive peptides that orchestrate key processes in human physiology.”
The authors outline in detail the possible interactions between ACE2 receptors and SARS CoV-2.
For those not interested in the scientific details in the paper, the Cliff’s Notes version of this article is below. Basically, we have insufficient data to know if patients taking RAAS inhibitors are at higher or lower risk for serious SARS-CoV-2 infection.
KEY POINTS RELATED TO THE INTERPLAY BETWEEN COVID-19 AND THE RENIN–ANGIOTENSIN–ALDOSTERONE SYSTEM
- • ACE2, an enzyme that physiologically counters RAAS activation, is the functional receptor to SARS-CoV-2, the virus responsible for the Covid-19 pandemic
- • Select preclinical studies have suggested that RAAS inhibitors may increase ACE2 expression, raising concerns regarding their safety in patients with Covid-19
- • Insufficient data are available to determine whether these observations readily translate to humans, and no studies have evaluated the effects of RAAS inhibitors in Covid-19
- • Clinical trials are under way to test the safety and efficacy of RAAS modulators, including recombinant human ACE2 and the ARB losartan in Covid-19
- • Abrupt withdrawal of RAAS inhibitors in high-risk patients, including those who have heart failure or have had myocardial infarction, may result in clinical instability and adverse health outcomes
- • Until further data are available, we think that RAAS inhibitors should be continued in patients in otherwise stable condition who are at risk for, being evaluated for, or with Covid-19
So my recommendations (and more importantly the recommendations of every major society or organization which has weighted in on this topic) to patients remain the same: don’t stop your ACE inhibitor or ARB due to concerns about coronavirus.
13 thoughts on “An Update On ACE2, RAAS and Covid-19: Still No Reason To Stop Or Change Your Blood Pressure Medication”
How does the recent article in PNAS (https://www.pnas.org/content/118/1/e2021450118) affect your thinking on ACE inhibitors/ARBs in relation to Covid-19. (Fyi I take 40mg of Lisinopril/day.)
Anthony: I love you, man… THANK YOU!
Great information! I have read several studies in the past targeting Corona type virus binding sites with monoclonal antibodies, essentially blocking the expression of ACE2. Since the advent of monoclonal antibody therapy in inhibiting PCSK9 for LDL control, I wonder if anything is in the works for such a therapy with ACE2 a therapy that could potentially function as a prophylaxis of Corona type viruses and an anti-hypertensive or RAAS? As a primary drug to treat hypertension, doubtful since I am sure it would be much more expensive than legacy drugs. However for those high risk patients who might be neutropenic or at higher risk of serious complications, this could be very beneficial. Maybe I am reaching 🙂
i’ve been on losartan for at least 4 years…now due to availability issues…i will soon be taking irbesartan.
any differences to watch for and should i monitor my BP to see if the stability with losartan continues with new med?
thank you so much!
What if the patient comes down with CV19? Is there any reason to think that their medication should be discontinued?
” Until further data are available, we think that RAAS inhibitors should be continued in patients in otherwise stable condition who are at risk for, being evaluated for, or with Covid-19″
Now, once you become quite ill with any infection we tend to see drops in blood pressure and worsening of kidney function.
under those circumstances as with other serious infections we will reduce or stop the RAAS inhibitors (and often other BP medications) until BP and/or kidney functions improve.
There are RCTs started on this very question of ACTIs, ARBs, and COVID-19.
They’ll be able to tell us something fairly definitive in April.
April of 2021 that is!
It’s good that such care is taken to determine the facts of it all. It’s how good science is done.
How abysmally late will that be for how many of us, whether we’re not avoiding the harm or missing out on the benefit ––– NOW??
True. I feel that we will come up with treatments for the virus but it will take time. It should give all even more motivation to do the things we know will prevent virus spread and delay getting infected.
How does this information specifically apply to oral administration of Coreg (or Carvedilol) 6.25 mg twice daily? Any suggestions?
It doesn’t apply to Coreg. Coreg is a beta-blocker. To my knowledge, no concerns raised about beta-blockers
As I understan dit, Carvedilol is both a non-selective beta adrenergic receptor blocker (β1, β2) and an alpha adrenergic receptor blocker (α1). The S(-) enantiomer accounts for the beta blocking activity whereas the S(-) and R(+) enantiomer have alpha blocking activity.
My concern is specifically for the Alpha ARB portion. Any concerns?
You are correct, it does block both alph and beta ADRENERGIC receptors. These are both componenets of the sympathetic nervous system. To my knowlwedge alpha adrenergic blockade is unrelated to angiotensin receptor blockage or to the RAAS
Acknowledged. Thank You!