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A lot of people have written to me asking about the safety of taking ACE inhibitors during the COVID-19 pandemic.

I therefore thought I’d do a blog to clarify my understanding of this subject. It is important to note that given the very rapid and terrifying pace of growth of the pandemic, we have very limited data to make absolutely definitive conclusions and the advice may change as results from more research become available.

What are ACE inhibitors and why are they used?

ACE (which stands for Angiotensin converting enzyme) inhibitors are a class of drug that are used in patients who have high blood pressure, heart failure and even in patients who suffer from diabetes.

You may recognise them as medications with names that end with the suffix –‘il’ – such as Ramipril, Lisinopril, Enalapril etc.

When the heart is under any kind of stress it struggles to get as much blood around the body as it should. The kidneys, which are extremely sensitive, detect this minute reduction in the blood supply and release hormones, which act to increase the body’s stress responses and also increase the absorption of water that would normally be passed out in the urine. This is to try and restore the amount of blood getting to the kidneys. Whilst this may be desirable for a very short time, the problem is that over a prolonged period, the on-going stress response and fluid retention puts on an ever-increasing load on the heart and eventually the heart will start weakening.

Some of the enzymes that regulate this response are called Angiotensin Converting enzymes (ACE) and ACE inhibitors stop one of these enzymes (ACE-1) from participating in this ultimately damaging process. There are other Angiotensin converting enzymes that are also involved in this process such as ACE-2 but ACE inhibitors work on ACE 1. There is a lot of very good evidence that long-term treatment with ACE inhibitors can help improve prognosis. There is also reasonable evidence that if a patient is nicely stabilised on an ACE inhibitor then withdrawing the medication can cause deterioration and decompensation of heart failure.

An Interesting observation that has been made is that for some reason, the urine levels of ACE-2 seem to be elevated in patients who are taking ACE inhibitors suggesting that perhaps ACE-2 levels are in some way increased in these patients.

The relationship between COVID-19 and ACE

Basically what we have come to understand is that the coronavirus (called this because of crown-like spiky projections on its surface) actually needs the presence something called the ACE-2 receptor to enter the lungs where it can be so damaging. We also know that patients who high blood pressure, diabetes and heart failure (i.e. all the patients who would be taking ACE inhibitors) who get COVID tend to suffer more aggressive and possibly lethal disease.  

Given the observation that ACE-2 levels are increased in patients who take ACE inhibitors and that the virus needs ACE-2 to get in to the body, scientists have therefore raised the question as to whether perhaps one mechanism may be that these patients have higher levels of ACE-2 and therefore a greater target for the coronavirus to inflict more damage. Whilst this is a plausible hypothesis, at present there is no definitive evidence that it is the ACE-inhibitor, which is definitely the cause for more severe disease in patients taking it. This may simply be a case of association rather than causation.  Patients taking ACE inhibitors are generally older, frailer and sicker. We also know that they are more likely to have significant additional co-morbidities, which would reduce their body’s reserves to fight infection. There are so many confounding variables that we cannot automatically make the assumption that the ACE inhibitor is to blame.

What we do know however is that ACE-inhibitors stabilise heart disease and abrupt withdrawal them can destabilise the underlying condition that they are taken for (such as heart failure) and the risks to a destabilised patients from coronavirus are likely to be significantly greater than to a stable patient.


So at the moment, there is not enough convincing evidence that the ACE-inhibitor is the responsible culprit and the risks of stopping the ACE-inhibitor abruptly are greatly likely to outweigh the benefits. All the major cardiac associations and bodies around the world have echoed this.

As mentioned earlier, advice may change as more research accrues but for the time being it is best not to risk destabilising a chronic condition like heart failure and making oneself even more vulnerable to the risk of COVID-19.

I hope you found this useful and would be very interested in hearing your thoughts. Here is a video I have done on the subject:

Keywords: COVID-19, Coronavirus, ACE-Inhibitors, high blood pressure, Sanjay Gupta, YORKCARDIOLOGY


This post is also available in: हिन्दी (Hindi)