As can be seen above, hypertension in the general populationclosely associates with increasing age, hence any association with hypertension may merely represent confounding due to age, and should be interpreted after careful analysis.

A recent Italian study (via Bloomberg) reports a high prevalence of hypertension amongst those who died. It is hard to know what to make of those raw rates, as can be seen above, the patients who died were also quite older. The prevalence of HT in those who died (76%) was higher than diabetes (36%), heart disease (33%) and CKD (18%). However, the median age of those who dies was 80.5 years. The prevalence of hypertension goes up with age, as an example was 76% in those 75 and older in this report. Hence this prevalence might just represent the expected prevalence for this age group. Additionally, from the Seattle outbreak study (McMichael et al, NEJM), it is clear that the prevalence of hypertension was indeed high in the older care facility residents who developed COVID-19, but not so much in the younger visitors, and staff who worked there.

Thus hypertension does seem to be a common comorbidity, even more so than diabetes - but these are mostly data from China, and one brief report from Italy (latter with much higher hypertension rate) and one from US, so one should be careful before generalization. It is also not clear how hypertension was coded - we can speculate that it might be based on use of hypertension medications rather than actual BP measurement. We do have data on actual BP from two studies:

In one study by (Huang et al, Lancet), the median systolic BP, on admission, in the 13 patients with COVID-19 who required ICU care later was 145 mm Hg compared to 122 in the 22 patients who did not. The patients needing ICU care were similar in age to those who did not need ICU care (median age 49 years)

In another study (Chen et al, BMJ) the median arterial BP, on admission, was 137 mm Hg among those who died compared to 125 mm Hg amongst those who survived. In this study, the patients who died were older (median age 68 years) than those who survived (median age 51 years)

Without better adjusted or stratified data, it is hard to say what this represents.

Does being on ACEi or ARB increase risk of contracting COVID-19?

We don’t yet know that having hypertension is a risk factor (independent of age) for developing COVID-19, or serious disease. Roughly 15 - 30% of patients with COVID-19 had hypertension, in the reported literature so far (see table above). The proportion of these who might have been on an ACEi or ARB will be a smaller subset of this 15-30%. There are no clinical data to support that being on an ACEi or ARB increases a risk, nor does the basic science discussed below support a clear association.

But even if there is a doubtful or dubious association, what’s the harm in switching to a different BP medication?

From the science, it’s not just that we don’t if know ACEis or ARBs (looked at separately) increase the risk of COVID19, or the severity, we don’t even know whether these drugs might be beneficial. To reiterate:

We don’t know if there is an association between ACEi/ARB and COVID19

If there is one, we don’t know the direction of association (beneficial or harmful)

We don’t know the magnitude of any possible association

ACEis and ARBs are useful drugs. They don’t just reduce blood pressure, they decrease risk of progressive kidney disease, of dying if one is at high cardiovascular risk, and if one has heart failure.

Stopping these drugs for an unknown potential benefit can make these conditions worse. The patient will need a replacement drug (more contact with an already stretched medical system), visit pharmacies (when one should be practicing social distancing), and may even need follow up lab investigations or medical visits to ensure the replacement drugs are working as they should.

Moreover, how long does it take for any biological effect on ACE2, to wear off, and make a tangible difference?

Should these drugs be started or stopped in patients with suspected or confirmed COVID-19?

The same discussion largely applies here: in addition that if the virus is in, and has bound to ACE2, will stopping the ACEis or ARBs now have enough of an effect of ACE2 to make a difference?

There is several clinical trials ongoing, or planned to answer these questions in patients with COVID-19, along with several large scale observational studies (see below). Until then, the actual decision for an individual patient should be an individualized one, based on the specific needs, benefits, and hemodynamics. We do hope more data become available in the coming days to allow us to make more informed choices.

RAS activation and long term outcomes

Patients who survived SARS-CoV have altered lipid metabolism even 12 years later and thus may have worse long-term outcomes including cardiovascular disease. Thus data on long-term outcomes of patients who survive SARS-CoV-2 will be important, especially because the RAS can be programmed to chronically upregulate ACE/Ang II at the expense of ACE2/Ang-(1-7) in otherwise healthy adolescents and young adults.

ACEi/ARB use and Clinical Outcome Data

This section started off with a few case series, but has some large observational studies now. The caveats we mention at the start on being careful in drawing conclusions from these studies are even more necessary here. Nevertheless, as these data start trickling in, expect this section to grow, and check back here for updates.

A previous version of this blog page had a longer discussion of the results of all the studies conducted in this area. In the pursuit of brevity, we have archived most of that discussion, which is now available here. Below, we summarize the some recent epidemiological studies published, which are of higher quality and large numbers.