http://www.nephjc.com/news/covidace2

This has been discussed previously. But I would like to hear other docs opinions re this very controversial subject. Especially whether ACE-I or ARB pts with HTN should stop or continue their meds.

The above review is excellent. The COVID-19 virus enters the type 2 respiratory epithelial cell via binding to the ACE-2 receptors on cell surface thru the viruse's spike like S proteins. ACE-I and ARB's upregulate ACE-2 in in vitro studies. A hypothetical review recommended against ACE-I and ARB in COVID-19 pts. They hypothesized that these pts would suffer worse ARDS due to increased type 2 cell entry related to increased ACE-2 receptors on type 2 cell membranes.

But a rebuttal paper from Europe argues against this, with animal data suggesting ACE-I and ARBs may be actually beneficial in COVID-19. And there is a study (highlighted on this forum) looking at losartan and HCQ as a THERAPY for COVID-19.

I am on losartan!!! Have mixed emotions.

HTN pts have higher mortality from COVID-19 infections FYI as you know. Independent variable. Not clear why.

So - what are ya'lls thoughts? Are you stopping or continuing ACE-I and ARBs for HTN in this COVID-19 era?

Very interested in what you guys have to say on this since I am on Omesartan. 10mg per day

Sticking to my Lisinopril (ace-I). I'm 40 and have the fats, but other than that I'm relatively healthy so I like my odds vs CoronaVirus more than my odds vs high blood pressure or trying to switch meds in this environment.

/Not a doctor.

jgo said:

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Very interested in what you guys have to say on this since I am on Omesartan. 10mg per day

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Olmesartan? I'm on the same. Curious as well.

Current guidelines - from American and Europe major medical scocieties, is to not alter therapy with ACE-I or ARB with pts on these drugs with COVID-19.

Not enough data to either start or discontinue ARBs in patients with COVID-19, moreso that one putative mechanism is beneficial and the other harmful. But I wouldn't hesitate to act on a sick patient if even preliminary data suggested a benefit one way or the other.

I would think he just don't have enough data to know if ACE inhibitions increase ACE2 expression in vivo. There was just a paper out that suggests ACE2 is interferon stimulated which we didn't know either.

Ramipril here (ACE inhibitor) ... 5 mg. I'm 39 and "healthy" other than HBP and high cholesterol (Lipitor). I know if I called my general practitioner and asked about these studies I would be able to hear his eye roll over the phone. 0% chance he'd change my meds. Stroke or C19? I guess I'll just roll the dice and take my chances with C19.

How does amlodipine figure into all of this?

Posted this on other thread but American Heart Association is recommending patients on ACE-I to not stop therapy out of concerns for Covid. Data not conclusive enough to alter treatment of pre-existing conditions.

BowSowy said:

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How does amlodipine figure into all of this?

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Doesn't really figure into it. It is a calcium channel blocker, different type of drug with different mechanism of action.

BowSowy said:

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How does amlodipine figure into all of this?

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Probably not much as that's a calcium channel blocker and to my knowledge has no effect on angiotensin cascade, lung cells.

Well ***** I'm on losartan too.

Not gonna stop taking it but still.