The Future of COVID-19 and Thromboprophylaxis Treatment

JUNE 19, 2020
HCP Live


Transcript: 

Gregory Piazza, MD, MS:
What’s going to be the landscape following this coronavirus pandemic? Certainly, there’s renewed interest in extended thromboprophylaxis for the medically ill. Something that many of us were hoping for is that we would get people interested in medically ill patient prophylaxis, and now we have this pandemic doing that. How are things going to change? What do you foresee for extended-duration thromboprophylaxis in medically ill patients, even considering those who don’t have COVID-19 [coronavirus disease 2019]? Is this going to change? I’ll start with Alex and then go to Vic.

Alex Spyropoulos, MD, FACP, FCCP, FRCPC: Conceptually, I think of this as 3 phases. In the prehospital phase is a subset of high-risk patients who have never entered the hospital that we should study? Indeed, we’re trying to assess a randomized trial looking at this question, whether there’s a subset of the ill outpatient population with polyvascular disease or key risk factors that would benefit from a purely outpatient-based thromboprophylactic strategy. The majority of data in the medically ill prophylactic space in terms of a DOAC [direct oral anticoagulant] are with rivaroxaban [Xarelto]. The majority of data, especially data that are relevant to the COVID-19 crisis, relate to D-dimer elevation. We’ve seen that using D-dimer elevation and a thromboprophylactic strategy with low-dose rivaroxaban produces a net clinical benefit in terms of an appropriate risk reduction without an appropriate increased bleed risk. That’s the first phase. The second phase is the in-hospital phase that we just talked about. Is there a strategy that uses more aggressive, or even therapeutic, doses of anticoagulants that confer advantages?

And lastly, as you just said, there’s the posthospital discharge phase. In that sense, is there an optimal thromboprophylactic strategy? Can we interchange DOACs? Can we use apixaban versus rivaroxaban? I don’t know. A lot of the data are with rivaroxaban. It’s FDA approved. Apixaban is not. Can we use aspirin? I doubt it. Can we use long-term low molecular weight heparin, like enoxaparin 40mg? Yes, there’s the EXCLAIM trial that Vic and I were part of. But again, there was a lot of bleeding in EXCLAIM as well. If I had to guess, my sense is that maybe these patients would benefit from a dual-pathway inhibitory approach, something like low-dose anticoagulation plus an antiplatelet therapy. More and more data suggest that there is an antiplatelet-derived process, especially with oxidative stress, as well as the classic thrombin-derived process that is leading to the thrombosis. I would love to study a dual-pathway or COMPASS-type regimen in these patients with a low-dose anticoagulant and low-dose aspirin. Those are the 3 phases that I think should be evaluated.

We’re in the tabula rasa, right? This is brand-new territory. We can extrapolate only from what we know, but we know very little in terms of the thrombotic risk in the COVID-19 era. 

Gregory Piazza, MD, MS: Vic, what do you think?

Victor Tapson, MD, FCCP, FRCP: Alex covered it very well, Greg. I’ll echo what he said. I was thinking about COMPASS when Alex mentioned that. Maybe we need a COMPASS-type study for VTE [venous thromboembolism]. Maybe we need a low-dose Xarelto, a low-dose DOAC, together with an antiplatelet drug in everybody. Maybe we need a huge study of 50,000 patients. Maybe we’ll see that many of us in the population could really benefit from this, even if we don’t have any obvious or visible risk factors for VTE. Something like that should be done. If quarantining goes on or comes up again, we may have to look at patients who don’t have COVID-19: people who are getting around and pretty healthy but who are sitting around a lot more. We might look at telemedicine and things like that. How do we study those folks?

Alex covered those things well. I’m going to finish with an optimistic point and say there’s so much going on right now. Most of our protocols at Cedars Sinai have been cut off for COVID-19 protocols. We’re using COVID-19–VTE protocols and other COVID-19 protocols, using a lot of different drugs. What about BCG? What about an actual killer cell? There are a lot of things we’re studying right now. We’re going to get a handle on this, but it’s going to come around again. It took us millions of years to evolve as humans to get our genome where it is. It took this virus a couple of months, a few weeks, so it’s a scary time. We’ll get a lot of antiviral funding, and we’re going to learn a ton in the future here.

Gregory Piazza, MD, MS: I agree. That brings us to the end of what’s really been a wonderful discussion with a lot of terrific insight to how we approach this pandemic. One of the things that lifts my spirits a little, as I try to keep my children from assaulting each other during this no-school period, is the fact that we have so many great minds working on this. Our research infrastructure is so strong that if there are inroads or handholds that we can find to boost ourselves up and improve care in this setting, we’re going to find them. I’m encouraged by that. Getting to work with you, Vic and Alex, on these things also makes me feel good, and we all need a little bit of that right now. I want to thank you both for being amazing friends and even better faculty. We reviewed great information.

I want to thank everybody who watched this HCPLive® presentation. Hopefully this will entertain you for a little while at home as you’re staying locked down. We found this to be fantastic. I learned a lot, and hopefully we’ll do more of these Peers & Perspectives® discussions focused on COVID-19 and how we can care for these patients better. I want to thank all of you.


Transcript Edited for Clarity

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