Acute PE: Increased Role for Cardiologists

Samuel Z. Goldhaber, MD; Seth Bilazarian, MD


April 23, 2015

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Cardiologists Treating Acute Pulmonary Embolism

Samuel Z. Goldhaber, MD: Hello. This is Dr Sam Goldhaber for the ClotBlog at on Medscape speaking to you from the American Heart Association (AHA) Scientific Sessions in Chicago.

We are very fortunate to have my good friend and colleague Dr Seth Bilazarian here with us today. Seth is also a blogger for on Medscape. We love to use this opportunity at the AHA to get together and talk about various issues that we have in common. What we decided to talk about today is one of my favorite topics, the role of the cardiologist in treating acute pulmonary embolism [PE].

Seth, you had suggested we speak about PE and how the role of the cardiologist is really increasing, particularly as we have more technological tools to offer and more advanced tools for the type of generally complex patients with pulmonary embolism whom we're asked to consult on. Do you want to expand on this a bit and tell us about your own experiences?

Seth Bilazarian, MD: It's a very interesting topic because cardiologists have many of the tools. I imagine many in our audience had a similar experience to me and went through cardiology training and are well trained in the arteries but not the veins. We feel some hesitancy about the right heart and veins. We lack confidence. Over the years I've relied heavily on my relationship with you to ask questions when I'm dealing with a patient who has a submassive or massive PE, and you've always been very helpful. But I'd have to say with the increasing experience that I've gained through novel oral anticoagulant [NOAC] use for atrial fibrillation, I'm coming into greater confidence in using those therapies for PE and deep vein thrombosis [DVT]. Catheter-directed thrombolysis is something that we've implemented in our community hospital. I thought we could take this opportunity to have you, an international expert who has dedicated a career to this area, and myself, a nascent user of technology and therapies in this area, to help others either begin or move along in this process.

Venous Disease, Arterial Disease

Dr Goldhaber: I agree with you that cardiologists are now embracing with enthusiasm the management of acute PE and acute DVT. It's only natural because we have the same set of NOACs that we use for stroke prevention and atrial fibrillation. I think even biologically we used to think that venous disease was quite separate from arterial disease, but now we've learned that the risk factors are virtually the same for coronary disease as for venous thromboembolism. And, as you and I have talked about as we prepared for this ClotBlog, a lot of the pathophysiology, including inflammation, is exactly the same as well. Really it makes sense to lump rather than to split.

I think we are asked to see probably the 30% or so of patients with either massive or submassive PE and not as often asked to see the patient with an uncomplicated DVT or PE, but that may be coming, because you can't always be sure when the patient presents whether it will eventually become complicated or uncomplicated.

What has your experience been in terms of working with your colleagues to make important decisions about when to use anticoagulation alone in a PE patient, when to go to the cath lab and use catheter-directed or ultrasound-facilitated catheter-directed thrombolysis, when to use systemic thrombolysis, when to send the patient for open surgical embolectomy, or when to put in an inferior vena cava (IVC) filter?

Dr Bilazarian: That's an enormous number of questions. Our current hospital practice began a program of catheter-directed thrombolysis and very quickly we have accumulated good experience. Our technicians, our nurses, and our physicians are really very comfortable using it now after our initial experience. It speaks to what we've been saying. We know how to put catheters into the pulmonary arteries.

Dr Goldhaber: It's part of our culture, right?

Dr Bilazarian: Right. We know how to do that, but you're right. Just like in the area of interventional cardiology, much of the important part of the procedure is the decision-making about who should receive it. Through your teaching and others we are limiting that to submassive patients defined as an RV/LV ratio ≥1 on [computed tomography] CT. We've had good success with that, but like many things, this is an evolving area. We are excluding very old patients because the trials excluded very old patients. We're not sure if that's the right thing to do. There's a lot that's unknown, and that speaks again to that lack of confidence because it's an area that is evolving as cardiologists are entering it as well.

Using NOACs to Treat PE and DVT

Dr Bilazarian: May I ask you a simple question before we get to the procedure aspect of it, for those in the audience who are very familiar with NOACs (we've had the first NOACs now for more than 4 years, when will we stop calling them novel?)? For a cardiologist who is very experienced and comfortable with NOACs for afib, is there any caution for using them with PE and DVT, other than knowing there are dose differences?

Dr Goldhaber: Well, the first principle is that the NOACs have much less major hemorrhage than low-molecular-weight-heparin bridging to warfarin, and a lot of our colleagues are not yet aware of that. There's this idea on the street, I sense, that NOACs are somehow more dangerous that warfarin. Have you picked up on that theme at all?

Dr Bilazarian: The lack of an antidote is something that comes up frequently from referring physicians and from patients. So yes, I think that there is that concern, and we can share our afib experience knowing that bleeding in general is less with NOACs.

Dr Goldhaber: Right. You look at all of the pivotal trials[1,2,3,4] and even without an antidote, which I imagine wouldn't be used that often anyway, not only is the intracranial hemorrhage cut by 50% across the board regardless of the NOAC or the dose of the NOAC, but also general major bleeding is much lower with the NOACs, and fatal bleeding overall is much lower as well. I think that should give us encouragement to consider NOACs as first line.

Dr Bilazarian: When we talk about the NOACs in this indication, we're talking about something beyond even the convenience aspect of not having frequent INR checks, but also patients don't like to stick their bellies twice a day with low-molecular-weight heparin. It's quite uncomfortable.

Dr Goldhaber: Exactly.

Dr Bilazarian: So there's that issue. The other thing we can take a leadership position in is that we're all trying to be better stewards of healthcare dollars. We're participants in [accountable care organizations] ACOs and trying to save hospital systems money. The NOAC strategy rather than bridging can shorten length of stay. We need to get the message out. That's the point of our blog.

Dr Goldhaber: The other point is that, much like stroke prevention in atrial fibrillation, there is more and more evidence to suggest that because pulmonary embolism often is due to inflammation—and this is chronic inflammation—and many of these patients warrant indefinite duration anticoagulation.

Dr Bilazarian: Yes. That's one of those things that I see frequently and wonder why patients have had anticoagulation discontinuation for idiopathic—

Dr Goldhaber: Right, and in the past it's been because the bleeding complication rate was so much higher with warfarin, but maybe we're at a point now of safety that we have the luxury of continuing anticoagulation.

Getting the Drugs to the Patient

Dr Bilazarian: One thing I will mention—if we have any people in our audience from industry—we do still struggle with a very practical problem. Just recently we had a catheter-directed-thrombolysis patient immediately started rivaroxaban (Xarelto, Bayer), which our hospital's formula uses. The patient was doing exceedingly well. On day 3 they were preparing to go home and had difficulty getting it from the pharmacy-benefits manager for that patient's insurance. So the patient had to switch back to enoxaparin (Lovenox, Sanofi), low-molecular-weight heparin, and warfarin. It was a really unfortunate circumstance. Even though we have the drugs and we have the data, when the rubber hits the road we have to be able to get the patient the drugs. Sometimes that's the major impediment.

Dr Goldhaber: Right. Hopefully we can work through that process. I think pulmonary embolism is a cardiovascular illness.

Dr Bilazarian: You've made me a believer.

Dr Goldhaber: I'm thrilled that at the AHA and the ACC and ESC, there's a lot more attention to DVT and pulmonary embolism than there had been in the past. It's all being brought together in the same family.

Dr Bilazarian: Your work is bearing fruit.

Dr Goldhaber: It's fun to work with you and to discuss some of our challenging patients. Seth, thank you very much. This is Dr Sam Goldhaber, signing off for the ClotBlog.


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