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Interview

Dr. Victor F. Tapson Discussed Submassive PE with VDM at the Veith Symposium 2011

April 2012
2152-4343

Figure 1Q: Do you feel that hospitals need to change the protocol for the way that pulmonary embolism is treated and why?

A: Risk stratification for pulmonary embolism is extremely important and I think we’ve not tended to do that over the years as this has evolved. Risk stratification shows whether or not a patient can be simply anticoagulated or if they are at higher risk for mortality. If proven to have pulmonary embolism and severe right ventricular dysfunction by echo, we think aggressive therapy may reduce mortality. We don’t have proof in randomized trials, but we do have very compelling non-randomized trial data suggesting that if your right ventricle is enlarged, if your troponin is elevated, if you have DVT remaining in the legs at the same time you’re diagnosed with pulmonary embolism, your mortality may be higher without more aggressive therapy.

Some hospitals treat most PE the same way and just anticoagulate everyone. Most of us know that if you have massive PE with hemodynamic instability, more aggressive therapy should be considered. Some still don’t; they’re worried about the risks of thrombolytics. Now we have some aggressive catheter-based therapies that may reduce the risk of bleeding. We should always consider a team approach. A PE rapid response team or an integrated group that addresses difficult clinical scenarios should be considered. Participants could include pulmonary/ICU team, cardiology/echocardiography, chest radiology and interventional radiology, thoracic surgery, and hematology. In your hospital, consider getting a group of people together to discuss how team members would interface. Some may be against thrombolytic therapy; some may be for it. The interventional people may be aggressive or not aggressive in terms of catheter-based therapy. Getting an understanding of different opinions can make it easier to make a decision when the time comes.

Different hospitals function differently but I think that having a team understanding of how to deal with these patients leads to better patient care.

Q: Are interventionalists hesitant to perform pulmonary interventions due to risk factors?

A: There are some very aggressive interventionalists and some less aggressive ones. One of the things that may steer them away is that these patients are sometimes unstable or can become unstable. You can have a patient in the cath lab or the interventional radiology lab who has submassive PE, a heart rate of 100, stable blood pressures, is on 2 liters oxygen, and a few minutes later, he or she requires facemask oxygen and is hypotensive. Many of our interventional cardiologists are accustomed to working with sick people. Most are now getting used to this kind of approach, but the potential risk of the patients may steer some individuals away.

Q:  What evidence-based data do you have in this space and why is it significant?

A: The most recent ACCP Consensus Statement was published in February 2012 and it does not outline aggressive treatment in quite the detail that we need, primarily because we have inadequate data. The AHA published recommendations in 2011 with a little more detail on how to handle submassive PE and suggesting that things like RV/LV ratio >0.9 might be a reason to be more aggressive. It gives an algorithmic approach. The evidence base is not grade 1A evidence. We don’t have a big randomized trial yet that proves that patients with submassive PE do better and have better outcomes with aggressive catheter-based therapy or thrombolytic therapy. We base our evidence on non-randomized but compelling data indicating higher mortality when certain features are present in PE patients and suggesting that aggressive approaches would make a difference.

There’s a study right now, the PEITHOS study, in Europe that’s looking at randomizing patients with submassive PE to either thrombolytic therapy or placebo. It’s not a catheter-based study, but at least it’s one look. I think we need more randomized data and I hope our partners in industry or the NIH will help us get more data in that realm. With catheter-based therapy, I think we can do an efficient, safer job of handling submassive PE and even in some cases of massive PE. If patients can be transported and handled quickly, I think catheter-based therapy is a good way to go.

Q:  What are the areas to consider in risk stratification?

A: The echocardiogram is the focal point and looking at how the right ventricle is doing. That’s the key thing. Other things to consider include a troponin that is elevated, which suggests right ventricular damage. If someone requires facemask oxygen versus 2 liters, that person is clearly not doing as well. We don’t have a lot of data to support that oxygenation is a predictor but clearly it is, as it measures how sick people are. Just a physical exam that shows someone’s heart rate is 140 is far more concerning than if it’s 70; it means the heart is stressed and having more difficulty so we put a lot of things into the equation but the echo is really the focal point. It’s how we define submassive PE.

Q: Do you know of any recent advances or research that have lead to better diagnosis and treatment or overall prevention of PE?

A: One of the things we learned from registries we’ve published like the ENDORSE registry, the IMPROVE registry, the NABOR registry, and the DVT Free registry, is that we underprophylax patients. It’s been eye opening to see that these patients are underprophylaxed. I think we’re doing better with that since the Joint Commission got involved. We had a task force that helped them come up with some recommendations that they should hold hospitals to in terms of prophylaxis. I think diagnostic testing is getting better. CT scanning is getting better. We have at least 128 detector scans, multidetector scans that are more sensitive. We’re doing better at making a diagnosis than when we just had a VQ scan or a lower generation scanner from 10 years ago.

The main thing is that because symptoms and signs of PE are non-specific, I think clinicians really need to be aware of it and have to think of it so that these patients don’t die undiagnosed. Sometimes you can’t help it because a patient dies suddenly; but sometimes there is chest pain and it’s assumed it’s angina or musculoskeletal pain or he or she comes in short of breath and it’s blamed on asthma. You have to look at risk factors. Do they have cancer? Did they just have surgery or trauma? Are they a medically ill patient? Some patients have no risk factors and they’re trickier. A 30-year-old patient may come in with shortness of breath and no apparent risks and you might not even think of PE or DVT. Someone has a charley horse in their leg and we might not realize it’s deep vein thrombosis.

I have a friend who called me recently while I was out of town and he said I have this bad pneumonia lately and it’s not getting better with antibiotics and I’m still coughing up blood. He said he tried to go for a ride on his bike and pulled a muscle in his leg. I talked to him and it turned out that he had DVT in his leg and pulmonary embolism, not pneumonia. We got him into the hospital; he was aggressively treated with thrombolytic therapy and fortunately, he didn’t die. Clinicians have to be aware that PE is kind of a masquerader. Sometimes PE appears to be pneumonia if someone has some infiltrates and a cough. You need to think of the disease and the risk factors. If clinicians do that, it’s a big step. If they’ll go beyond that and risk stratify patients, then I think we’ve really accomplished a lot.

Q: Is there anything we haven’t covered that you feel our audience would like to know about your research?

A: I think there are a lot of new techniques for interventionalists to look at. There are different forms of techniques that we call pharmacomechanical thrombolysis. We published data on that almost 20 years ago. We can find ways to break up clots more easily with catheter-based devices, suction devices. There’s an ultrasound catheter that you can put into the pulmonary arteries and the ultrasound waves help disperse the thrombolytic therapy and get into the clot better. There are a lot of new techniques out there. I think if interventionalists are aware of the techniques and if our clinicians can get the patients to the interventionalists, we can probably do a much better job with the patients. 

Dr. Victor Tapson is a professor of medicine in the Division of Pulmonary and Critical Care and Director of the Center for Pulmonary Vascular Disease at Duke University Medical Center in  Durham, North Carolina. Dr. Tapson earned his MD at Drexel University College of Medicine in Philadelphia, Pennsylvania. He completed a residency in internal medicine at Duke University Medical Center and a residency in pulmonary medicine at Boston City Hospital.


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