Dr. Lichaa Sit Downs: Dr. Vladimir Lakhter On CTEPH Interventions - Part 2

By Hady Lichaa, MD - Last Updated: January 25, 2023

In the second half of a two-part interview, DocWire News partner Hady Lichaa, MD, FACC, FSCAI, FSVM, RPVI, spoke with Vladimir Lakhter, DO, to discuss the topic of chronic thromboembolic pulmonary hypertension (CTEPH) interventions. Dr. Lakhter provided what Dr. Lichaa described as “a tour de force on chronic thromboembolic pulmonary hypertension treatment.”

Dr. Hady Lichaa: When you have a patient who is a perfect candidate for balloon angioplasty, what I noticed as an interventional cardiologist is this is absolutely different than atherosclerosis in the systemic circulation from a treatment. One can think a balloon, what is a balloon going to do? In our world, the arterial world, balloon angioplasty is not that effective. Could you elaborate why balloon angioplasty is so effective in the pulmonary team?

Dr. Vladimir Lakhter: That’s an excellent point, Hady. If you look at the histology of patients’ pulmonary arteries in those patients that have CTEPH, you’ll see that there is really no calcium, to your point, but atherosclerosis. More often than not, you have some degree of calcification, so that’s number one. There is really no calcification in these lesions. Now, I’ll say that we have seen calcific chronic thromboembolic disease, but that’s extremely rare. There’s just a very, very few percent of patient, so majority of these patients do not have calcific disease.

If you’re looking at the vessels, the most common lesions that we treat are webs or stenoses or ring-like lesions. If you did an intravascular ultrasound of the pulmonary artery, you’ll see that essentially the pulmonary artery looks like a Swiss cheese. You have multiple channels through the pulmonary artery. It’s almost like a coronary artery that’s dissected and has multiple dissection planes, some of which are connected to the true lumen, so effectively it’s not one circumferential stenosis most of the time. There are many, many different channels, micro-channels.

The actual histology of it, it’s a fibrous tissue that used to be thrombus. Then through a process of remodeling, probably through inflammatory responses, cytokine responses, ultimately there’s really no clot anymore. Most of the time it’s really just this fibrous tissue that’s non-calcified. There’s pretty good data to show that once you perform balloon angioplasty on these webs, you’re essentially taking one of these small channels, and you’re creating a much larger dominant channel by essentially ripping through the webs. Although that may not be sufficient in an atherosclerotic process because there is going to be restenosis, and the patency rate of something like that at one year is probably 50% with a plain old balloon angioplasty, but the data from balloon pulmonary angioplasty and follow-up of patients that have had balloon angioplasty alone for CTEPH have shown fairly good durability in patency.

Mostly, we may not be bringing these patients back for repeat pulmonary angiograms to see if there is restenosis, but what we can follow is their six-minute walk test. This walk test, we can perform a right heart catheterization down the line and see. Is the PVR and the PVR cardiac output, mean pulmonary artery pressure that I achieved initially acutely after a balloon pulmonary angioplasty, is it the same or has the pressures gone up?

You’ll see a lot of times that when you follow these patients up with a right heart catheterization six or 12 months out, you’ll see that frequently they still have the same PVR as you left them with. Sometimes the PVRs and mean pulmonary artery pressures actually continue to reduce. So really, really nice that at least so far, what we know about this disease process, that you don’t really need to do more than balloon angioplasty. You don’t have to stent this. You don’t necessarily have to use drug-coated balloons, but maybe we’ll learn down the line that there are certain lesions, the types that benefit from more aggressive treatment. We just don’t know at this time.

Dr. Hady Lichaa: Could you tell the audience why patients have to come in multiple sessions and have? Tell us about your experience and how many segments or sub-segments you treat per session and why you do that.

Dr. Vladimir Lakhter: Yeah, so frequently you’ll see that patients coming in for balloon pulmonary angioplasty or patients coming in for surgery will have bilateral disease. It’s very unusual to see that only one or two segments are involved and that’s essentially it. Frequently what you’ll see is diffuse involvement of multiple segments involving all or most of the lobes of both pulmonary arteries, so when you’re talking about revascularization of these patients, you’re really talking about on the order of 20, 30, 40 arteries that you need to treat. You’re not necessarily treating 40 segments. There is no 40 segments, but you’re going to find that you’re treating a segment. Then you’re treating a sub-segment, and then you may be treating a sub-sub-segment, depending on how far out is safe to balloon.

Obviously, these arteries taper. You’re not going to be able to treat the tiniest of the vessels, and you probably don’t have to do that. That’s what the medications are for, but it’s impractical to treat somebody’s right lung in its entirety, and you’re running into multiple issues there. One is that you’re going to be using a lot of contrast. You’re going to be using a lot of radiation in trying to treat 10 arteries. I would say that on average we’re probably treating anywhere from six to 10 vessels. Whether that’s segments and sub-segments and sub-sub-segments combined, those are the most common lesions that we treat.

If you’re treating more proximal disease, for example an interlobular artery or a basal trunk, you’re running into a risk of reperfusing too much and running into risk of reperfusion pulmonary edema, so you really have to be mindful of how proximal your disease is. If you have very proximal disease and you’re treating somebody who is technically a surgical candidate but for whatever reason are not getting surgery, and you’re treating those patients, you really want to limit your treatment to that basal trunk or to that interlobular artery. You certainly don’t want to be treating anything else in that lung, and you definitely don’t want to be treating anything in the other lung.

I think for most of our patients, they’re requiring anywhere from four to five BPA sessions, and each one of those sessions we’ll treat anywhere from six to 10 vessels, I would say. Our usual approach is that we’ll treat the lower lobes first if we can, and that’s because the V/Q matching physiologically is the best in lower lobes. If we’re able to revascularize the lower lobes, we’re going to get the most bang for the buck in terms of restoring perfusion to the areas that are most ventilated. Then we’ll work our way up to the middle lobe and the upper lobe, and we’ll usually alternate. We’ll treat right lung during the first session. Then we’ll bring the patient back for the left lung if they have disease in the left lung. Then we’ll go back to the right, and we’ll alternate that way until we’re completed our treatment, so that’s the general approach that we have.

Dr. Hady Lichaa: Excellent. To finalize the interview, I just wanted to find out from you what’s the overall morbidity of the procedure? What is the data saying about complication rates, and how is this improving with time and your understanding of the anatomical differences of the pulmonary segments?

Dr. Vladimir Lakhter: Yeah, so that’s probably the most important thing to consider in these patients because a BPA that’s performed in a non-careful manner can definitely lead to pretty drastic complications that may be very difficult to deal with. So, initially when the BPA procedure was developed and reported on almost two decades ago at this point, the morbidity and mortality was fairly significant. The major reason for this morbidity and mortality was reperfusion pulmonary edema. It was probably that there were too many vessels that were being treated, and the balloon sizes that were being used to treat patients’ vessels were too big.

For that reason, the balloon pulmonary angioplasty initially fell out of favor for about 12 or 13 years, after which it was refined. The refinement of that procedure was initially done by using IVUS imaging to guide balloon sizes and to limit the treatment to a limited number of vessels, so not over-treating too many vessels and also not using too big of the balloons. Just with that adjustment alone, the morbidity related to reperfusion pulmonary edema fell dramatically.

I would say that the main things that we see and we worry about when performing balloon pulmonary angioplasty, one is hemoptysis. I think that’s an intuitive thing. You’re using a wire to try to cross a lesion. If the wire exits the vessel or the wire is in a bad spot and you oversize the vessel, you can rupture the pulmonary artery and you can have hemoptysis. You can have massive hemoptysis that the patient may not survive, or you can have very mild hemoptysis where the patient just coughs. They bring up some blood colored sputum, and that’s all they see. Most of the time, if we see hemoptysis, it’s really just a blood-tinged sputum. The risk of massive hemoptysis is very, very low, thankfully.

If you’re limiting the procedure to focus treatment of the lower lobe, middle lobe and limiting yourself to six to 10 segments, I think the risk of a perfusion pulmonary edema is fairly low. One of the ways that we try to reduce the risk of pulmonary edema in our patients we found to be successful is to give diuretics to all patients at the end of the procedure, so we’ll usually give about 20 or 40 milligrams of IV Lasix, unless the patient’s wedge pressure is very, very low. Most of the patients will get Lasix, and we’ve really found that that has reduced the risk of reperfusion pulmonary edema.

I think the risk of hemoptysis that we have seen, of mild hemoptysis is probably on the order of 5% of all cases, definitely less than 10%. The risk of massive hemoptysis, we’ve probably only seen one. I think one patient had that, and thankfully we were able to treat them successfully. I think that the data, and a lot of this data that we have on balloon pulmonary angioplasty in the last decade has come from Japan. They’ve treated the most patients, and they’ve done the most sessions. I think that’s fairly consistent with the outcomes that they’ve had of 5% risk of hemoptysis and a couple percent risk of significant reperfusion pulmonary edema.

Dr. Hady Lichaa: Well, that was a wonderful conversation, a tour de force on chronic thromboembolic pulmonary hypertension treatment. This field is really expanding, and you’re having a huge part of this expansion in all the great work that you and your colleagues are doing. Thank you very much for your time, and hopefully we’ll talk about this topic sometime soon. Thank you.

Dr. Vladimir Lakhter: Absolutely. It’s my pleasure. Thank you so much. Thank you very much.

Dr. Hady Lichaa: Thank you.

Dr. Vladimir Lakhter: Thank you.

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