Journal Home
Search for

Volume 45, Issue 1, Pages 23-24 (January 2007)


View previous. 14 of 73 View next.

Discussion

published online 29 November 2006.

Refers to article:
Popliteal artery volume flow measurement: A new and reliable predictor of early patency after infrainguinal balloon angioplasty and subintimal dissection , 29 November 2006
Enrico Ascher, Anil P. Hingorani, Natalie A. Marks
Journal of Vascular Surgery
January 2007 (Vol. 45, Issue 1, Pages 17-24)
Abstract | Full Text | Full-Text PDF (167 KB)

Article Outline

Copyright

Dr John Blebea (Philadelphia, Pa). There appears to be a big discrepancy between the outcome with subintimal angioplasty versus standard transluminal angioplasty in terms of patency rates. There is also a major decreased patency among those vessels with low flow rate. Were the overall flow rates within the popliteal artery less for the patients undergoing subintimal angioplasty as a group, not just the proportion that thrombosed or had low flows later?

Dr Anil P. Hingorani. No, they weren’t. They were actually pretty similar when we looked at the popliteal artery volume flows at the end of the procedure. We were not able to differentiate between these two groups.

Dr Jacob Schneiderman (Tel-Hashomer, Israel). How do you verify that there were no distal emboli related to the procedure? Are you doing any completion evaluation of the distal tree?

Dr Hingorani. As we mentioned before, with the duplex imaging, before the procedure we look at the tibial vessels, and after the procedure we also look at the tibial vessels. With duplex imaging, you can actually see all the way down to the pedal vessels.

Dr Schneiderman. So you feel confident with this ultrasound evaluation to conclude that no emboli went to the distal tree?

Dr Hingorani. We’ve already had over a thousand patients that we’ve evaluated preoperatively for open procedures, not only including the femoropopliteal segment but all the way down to the tibials and the pedal vessels, and done bypasses based upon those.

However, the limitations are actually, I think, the key. You don’t want to be doing these patients who have very calcified vessels where you can’t see what’s going on very well. You don’t want to be doing this in patients who have a tremendous amount of tissue edema because you’re not going to be able to evaluate the vessels well. You don’t want to be doing this in patients whose SFA is 6 cm deep, you’re not going to be able to visualize and get enough information to do these types of procedures.

Dr Hasan Dosluoglu (Buffalo, NY). I have two quick questions. You have studied a good number of stented patients, so could you identify those who had developed more restenosis, depending on the flow patterns. If you end up with a patient who has suboptimal flow, and you cannot identify why that is, what do you do with these patients?

Dr Hingorani. That second question is actually, I think, one of the more important points. Those types of patients we persistently try to look for an inflow lesion or an outflow lesion. Maybe we missed something on the inflow and we’ll go back up and look at the iliac arteries to make sure we didn’t miss anything. Unfortunately, we haven’t very often found an inflow or an outflow problem. And when you don’t, I usually don’t reverse the heparin and don’t administer the protamine in these types of patients.

In general, we thought we were actually doing okay, because in the recovery room they seemed to be doing all right. But, however, when we looked at them long term, these patients seemed to do much, much worse. They had much higher rates of early thrombosis despite our maneuvers of not reversing the heparin.

We were not actually able to differentiate which patients, even with or without stenting, would have long-term patency based on this data set.

Dr Rumi Faizer (Columbia, Mo). A few questions. First, you must have a good reason why you’re using flow volume and not peak velocities and waveforms. And I was wondering how you came to that determination?

Second question. Many of us have been impressed with how you can see a pressure gradient down the SFA and not a clear stenosis on imaging with angio. And I thought that’s a wonderful place for this to show itself. I was wondering if you had any correlation between intravascular pressure gradients versus waveforms that you’re seeing?

And then, lastly, I was a little bit confused with how you had such a high proportion of TASC C and D lesions, and yet the ABI is averaging 0.68. Why such a discrepancy? I would have expected lower ABIs in this population.

Dr Hingorani. Initially, when you want to try to start doing these types of protocols, you don’t want to be doing the TASC Cs and Ds. You want to start off with the thin patient, whose vessels you can easily see, with a short focal stenosis. When you want to start off doing these, we actually suggest that you start doing it preoperatively and not in the operating room, and compare it to angiography for at least the first 25, until you’re certain that your results that you’re getting from the technologist are greater than 95% accuracy.

We have not compared pressure gradients to these patients. But I think you’re actually bringing up one of the clear advantages that other people have already shown in data sets, that duplex imaging, if you take your patient that you did an SFA angioplasty and you immediately do a duplex, you’ll find a fair number of lesions that you missed on angiography, even with biplanar angiography, unfortunately. So I think that actually may contribute to one of the reasons why we are stenting a lot more patients as compared to our angiogram patients, because I think we are seeing a lot more lesions that may have been missed. We are seeing a lot more recoil. We are seeing a lot more dissection. We are seeing a lot more residual stenoses that I think we are missing on angiography. But we don’t have data comparing it to pressure gradients.

We do use peak systolic velocities routinely. We do use mode B imaging before, after, and during the procedures. This data set right now is just mostly looking at the next step, looking at popliteal artery volume flows.

The average ABIs, I wouldn’t be able to say. That’s what the numbers were, 0.68. 68% of our patients were claudicants, so I would not be that surprised if their ABIs were on the order of 0.5, 0.6.

Dr Charles Brantigan (Denver, Colo). Let me change the focus of the discussion for a moment from the technical to the physiologic. The last statement in your conclusions in the abstract says that “Perhaps pharmacological manipulation in this high-risk group of patients may enhance patency rates.” I am assuming you are talking about vasodilator therapy of some type. What therapy are you proposing, and for how long are you proposing to use it to enhance the patency rates?

Dr Hingorani. Unfortunately, as you know, the vasodilators have really not really been that helpful. And right now, as I said, all we are doing right now is not reversing the heparin. All of these patients are on Plavix preoperatively and on indefinite aspirin after the procedures. And actually, we are leaving them on Plavix for at least 3 to 6 months after these procedures, irrespective of the popliteal artery volume flows. If we encounter a low popliteal volume flow, we’re routinely not reversing heparin, but we are not using any dilators or such.

Dr Brantigan. So you are not actually proposing any different pharmacologic management for the two groups of patients?

Dr Hingorani. Not yet.

Dr Brantigan. Except, perhaps, not reversing the heparin, which many people wouldn’t do anyway.

Dr Hingorani. Not yet. I don’t think we really have that many alternatives as of yet. That would be a point of discussion and a possible route of further investigation.

PII: S0741-5214(06)01838-6

doi:10.1016/j.jvs.2006.09.054


View previous. 14 of 73 View next.