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Angioplasty.Org Interview Series: Transradial Approach
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Interview with Samir B. Pancholy MD, FACC, FSCAI

In this interview, Angioplasty.Org talks with radialist Dr. Samir Pancholy about his findings regarding the prevention of radial artery occlusion, one of the few complications associated with the transradial approach to catheter-based procedures. Dr. Pancholy has authored or co-authored a number of studies on aspects of transradial access, most recently appearing in the Journal of Invasive Cardiology and Catheterization and Cardiovascular Interventions. He has also been published in the American Journal of Cardiology, the American Heart Journal and the Journal of Nuclear Cardiology, among others.

Dr. Pancholy is currently affiliated with Mercy Hospital and Community Medical Center in Scranton, Pennsylvania, as well as several other Scranton-area hospitals. He is considered an expert in the transradial approach and has conducted courses on this technique. He is board certified in Internal Medicine, Nuclear Medicine and Interventional Cardiology. He is a fellow of the Society for Cardiac Angiography and Interventions and has served on SCAI's Credentials Committee.

For more about the transradial approach, visit our Radial Access Center.



Samir B. Pancholy MD, FACC, FSCAI
Samir B. Pancholy MD, FACC, FSCAI -- Mercy Hospital & Comm. Medical Center, Scranton, PA

Q: What is radial artery occlusion?
Dr. Pancholy: Radial artery occlusion is basically obliteration of the lumen of the radial artery (in the wrist) which becomes 100% blocked. The most common reason is either traumatic or an occlusion that occurs after a catheter-based procedure that uses the radial artery, either catheterization or angioplasty. It is very infrequent, but it remains one of the few complications of transradial procedures.

Q: What causes radial artery occlusion?
Dr. Pancholy: Surprisingly, until about a year ago, we did not know the cause. We were hypothesizing as if we knew, but we had no proof. We had a number of imaging studies, ultrasonography, every once in a while contrast angiography, which would show us that the radial artery was occluded, but we never really got into the mechanism. There were lots of theories, such as growth of extra tissue, scar growth which will then occlude the lumen like it does in the coronary artery after we do angioplasty. A lot of people thought, “Well clot’s got to be a player. Blood clotting at the local area because of the trauma to the artery is definitely a mechanism and then afterwards it becomes organized into a scar.” But there was no proof for this.

Q: Why was it so difficult to find the cause of radial artery occlusion?
Dr. Pancholy: The reason there was no proof was because radial occlusion is such a benign complication that nobody ever needs to go to the operating room to get it fixed. So there had been no direct look at the radial artery of a patient who had this problem. The most we did was a sonogram and we found out the artery was occluded, but the patient was asymptomatic and so we used to tell them there's no harm done, you're going to be fine.

Q: But you finally were able to determine the cause of radial artery occlusion?
Yes. About a year ago here in Scranton, one of my patients had no femoral artery access at all. Her left arm had a hemodialysis fistula so I could not use the left radial or brachial artery, and I had to use the right radial artery for the catheterization. Turned out she had coronary blockages, so I was planning to go back in and fix them, but I decided to wait a few days because of her other issues.

When we brought her back, we saw that the radial pulse was extremely diminished, which was brand-new because, when I had done the catheterization, she had a nice right radial pulse. So we did a sonogram and found out that the radial artery was occluded.

We now had two options. We either go to the right brachial artery or we somehow get back in through the occluded radial artery. Brachial access historically has been known to have the most complications -- higher than femoral access and clearly higher than radial access. So I decided to enter the radial artery distal to the occlusion and I documented that with contrast. Once I knew I was in the correct lumen, I put a wire into my needle hub and gently advanced it -- and I was able to cross the radial occlusion. I was extremely happy that I was in the radial artery, but when I put my sheath over that wire and took out the dilator, there was no blood flow. So I'm looking at it saying, my goodness, I think I am in a false lumen.

Samir B. Pancholy MD,

However, we applied some backward pressure through a syringe and suddenly some blood came out of the sheath into my syringe and the blood started flowing. We carefully retrieved the blood out of the syringe without compromising it and I sent it to the pathology lab -- and we were able to see under the microscope that it was organizing thrombus with very rapid growth.

This was one of the first times that the pathologic mechanism of radial artery occlusion was documented. It was actually thrombus that should not have started organizing so fast, but we know that it was thrombosis that goes on at the local spot and what our sheath did was to dislodge the thrombus forward and then we sucked it out with a syringe when we were aspirating and trying to re-establish blood flow.

One month out from the angioplasty, we re-ultrasounded the radial artery and it was wide open. I've been following her since August of last year and she continues to stay open. In that series I had 14 patients in whom I was able to re-access 12, and the majority of them stayed open.

Q: As you’ve written, although radial artery occlusion is infrequent, it is the chief complication of the radial approach – benign for the patient, but it may prevent re-use of the artery as an access site for future procedures. So being able to use an occluded radial artery for subsequent procedures is important?
Dr. Pancholy: Correct. And we published these findings in the December 2007 issue of the Journal of Invasive Cardiology (“Transradial Access in an Occluded Radial Artery: New Technique”).

Q: So you verified thrombus as the cause of radial artery occlusion, but what causes the thrombus and is there a way to reduce the risk?
Dr. Pancholy: Our hypothesis was that occlusive hemostasis was the reason for radial artery occlusion. There was some proof to that effect from previous retrospective databases: one small study from Sanmartin in Spain showed that it was a potent predictor of occlusion. So we thought, well, when a blood vessel gets traumatized, for example during balloon angioplasty, what do we do to make sure it doesn't clot up? One thing is to establish constant blood flow so that the thrombus doesn't get a chance to propagate. So we thought that occlusively compressing the radial artery to achieve hemostasis was making chronic occlusion of the radial artery more frequent than it would have been otherwise, just based on trauma.

Q: You tested this concept in the PROPHET study, where your conclusion was that “Patent hemostasis is highly effective in reducing radial artery occlusion after radial access; guided compression should be performed to maintain radial artery patency at the time of hemostasis, to prevent future radial artery occlusion.”
Dr. Pancholy: Yes. There's an abstract online of the PROPHET study, and the full study is going to be published in a forthcoming issue of Catheterization and Cardiovascular Interventions. We wanted to test our theory that if you don't compress the radial artery very hard, and don’t occlude the flow through it during the process of hemostasis, then you might actually lower the risk of occlusion -- and this was what we called the concept of “patent hemostasis.”
    Catheterization and Cardiovascular Interventions

Q: You’ve just recently completed a new study, a summary of which we’ve posted at Angioplasty.Org. It’s similar to the PROPHET study, except you’ve added a specific piece of equipment to the mix: Terumo’s TR Band, to aid in achieving “patent hemostasis” and “guided compression”. Tell us more about both the PROPHET results and your new study.
Dr. Pancholy: At the time that PROPHET was started, we did not have the TR Band in the U.S., so we were still using the old hemodialysis band, called the HemoBand. And the HemoBand almost looks like a zip tie that you essentially apply to the site of the sheath entry and then just click it on and tighten up as you need to.

Because the radial artery is so isolated and against the bone, it's very easy to apply a lot of pressure and not get into any trouble. The patient tolerates it very well. They might feel a little bit of pressure there. But it gives you very guaranteed hemostasis. However, most operators I have observed actually want to over-pressurize the radial site, once they take the sheath out, just to be sure they don't get any bleeding.

With the PROPHET study, we took half of the patients and did our standard pressure band application, and we randomized the other half to get patency documented after the case, where we made sure that we applied the band and then we liberated the pressure to some extent until we got patency.

Diagram of Radial and Ulnaer arteries in the hand    

Q: How were you able to measure that you got patency?
Dr. Pancholy: We were able to measure it by doing plethysmography of the index finger. We applied a pulse oximeter probe to the finger and we would occlude the ulnar flow by applying direct pressure on it. We wanted to see persistent flow going on in the radial artery which gives you proof that the radial artery is widely patent at that time.

Most of the time in the PROPHET study we would find that the radial was occluded with our pressure band, so we would start loosening the band, and either we would get radial flow as evidenced by return of the plethysmograph signal, or we would get bleeding, in which case we would convert our hold to a manual hold.

Q: The PROPHET study showed significant reductions of radial occlusion, on the order of 60% at 24 hours, for the group that had documented patency and “guided compression”. What was the motivation for adding the TR Band in for your new study?
Dr. Pancholy: In August of '07 the TR Band was approved by FDA to be marketed in the U.S. As soon as it was available, we started using it exclusively on everybody because it's much more comfortable than the HemoBand. Obviously we had collected a lot of patients who underwent transradial catheterization with the TR Band since its availability, so we went back and looked at the occlusion data on people who received HemoBand after the transradial cath vs. those who received the TR Band after the cath and we found with the TR Band a very significant reduction in the risk of occlusion that follows these procedures, at 24 hours and at 30 days.

And it was surprisingly striking. So then we started wondering, why are we having this difference? What's the mechanism of it? We had actually been intrigued by the fact that the TR Band has an inflatable chamber anyway. The HemoBand, once you apply it, actually maintains the pressure that you applied initially for the duration that you leave it on, unless you go to the HemoBand and manually click it down to a lower pressure, or you essentially untie the HemoBand.

The TR Band, on the other hand, has an inflatable chamber which we inflate with 15cc of air according to the package insert. And what we noticed was that the TR Band actually deflates over the first hour or so. So we measured pressures in the chamber of the TR Band. We were able to see that the initial pressure is usually around the low 200's -- the mean was 240. And at half an hour that pressure comes down to about 150, and at one hour it's about 130 or so -- without any intervention from us. So this is almost a self-deflating band. What it does is to allow the radial artery to go from an occlusive application to a non-occlusive hold. And we did not see any bleeding complications from the TR Band at all, so it wasn’t losing its efficacy as far being a hemostatic device.     TR Band hemostasis device
TR Band hemostasis device

Q: Back to your study -- what was the magnitude of reduction of radial artery occlusion using the TR Band?
Dr. Pancholy: Very, very significant. In our database which was 250 patients in each arm, we had about 55%-60% decrease in early and chronic occlusion with the TR Band vs. the HemoBand, which is a real big deal because occlusion is by far the only complication of the transradial procedure that is considered to be worthwhile as far as being concerning and one which limits future access.

Q: Does this method of using the TR Band and deflating it take more time and can it be performed by nursing staff?
Dr. Pancholy: It is automatic. The TR Band gives you an opportunity to "keep your own protocol that you have now", and not worry about occlusion as much as you would with other non-deflating or non-releasing devices out there. We used to use the HemoBand because it's the cheapest and most generic device -- it's probably the most commonly-used device worldwide because it's so inexpensive, but it comes with a price to pay, because you are not able to walk away from the patient for two hours and get a low risk of occlusion like you do with the TR Band.

Q: In your study, even after the reduction, the chronic radial artery occlusion rate was 18 out of 250 -- that's still higher than is quoted in some literature.
Dr. Pancholy: Yes. My rate of occlusion had been very low. But that was before we brought every patient in for follow-up. After we started examining every patient at 24 hours and 30 days, we found that the actual occlusion rate was much higher, because it is a totally asymptomatic kind of a complication, so you're not ever going to get a patient come in and say I think I have an occlusion.

In my practice we have a constant 24 hour and 30 day follow-up going on for radial artery occlusion for everybody that goes through a transradial procedure. In fact we have radial weekends, where on a Saturday morning, I call people into my office for bagels and donuts, and we examine them for occlusion. It's a free visit and they come and have a little breakfast and go home. This way we get very tight data collection on every procedure. So if you bring everybody back and look for a radial occlusion, you will see more.

Q: So the take-away here is that compression for too long at too high a pressure will lead to an occlusion. Would you say that the idea of using “longer and stronger” compression is a mind set coming over from people whose experience is with the femoral approach, because in that situation you absolutely need to use higher compression for a longer time? Could we say that: "Long and strong in the radial is wrong"?
Dr. Pancholy: You're absolutely right. There is a mentality of reinforcement and over-application and longer application from the femoral experience and that actually is very counter-productive in the wrist.

Q: You’re looking to establish a protocol about this?
Dr. Pancholy: Yes. What all these data are trying to say is that patency is a very big necessity when you are obtaining hemostasis after a transradial procedure and systematic protocols for maintaining patency need to exist. If you make an attempt at instituting a patent hold, that may not be good enough. You have to document it, you have to prove that you're creating patency, you have to monitor it. And not use excessive pressure or excessive duration.

There is a difference between trying and protocolizing. And I think we need to incorporate this as a protocol after the procedure, not just an attempt. Because if it becomes a protocol, then everybody follows it and it improves outcomes quite significantly.


This interview was conducted in August 2008 by Burt Cohen of Angioplasty.Org.