Cath Lab Digest

Why do you think that distal embolic protection has only relatively recently become a topic of interest in invasive cardiology?

In 1977, before Gruentzig did his first catheter-based angioplasties during bypass surgery, he evaluated for arterial debris by collecting the effluent from an artery dilated during surgery, and looking for embolic particles (none were seen). Clinically, when you look at the literature up through the mid-1990s, the only reports of embolization are in patients with thrombotic lesions, where a chunk of clot breaks off, embolizes and blocks a distal large branch on the angiogram. There was nothing compelling people to think about distal embolization or protection against such embolization. There were, however, some unexplained problems. The two biggest examples are:

1. Elevations of CK after otherwise successful procedures;

2. The no-reflow phenomenon, where antegrade flow in the coronary is reduced and patients have chest pain with ST-segment elevation even though the large vessel is open.

In 1990, we were one of the first groups to suggest that no-reflow might be due to spasm not of the big arteries but of the small vessels.1 We recommended treatment with intracoronary calcium channel blockers like verapamil, diltiazem, and cardipine, which most of the time seemed to improve the flow. However, these drugs didn’t really work in a preventative way. You could give them before an intervention but you might still get no-reflow.

Next, there arose a great deal of interest in the glyco-protein IIb/IIIa receptor blockers to prevent platelet adhesion, with the belief that maybe platelet clumping was causing no-reflow. However, at least in saphenous vein graft interventions, the randomized trials of GP IIb/IIIa inhibitors did not show a reduction in adverse events in saphenous vein grafts.

Finally, the first of the distal protection devices, the PercuSurge GuardWire (actually developed with the hope of preventing stroke during carotid interventions), underwent testing in vein grafts in the SAFER trial.² The trial showed that embolic debris was being recovered and demonstrated a dramatic reduction in the incidence of CK elevations and no-reflow in saphenous vein graft intervention. There was a 42% reduction in CK elevations, from 16 to 9, and more than a 50% reduction in no-reflow, if I remember correctly, from 8.3 to 3.3.

The SAFER trial really was the turning point where people went from saying, Embolization doesn’t occur why should I worry about it? to understanding that in fact it occurs very frequently, in almost every case with saphenous vein grafts, and protecting against embolization reduces these otherwise unexplained adverse events.

What are some of the ongoing challenges of creating an embolic protection device?
There are 3 classes of device:

1. Distal occlusion. The PercuSurge GuardWire utilizes distal occlusion, which temporarily blocks the flow of blood while the intervention is done. Any debris trapped in a stagnant column of blood can be aspirated before the distal occlusion is released.

2. Distal filters

3. Proximal occlusion. This type of device interrupts the flow of blood upstream of the blockage.

There are pros and cons of each type of device, and I think one of the unsolved questions is which class of device and within that, which device is going to be the best, in terms of deliverability, maintaining flow, recovery of debris, and so forth.

The second big question is, how far can you generalize this model beyond saphenous vein grafts? We chose vein grafts as the initial testing ground, because they had a very high complication rate, and there’s a lot of viable debris. Regardless, whenever people have looked at intervention in other atherosclerotic vessels, be they carotids or renals, people have also found debris, and have shown that embolic protection reduces complications. The same thing probably should hold true for native coronary intervention, because people have certainly shown that debris is released, particularly in acute myocardial infarction (MI) interventions, and probably also in vulnerable plaque/unstable angina-type interventions.

We’re still struggling with demonstrating the clinical benefit of embolic protection. The EMERALD trial, which was just reported at the American College of Cardiology meeting by Gregg Stone, was the trial of the PercuSurge GuardWire in acute MI interventions. Even though the pilot data suggested that it improved outcomes, that was not demonstrated in this big, randomized trial.

My view is that embolization is a common in fact, one could almost say ubiquitous complication of dilating atherosclerotic stenoses in any vessel. The end organ being perfused by the vessel is sensitive to such embolization, which is certainly the case in the brain, heart, and probably the kidneys as well. The incidence of adverse outcomes would be reduced by embolic protection. I believe we’re headed for a situation where embolic protection becomes more of a routine part of intervention, the same way stenting is a routine part of intervention.

Do you feel that embolic protection is still important even with direct stenting?