What were some of the issues in treating certain vessel sizes in the past?
Five years ago, any vessel less than 3.0 mm in diameter was considered a small vessel. Now, small vessels are those that are less than 2.5 to 2.75 mm. Treating disease in these vessels is becoming more critically important, both in terms of women with heart disease and in diabetic patients who may have long diffuse disease. Furthermore, if you perform an angioplasty or stenting in a proximal vessel, it is still imperative to maximize blood flow to the muscle itself by ensuring smaller run-off vessels are open.

In the past, with angioplasty or bare-metal stents (BMS), restenosis rates were quite high, sometimes upwards of 50% angiographically. This has changed with drug-eluting stents (DES), which have become extremely effective in treating vessels that are 2.75 mm or even smaller. Therefore, we have a new modality that not only treats the patient acutely but also is beneficial in the long run by decreasing the chance that blockages will recur.

How has contemporary stenting impacted your approach to treating various vessels sizes?
With contemporary stenting, we can now treat almost any lesion that involves the epicardial coronary vessels, whereas before we were limited by lesion length and complexity. Previously, proximal lesions were considered higher risk, but with the advent of stenting, these patients can expect incredible safety and decreased likelihood of restenosis. Additionally, we were once reticent about stenting in left main disease and proximal left ostial disease, particularly if the left anterior descending artery fed the right coronary artery by collaterals, because you could basically lose two vessels in the pursuit of saving one.

What data do you anticipate will help support or further change practice patterns?
From a data standpoint, we are still unsure of how to treat patients that require multiple overlapping stents “ patients with bypass graft disease, patients with left main disease that are unprotected and patients with severe three-vessel disease with multi-lesion, multi-vessel disease. The SYNTAX study will help elucidate whether three-vessel DES treatment is non-inferior to bypass surgery and whether the same holds true for left main disease. I think there is now general agreement that bypass grafts should be treated with embolic protection devices, followed by stenting, but to date there is not a randomized trial comparing DES and repeat bypass surgery in these patients. There is also some question about DES in patients with acute myocardial infarction; HORIZONS AMI will provide guidance in this area.

What role does late loss play in DES? What data exist to show what happens to late loss as vessel size decreases?
Late loss is the difference in the amount of ingrowth of tissue that occurs from the time the stent is put in to the time that one performs intravascular ultrasound at a later date. With DES, there is no clinically significant difference once you are in the range of 0.2 mm to 0.4 mm in late loss. In other words, a late loss of 0.2 mm to 0.4 mm does not correlate with any clinical outcome, such as the need for revascularization or a myocardial infarction. On the other hand, late loss below 0.2 mm may indicate improper healing around the stent due to poor endothelialization, which can result in stent thrombosis. I prefer to see late losses between 0.3 and 0.45 mm because this is in the range where you are safe relative to the healing effect, but not overzealous in potentially causing restenosis.

In the TAXUS V trial, we saw a decrease in late loss as the size of the vessel decreased. However, in the SIRIUS 2.25 registry and GESTALT, you see a paradoxical opposite, which is somewhat interesting. With the sirolimus stent, the late loss in the smaller vessels was actually higher than the late loss in 3.0 and 3.5 mm vessels. We are not sure whether this has a significant correlation to a clinical outcome, but there is obviously something interesting in that data.

Even with the advent of contemporary stenting, what technical considerations still remain?
There are several things to keep in mind. First, as a vessel tapers distally, you may find yourself a little bit handcuffed in terms of not having a 2.25-mm or 2.0-mm DES if you have a distal dissection. This means you have to be careful to cover any injury zone and any disease during stent placement if you don™t want restenosis or propagation of the dissection to a vessel that you can™t pack up with stent. The second thing to be cognizant of is that there may be a little higher enzyme leak when treating very long, diffusely diseased vessels with multiple overlapping stents. I prefer to treat these vessels with one, longer stent and dilate the more proximal segment if needed. For example, if a vessel tapers from 3.0 mm to 2.5 mm, I prefer to put in a 32 x 2.5-mm stent and then dilate the proximal segment with a 3.0-noncompliant balloon.

How will future DES technology enhance treatment?
We may potentially see multiple DES options “ multiple platforms and potentially multiple drugs “ on our shelves. This will mean that we will need to weigh the importance of stent strut thickness, different drugs, different polymer combinations, and flexibility and trackability of different designs. As we look even further into the future, we will probably have platforms that are completely bioabsorbable and may deliver anticoagulation to the endoluminal surface of the blood flow, while delivering drug to the abluminal surface of the vessel. The potential for such a broad selection is an exciting prospect for both interventionalists and patients.

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