Huge progress needs to be made before bioresorbable stents can replace permanent stents


When Abbott Vascular received the CE mark for its bioresorbable coronary scaffold Absorb in January 2011, it marked a new era of bioresorbable stents. As well as Abbott, several other companies—such as Elixir Medical (Desolve) and Biotronik (Dreams)—have also developed bioresorbable stents for the treatment of coronary artery disease. Renu Virmani, medical director, CVPath Institute, Gaithersburg, USA, spoke to Cardiovascular News about bioresorbable stents and their potential impact on the future management of coronary artery disease

What are the perceived benefits and disadvantages of bioresorbable stents compared with (new generation) drug-eluting or bare metal stents for the treatment of coronary artery lesions?

With conventional drug-eluting stents, a permanent polymer can induce greater late stent thrombosis, inflammation, granulomatous reaction, and greater long-term neo-intimal formation (late catch-up)

They remain even after the drug is fully released and no longer needed and can induce early neoatherosclerosis ie. within 15 months (40% of drug-eluting stents show some atherosclerotic change)

Bare metal stents have the disadvantage that the foreign body (stent) is present forever even when not needed. They induce chronic inflammation and are associated with restenosis and long-term induce neoatherosclerosis after five years.

What is the evidence so far for bioresorbable stents?

Studies have shown that these stents are associated with low stent thrombosis and low late stent restenosis (but the number of patients in these studies is too low to draw conclusions). Also, they do disappear after two to three years and, therefore, the artery is no longer “jailed”. Thus, there is no late restenosis and there is probably a reduced risk of neoatherosclerosis as well.

What are the research priorities in this area?

For me the most important priority is that they need to get thinner (<100micron). Also, they should disappear between 12 months and 18 months after implantation but they must maintain integrity (ie. we do not want to lose the outward force that a stent exerts on the arterial wall). In the case of bare metal stents, they should remain until three to four months afterwards and this timeframe should be longer with drug-eluting stents—nine to 12 months,

When Absorb received the CE mark in 2011, you told Cardiovascular News that you saw it being used in “young individuals with proximal discrete lesions” rather than patients with heavily calcified or very complex long lesions. Is this still your view?

Yes, my view remains the same because the bioresorbable scaffold does not have the integrity and strength the metal stents have. The calcified area of the vessel wall does not break or crack with the balloon angioplasty and it has to be pushed outward—a strong stent is needed to achieve this. In the days of percutaneous balloon angioplasty, closure rates were high because the plaque prolapsed into the lumen and caused occlusions. If the scaffold is not strong, the same thing will happen.

Drug-eluting stents with biodegradable polymers are also being investigated. What are the potential advantages and disadvantages of drug-eluting stents with biodegradable polymers compared with bioresorbable stents?

Permanent polymers remain even after drug is fully released when they are no longer needed. With bioresorbable polymers, the disadvantage of the stent remains (ie. that there will be a constant foreign body present in the arterial wall, which will induce inflammation and eventual restenosis). Therefore if one can get rid of the stent, then the chances of late effects of late catch up (restenosis) in drug-eluting stents and neoatherosclerosis are reduced.

Do you think bioresorbable stents will eventually replace drug-eluting and bare metal stents?

I think if the technology improves, then that is indeed likely. However, we need to make a huge progress before this is achieved as we need to have a better understanding of bioresorption and what it does to the artery wall. For example, does it induce inflammation? If so, we will have the problem of restenosis and neoatherosclerosis. We still have to deal with the thickness of these scaffold,150 microns, which is too thick for endothelialisation to occur rapidly.