Last year's great debates

In the first of the debates at the 2004 meeting, Sir Peter Bell (Leicester, UK) clashed with Klaus Balzer (Mülheim, Germany) over the proposal that plaque type is a pointless pursuit. Sir Peter Bell, who was speaking for the motion, said he believed that physicians should "treat the patient not the plaque". He asked why physicians bothered with plaques, suggesting that they provide endless research opportunities and allow endless speculation, while clouding the issue of treatment.

Bell said that the patients who should be treated are those with symptoms and a severe stenosis > 70%. He continued by saying that few if any asymptomatic lesions should be treated invasively as the risk of stroke is about 1% per annum with no treatment. "The importance of plaque type is therefore based on little evidence and its characterization is being used to justify treating patients who don't need treating by angioplasty and stenting, another unproven technique," declared Bell. He concluded his talk by asking, "After almost 25 years of research activity, none of which has brought any obvious benefits to patient care, isn't it time to stop this pointless exercise and do something more useful with the money?"

Klaus Balzer responded by stating that plaque morphology provides the right patients for the right procedure. He referred to the ICAROS international multicenter registry and declared that he believes that advances in plaque identification need to be monitored by vascular surgeons. "We are in competition with interventionalists and need to follow plaques or risk losing this field."

The audience overwhelming supported Balzer's view that plaque type is important.

Other debates included:

"That cerebral protection with stenting is of proven value"

Supported by Takao Ohki (New York, US) and Klaus Mathias (Dortmund, Germany).

Opposed by Giorgio Biasi (Milan, Italy) and Sumaira MacDonald (Newcastle, UK).

Ohki quoted his opponents previous publications to support his case. He admitted there was no Level 1 or 2 evidence available, "only circumstantial and common sense". Biasi said that ideally what is really needed is protection before, during and after the procedure. He presented data from the ICAROS international multicenter registry and indicated that he believed that the best protection available was identifying the plaque (through Gray Scale Median) and then using brain protection devices only in certain patients. Macdonald emphasized that in this area there are "strong opinions and weak evidence". She said that recent improvements in outcomes could be attributed to other advances, with learning curves and drugs being important. Macdonald also asked Mathias why the SPACE study in Germany was so unwilling to use cerebral protection.

Honors were even after this debate, with equal support from the audience for both camps.

"Endotension is hogwash"

Supported by Brian Hopkinson (Nottingham, UK) and David Kessel (Leeds, UK).

Opposed by Geoff White (Sydney, Australia) and Geoffrey Gilling-Smith (Cheshire, UK).

According to Hopkinson endotension is "a slightly nebulous concept based on some false assumptions and is a very, very small part of the management of endovascular problems." Hopkinson highlighted, "It is something that cannot be measured very easily. It is designed as a lack of endoleak - expansion without any definable endoleak and therefore is really of no significance."

However, he did say that sac pressure is quite different. "Endotension is designed as an expansion of sac volume with no detectable endoleak - totally different. Sac pressure is potentially very interesting. There are lots of snags and hazards and problems about it, but it is a much more important and significant advance rather than this rather ethereal concept that you can have an expansion without an endoleak. It could occur if there was fermentation going on inside and bugs were in there producing gas. Or it could occur if there was a dialysing process, such as we get across grafts that are leaking fluid but not blood. It is difficult to see that those are in anyway dangerous compared with true sac pressure. Which must be one of the factors that can lead to expansion and rupture and death."

Geoff White pointed out that there are over 350 articles on Medline about endotension and that it is recognised by the US government. He decried what he sees as the Hopkinson approach of "I don't understand it therefore it must be swill". White concluded by declaring, "endotension is science". David Kessel's main message was "If there is no flow it cannot grow," claiming that there is no evidence endotension exists and complained that its definition keeps changing. He concluded by stating that he believes that "endotension is an endoleak".

Gilling-Smith provided the definition of endotension as persistent or recurrent risk of rupture after endovascular repair. He said that what was being talked about was pressure and that pressure is important as this leads to expansion and rupture. Therefore "endotension matters", said Gilling-Smith.

The audience, however, supported the Hopkinson team.