By Michael Jenkins
Let us not be under any illusions, what we have heard from Wyss and Schanzer are very important data. I think healthcare commissioners who are looking for “value for money” would be very interested in these data and there is a need to justify the long-term durability from EVAR.
The critics of EVAR will say, “I told you so,” and the endovascular evangelists will say “These are old data, and old devices and we have gone through this learning curve.” It is best to stick to the facts. Wyss’ paper shows that actually the explanation for “catch-up” mortality is because of rupture. There were 27 ruptures in 848 EVAR procedures and that does explain the late “catch-up” mortality.
I think by dividing these patients into anatomical issues i.e. top neck diameter, iliac diameter and neck length against failure of endovascular issues such as endoleaks, sac expansion, it is a little bit surprising that the so-called adverse anatomy did not show any significant risks.
But if you go back to the original EVAR data these were all deemed suitable for endovascular repair, so they were mostly well inside the instructions for use at the time and that makes me worry slightly for the ones that have been done since then outside the instructions for use where we really have expanded the indications. So for this set of data, the indications are pretty good.
If we go back to that cluster of risk problems, i.e. increasing sac diameter, endoleaks and migration, it is somewhat helpful to show that we can identify the risks that lead to rupture and this had a hazard ratio of 8.8. It is also a little bit reassuring that there were very few “out of the blue” ruptures or interval ruptures outside the surveillance programme (three out of 848, 0.35%) and that does show the benefit of surveillance. It also shows that when you find a problem, you have to fix it, because that problem has a high risk of rupture. This could mean potentially clearing the sac and the lead in to it, and arguably, this is a higher-risk situation than the original aneurysm. However, what we do not know is the number of patients that show sac expansion which did not lead to rupture.
It is interesting looking at the US data that 40% of sacs increased in diameter over a five year period. In Wyss’ paper, the data was looked at from the point of view of the rupture, not expansion, and whether they ruptured or not.
Other points to note are that there is no time that you can actually stop surveillance – aneurysms can rupture at six years – and that there is always an increasing risk of problems that need to be identified. The Wyss data show that ruptures occur at any and all stages of follow-up.
Comparing the UK data and the US data, what initially strikes me is that the mean diameter in the US data was below the threshold of what most of Europe would consider to put a device in. There are quite good data to suggest that there are fewer problems with small aneurysms and I suppose this makes sense because there is less room for migration to occur.
But actually when we look at US data, this is not necessarily true. Forty per cent aortic sac enlargement occurred in patients over the five-year period, even with small diameters. The other thing that is important is if you look at those curves in the Schanzer paper, it is remarkable that it is the newer devices which seem to lead to more sac expansion. These were newer devices, and put in further along the learning curve, so you cannot necessarily explain the problems by saying that these are the first generation, second generation devices and that is why the problem occurred.
It is obvious that EVAR only works when there is a seal and once you lose that seal, you have a pretty dangerous situation and when that occurs you need to fix it to get that seal again, otherwise you run the risk of leading to rupture.
Michael Jenkins, vascular surgeon, Imperial College, London, UK