"My name's Raj Kharbanda, I'm a cardiologist, I work in Oxford in the United Kingdom.
Yeah, so stroke still remains an important problem for TAVI and we're really trying to find ways of reducing stroke. The cerebral embolic protection devices, have been tested as a way to reduce stroke and there have been two large randomised trials. One, the protected TAVR trial, which enrolled 3,000 patients from the USA, Europe and Australia, and our trial, the BHF Protect TAVI trial, which enrolled over 7,500 patients from the UK. And both of those trials were testing the sentinel embolic protection device.

Both of those trials for the primary endpoint were neutral, but the idea was that we've got this data on 10,000 patients that we could combine at a patient level analysis to get a better understanding of some of the lessons about where it might be effective and if, you know, how we might use or understand embolic protection better.

The trials were very, very similar in terms of the primary endpoint was stroke. We had to obviously combine the data sets and, and the analysis is done with individual patient level data. That data is still being collected, if you like, in terms of making sure that the data sets are combined, accurately and there are more analyses to come out. But the data we've presented here have been the primary analysis of the initial findings from that, combination.

The, incidence of stroke which was the primary endpoint was 2.3% in the control group. Those patients who didn't get SEP, in the group that got SEP it was 2.2% and that's difference of 0.1% didn't reach significance. Disabling stroke was numerically lower and so overall, there was no difference in the primary endpoints for the trial.

So we've, one of the, you know, when you've got this, you want to get as much information out of a large trial like this as possible. One of the questions has been about, patients who were randomised to treatment, who didn't get the treatment. How did that impact on the result? What are those patients like? And there are a number of ways of looking at that analysis. So we've done a couple of analyses and there are some signals that it's possible that in certain people there is a reduction in stroke. But this is all hypothesis generating, if you like. And at the moment, what we've shown is that the routine use of embolic protection across a large population doesn't reduce stroke or disabling stroke. But understanding whether there are subgroups or particular patients who are at higher risk is really the next phase of our, investigation from this data set.

So are there groups who are at higher risk and can we identify those? And if we can, are they a group where embolic protection might be effective? So I think this is what we've shown is that a routine strategy is probably, isn't effective, but it doesn't rule out the fact that a selective approach might be better. But at the moment we don't know who those patients are. And it's probably a combination of things that, you know, give you an increased risk of stroke.

So I think that in terms of where it leaves the field, I mean, stroke still remains an issue. Embolic protection intuitively remains a good way of targeting procedural stroke. Now what I think we've learned is that perhaps it's a device effect, perhaps this was a first generation device, perhaps there are other devices that might work better. But I think it also tells us that the way that future trials need to think about this is possibly to focus on disabling stroke, rather than all stroke, and to perhaps have a more selective approach, so a more stratified, selective approach, focusing on hard clinical endpoints. So I think it raises questions rather than, you know, says we shouldn't do it, but it focuses the mind of what we should be concentrating on.”