I think this is a burning question or it is becoming a burning question in stroke medicine because we see an increasing number of patients who fail DOACs as one would say and go on to have a stroke despite being treated with anticoagulants. And people really don’t know what to do about these patients there’s really not much evidence and it’s quite variable what people actually end up doing in practice some will switch to another anticoagulant there are many discussions about you know switching to another anticoagulant with a different mechanism of action or with a different dosing frequency and what have you and many who wouldn’t switch...
I think this is a burning question or it is becoming a burning question in stroke medicine because we see an increasing number of patients who fail DOACs as one would say and go on to have a stroke despite being treated with anticoagulants. And people really don’t know what to do about these patients there’s really not much evidence and it’s quite variable what people actually end up doing in practice some will switch to another anticoagulant there are many discussions about you know switching to another anticoagulant with a different mechanism of action or with a different dosing frequency and what have you and many who wouldn’t switch. So unfortunately the state of the evidence is not very good on this question. We only have observational data and most of that actually retrospective in nature. The totality of the data that we have does not support switching or at least does not support routine switching between anticoagulants. We don’t see that switching from one DOAC say to another DOAC with say a different mechanism of action or a different dosing frequency might lead what might be associated with better outcomes. What we do see is a signal for worse outcomes in patients who are switched from a DOAC to a vitamin K antagonist. That’s the old class of anticoagulants. They tend to bleed more, which we kind of know already, and they also don’t seem to profit much in terms of a reduction of ischemic stroke. Bear in mind that this, again, are observational data. There’s all kinds of biases in this data which are inherent to these observational studies which you cannot really adjust for or wait for or really account for. And so take that with a grain of salt. What most people would consider doing in clinical practice with relation to these patients is not switch them to vitamin K antagonists, except for, you know, exceptional situations, exceptional scenarios. There are some even well-defined indications in small subgroups, you know, people with mechanical valves, people with antiphospholipid syndrome. But leaving these patients apart, these exceptional situations, most people wouldn’t switch, routinely switch to vitamin K antagonists. And then I think it’s kind of divided between clinicians, whether they would keep everybody on the same DOAC or whether they would switch them to a DOAC with a different dosing frequency or a different mechanism of action. I think both is fine in the absence of evidence, but we really need to do better. And it’s not just about switching because ultimately regardless of whether we switch or not these patients are at a very high risk of recurrence so we also really need even better preventive strategies so that transcends the question of switching really.
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