Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, May 17, 2026

Paradigm Change Coming in Secondary Stroke Prevention: OCEANIC-STROKE

 What is your competent? doctors current secondary stroke prevention? Will this replace the current protocol?  Or don't you even have a protocol?

Paradigm Change Coming in Secondary Stroke Prevention: OCEANIC-STROKE

This transcript has been edited for clarity. 

Dear colleagues, I am Christoph Diener, from the Faculty of Medicine at the University of Duisburg-Essen. In this month's video, I would like to concentrate on new developments in secondary stroke prevention, in particular, the OCEANIC-STROKE trial

From Aspirin to Factor Xa Inhibitors

Until about 20 years ago, for secondary stroke prevention, we only had aspirin, which was not terribly effective. Then it turned out that we had much more effective drugs in stroke prevention in people with atrial fibrillation. On one side, dabigatran, and on the other side, the factor Xa inhibitors, for example, apixaban, rivaroxaban, and edoxaban.

The big difference was that stroke prevention in atrial fibrillation with aspirin had a risk reduction of about 15%, but with new anticoagulants, we had risk reductions compared to placebo of 60%-70%. New anticoagulants were more effective, but they also had bleeding, so there is a need to develop new antithrombotic drugs that have lower bleeding risk and similar efficacy.

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This is why factor XI came into play. There are people who have a genetic disorder and they have no factor XI. Clinically, they have a reduced risk of ischemic stroke and myocardial infarction, and they have only a very small increase in the risk of bleeding, particularly in the urogenital tract and oropharyngeal tract if they have to undergo surgery.

Factor XIa Inhibitors

This is why factor XIa inhibitors were developed. There are small molecules, and I will talk today about asundexian, and there are monoclonal antibodies against factor XI, and one of them is abelacimab

Let me start with asundexian. The first trial was done in atrial fibrillation. The OCEANIC-AF study compared asundexian with apixaban. This trial was terminated prematurely because the drug was inferior to apixaban and had a similar bleeding risk. 

The next approach was to study this drug in secondary stroke prevention in people without cardioembolic strokes, and also in people who have high-risk transient ischemic attack (TIA). This is the OCEANIC-STROKE trial. This trial used asundexian as a factor XIa inhibitor, and following a dose-finding study, the final dose was selected. This was a placebo-controlled, international trial, and asundexian was given on top of antiplatelet therapy, which was initially the combination of aspirin and clopidogrel followed by long-term aspirin.

The primary endpoint was ischemic stroke — recurrent ischemic stroke in people who had a stroke or first ischemic stroke in people who had a high-risk TIA. The primary safety endpoint was International Society on Thrombosis and Haemostasis (ISTH) major bleeding. The key inclusion criteria were non-cardioembolic strokes and a history of atherosclerosis, either by imaging, ultrasound, or they could have a non-lacunar stroke on imaging; and they had to have antiplatelet therapy.

This trial had 6150 patients who received asundexian 50 mg once daily compared to placebo, and they were followed between 3 and 31 months. At baseline, they were on average 67 years old, about one-third were females, they had typical risk factors like diabetes and hypertension, and 25% were current smokers. The index event in the majority: 95% was an ischemic stroke. 

If we look at the cumulative incidence of ischemic stroke, there was a clear benefit of asundexian 50 mg compared to placebo, with a hazard ratio of 0.74, which translates into a 25% risk reduction, which was highly significant. The study was also positive for all the secondary outcomes. For example, all strokes or cardiovascular deaths or all-cause mortality, myocardial infarction, and stroke, and so on. 

Very importantly, in terms of safety, there were no differences in ISTH major bleeding events and there were also no statistically significant differences in the other bleeding events. The cumulative incidence of major bleeding had a hazard ratio of 1.10, which was not statistically significant. The benefit of this drug was shown in all subgroups. 

Ladies and gentlemen, this is a major step forward. For the first time in 50 years, we have a new drug, which is superior to aspirin or the initial antiplatelet therapy with clopidogrel and aspirin, and has no increased bleeding risk. This will change clinical practice. 

AF vs Stroke Results 

Now, you will ask, why was this drug not effective in people with atrial fibrillation? Why was it effective in people with atherosclerosis and ischemic stroke and high-risk TIA? We don't know, but there is a difference, obviously, compared with the monoclonal antibody abelacimab because abelacimab was effective in people with atrial fibrillation compared to rivaroxaban — not in terms of efficacy, but it had a significantly lower bleeding risk. This monoclonal antibody at present will undergo a study with secondary stroke prevention. 

Dear colleagues, ladies and gentlemen, our clinical practice will change once asundexian is approved. In future, this patient group who has ischemic stroke or high-risk TIA and has non-cardioembolic stroke and has atherosclerosis somewhere in the body will clearly benefit from this drug on top of long-term aspirin therapy. This is a change in the paradigm how secondary stroke prevention is performed. 

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