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Safer Paths Better Outcomes: Advancing Secondary Stroke Prevention Through Factor XIa Innovation | Module 2: Translating Factor XIa Inhibition Evidence into Practice

Stroke medicine
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Description

This program is supported by an independent education grant from Bayer. This education program is only available to healthcare professionals in the USA.

In this on-demand session, leading stroke prevention expert Dr. Jeffrey L. Saver discusses implementing evidence-based antithrombotic strategies for secondary stroke prevention. Drawing on landmark trial data and the latest AHA/ASA guidelines, the module translates complex evidence into practical algorithms for managing both non-cardioembolic and cardioembolic ischemic events in 2026.

Prefer to read instead? Read our Key Clinical Summary here.

Accreditation: AffinityCE designates this activity for 0.25 AMA PRA Category 1 Credit™

Session Highlights

  • Optimizing DAPT Timing and Duration: Mastery of early Double Antiplatelet Therapy (DAPT), specifically aspirin plus clopidogrel, initiated within 24 hours of a minor stroke or high-risk TIA and continued for 21 days to maximize ischemic reduction while minimizing bleeding risk.
  • Precision Medicine for Clopidogrel Non-Responders: Evaluation of CYP2C19 loss-of-function genotyping to identify the 20–30% of patients who may benefit more from DAPT with ticagrelor and aspirin rather than clopidogrel-based regimens.
  • Tailored DOAC Initiation in Atrial Fibrillation: Implementation of an infarct-size-based schedule for initiating Direct Oral Anticoagulants (DOACs), utilizing an "early" strategy (within 48 hours for small/moderate infarcts) to balance recurrent ischemia against hemorrhagic transformation.
  • Mechanism-Driven Therapy Selection: Insight into the pathophysiological differences between "white clots" (platelet-rich) in non-cardioembolic stroke requiring antiplatelet therapy, and "red clots" (fibrin-rich) in cardioembolic stroke requiring anticoagulation.
  • Clinical Application of the AHA Algorithm: Mastery of the updated AHA guideline algorithm, which incorporates NIHSS scores, allele testing results, and time from symptom onset to guide specific therapy selection (POINT, CHANCE, and THALES trial protocols).

Who Should Watch

  • Pharmacists
  • Neurologists
  • Multidisciplinary stroke care teams
  • Primary care physicians
  • Critical care physicians
  • Hospitalists
  • Advanced practice providers
  • Nurses
  • Care managers involved in multidisciplinary post-stroke care

Presented by

Jeffrey L. Saver, MD, FAHA, FAAN, FANA, is a Distinguished Professor and Director of the UCLA Comprehensive Stroke and Vascular Neurology Program. A world-renowned expert in stroke treatment and prevention, he has authored over 870 research articles and served as the principal investigator for landmark trials including FAST-MAG and SWIFT PRIME. Dr. Saver is a former Chair of the AHA Stroke Council, and a recipient of the World Stroke Organization Lifetime Research Award.

Continuing Education Information

Commercial support: This activity received monetary support through an independent education grant from Bayer.

This continuing education activity will be provided by AffinityCE and MedAll. This activity will provide continuing education credit for pharmacists.

Disclosures

Jeffrey L. Saver, MD, FAHA, FAAN, FANA has disclosed financial interests or relationships within the past 36 months with the following ineligible companies: Consultant for Abbott, Aeromics, Bayer, Biogen, Boehringer Ingelheim, BrainQ, BrainsGate, CSL Behring, Medtronic USA, Roche, Stream Medical, Johnson & Johnson, MIVI Neuroscience and Occlutech. Stock Options from MindRhythm, Neuronics Medical, Rapid Medical.

These disclosures are provided in accordance with ACCME standards to ensure transparency and uphold the integrity of continuing education. Dr. Saver does not intend to reference any unlabeled or unapproved uses of products during the presentation.

AffinityCE staff, MedAll staff, as well as planners and reviewers, have no relevant financial relationships with ineligible companies to disclose.

Mitigation of Relevant Financial Relationships

AffinityCE adheres to the ACCME’s Standards for Integrity and Independence in Accredited Continuing Education. Any individuals in a position to control the content of a CME activity, including faculty, planners, reviewers, or others, are required to disclose all relevant financial relationships with ineligible companies. Relevant financial relationships were mitigated by the peer review of content by non-conflicted reviewers prior to the commencement of the program.

Activity Accreditation for Health Professions

Physicians

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AffinityCE and MedAll. AffinityCE is accredited by the ACCME to provide continuing medical education for physicians.

AffinityCE designates this enduring material for a maximum of 0.25 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Physician Assistants

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AffinityCE and MedAll. AffinityCE is accredited by the ACCME to provide continuing medical education for physicians.

AffinityCE designates this enduring material for a maximum of 0.25 AMA PRA Category 1 Credits™. Physician assistants should claim only the credit commensurate with the extent of their participation in the activity.

Nurse Practitioners

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AffinityCE and MedAll. AffinityCE is accredited by the ACCME to provide continuing medical education for physicians.

AffinityCE designates this enduring material for a maximum of 0.25 AMA PRA Category 1 Credits™. Nurse practitioners should claim only the credit commensurate with the extent of their participation in the activity.

Nurses & Other Professionals

All other health care professionals completing this continuing education activity will be issued a statement of participation indicating the number of hours of continuing education credit. This may be used for professional education CE credit. Please consult your accrediting organization or licensing board for their acceptance of this CE activity.

System Requirements

Mobile device (e.g., large-format smart phone; laptop or tablet computer) or desktop computer with a video display of at least 1024 × 768 pixels at 24-bit color depth, capable of connecting to the Internet at broadband or faster speeds, with a current version Internet browser and popular document viewing software (e.g., Microsoft Office, PDF viewer, image viewer) installed. Support for streaming or downloadable audio-visual materials (e.g., streaming MP4, MP3 audio) in hardware and software may be required to view, review, or participate in portions of the program.

Unapproved and/or off-label use disclosure

AffinityCE/MedAll requires CE faculty to disclose to the participants:

  • When products or procedures being discussed are off-label, unlabeled, experimental, and/or investigational (not US Food and Drug Administration [FDA] approved); and
  • Any limitations on the information presented, such as data that are preliminary or that represent ongoing research, interim analyses, and/or unsupported opinion.

CME Inquiries

For all CME policy-related inquiries, please contact us at ce@affinityced.com.

Participation Costs

There is no cost to participate in this program.

This continuing education activity is active starting February 27th 2026 and will expire on December 31st 2026.

Estimated time to complete this activity: 15 minutes.

Learning objectives

Upon completion of this activity, participants should be better able to:

  • Interpret emerging clinical evidence on Factor XIa inhibition - including findings from PACIFIC-STROKE and ongoing Phase III studies such as OCEANIC-STROKE and LIBREXIA-STROKE - to inform treatment decisions in non-cardioembolic stroke.

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Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hello, everyone. Uh, this is Jeffrey Saver, professor at UCLA and the Stroke Program, and it's a pleasure to be speaking with you today on the topic of translating factor 11A inhibition evidence into practice. Here are my disclosures. And the learning objective for this program is to interpret the emerging evidence on factor 11A inhibition, including findings from a phase 2 Pacific stroke trial and ongoing phase 3 oceanic and lorexia stroke trials to inform treatment decisions in non-cardiembolic stroke. I'll begin with a couple of key framework aspects. And the first is, as we all know, the use of antithrombiotics, antiplatelet, or anticoagulant agents in, uh, prevention of ischemic stroke, uh, has advantages and disadvantages. Uh. It helps to prevent pathologic thrombosis all the way to the right that occurs in the lumen and allows clot to occlude the artery locally or by embolizing. Uh, on the other hand, it can also prevent hemostasis in the middle, which is needed to repair. tears in the arterial wall and prevent bleeding from happening. So we have this uh bleeding versus uh uh and hemostasis versus thrombosis trade-off, which transfers as clinically into a trade-off between more antithrombotic therapy, preventing more ischemic stroke, but causing more cerebral hemorrhage. And we have a variety of Risk factors for individual patients that indicate who's at greater risk for one or the other and might indicate uh when to be more aggressive. But there's a lot of overlap. So, uh, risk factor profiling only gets us so far. So this is the gap that the factor 11A inhibitors have been developed to address because there's reason to hope that the factor 11A inhibitors, unlike other agents in the coagulation cascade therapy realm, will be able to differentially affect. Hemostasis versus intravascular thrombosis. Factor 11 has only a minor role to play in the initial hemostatic plug, but a major role in the uh subsequent intravascular thrombosis. So a factor 11A inhibitor could Prevent intravascular thrombosis while not preventing hemostasis and thereby uncoupling the bleeding risk of antithrombotic therapy from the ischemic event prevention. And there's a strong suggestion that uh this uh could be the case if we get the right agent because uh genetic studies in individuals who have been born without factor 11 have shown first, they don't have a proneness to bleeding despite missing factor 11. And second, they do have less embolic stroke and, um, uh, and Non-cardibolic stroke than patients who have, uh, or individuals who do, uh, who have normal effect. 11. So, we'd like to reproduce this genetic state in patients with a pharmacologic agent. There are many agents now in development. Here's the coagulation, uh, cascade, and you can see our familiar 10A inhibitors in brown, direct thrombin inhibitors in pink and in purple are the many agents. Being developed for this promising target of factor 11. And today, we're gonna talk about three that are the furthest along. Two are small molecules, ascidexion and Milvexium, and one is a monoclonal antibody, abelasimab. We'll begin with ascidexion, which is the furthest along. Uh, it is a direct inhibitor, uh, with oral dosing once daily of factor 11A, does not increase the bleeding time and it, uh, has a very strong, greater than 90% inhibition effect on 11A without increasing, uh, clinical bleeding in, uh, initial, uh, normal control studies. Now, when we think about The patients in whom factor 11 inhibitors will be beneficial. Uh, the first thought is, uh, to go to this traditional distinction, uh, between non-cardiobolic and cardiobolic stroke. That in non-cardiobolic stroke, you have rapidly flowing blood that is interrupted by Plaques extending into the lumen causing this laminar flow and platelet activation and aggregation, so antiplatelet agents for these white clots would be more effective. In contrast, for Most cardiobolic sources like um atrial fibrillation, we have stasis. The non-beating atrium allows clot to slow uh blood to slow, and whenever blood flows, it tends to clot. And that's a coagulation cascade mechanism. So anticoagulants would be better for slow flow in the atrium. Yeah, and that has classic view has held up for many years, but has recently become more nuanced because, uh, Recent trials have confirmed that it could be helpful to um treat an additional mechanism of thrombosis that does occur in non-cardibolic stroke, and that is, uh, when you injure the vessel wall, uh with uh plaque development, you expose to the surface. Uh, tissue factor that's in the endothelial wall. And tissue factor is one of the most thrombogenic molecules we know. Uh, it activates the coagulation cascade. And that means that there may be some benefit of adding an anticoagulant to antiplatelet agents in patients with non-cardiobolic stroke and that, uh, was Actually shown to be the case in the Compass trial, which added a low dose DA to aspirin, uh, but, uh, Has, has not really had a wide uptake in clinical practice, uh, in, in part because it doesn't quite fit well with what we have historically been taught. So, here is the first polling question. And uh the polling questions are gonna be about the information that I will be turning to next, not the information that you've seen. So this is to motivate you to uh really pay attention in the uh slides to come. This first question says, in a patient with mild non-cardibolic ischemic stroke, given antiplatelet therapy within 4 hours of stroke onset, How might the Pacific stroke findings influence your antithrombotic choice in future clinic clinical practice if asendexion was approved? I won't read through each of the uh long answers. I'll give, let you read through those and, and choose that over the next 10 seconds. OK. Well, now let's turn to the data that speaks to that question by looking at the specific uh stroke phase two trial published in The Lancet in 2022. And uh this uh key aspects were it was in patients with non-cardibolic stroke with uh the study drug asindexion, a factor 11A inhibitor, or placebo begun within 48 hours of onset in patients who were gonna be getting antiplatelet therapy. So this is on top of standard antiplatelet therapy, not instead of it. And uh initially in Lower-risk patients uh with mild NIH stroke scale and no reperfusion therapies and then expanding to more moderate to severe patients in a stroke scale under 15 and patients who received thrombolysis or thrombectomy. And uh treatment was for 6 to 12 months.