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FAQs on Antiplatelet Management in Stroke
Antiplatelet Therapy, Bleeding Risk, and Reversal Strategies: Expert Answers to Your Questions

Released: March 11, 2025

Expiration: March 10, 2026

Deepak L. Bhatt
Deepak L. Bhatt, MD, MPH, MBA, FACC, FAHA, FESC, MSCAI
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Key Takeaways
  • Patients treated with antiplatelet therapy because they are at high risk for a thrombotic event, who receive a reversal agent during a bleeding event, may face an increased risk of thrombosis because of the temporary loss of the antiplatelet’s effect, highlighting the need for prompt resumption of antiplatelet therapy and careful management of prothrombotic factors during bleeding events.
  • Life-threatening bleeding is a low-frequency, high-impact event, so regular reviews on antithrombotic reversal agents are beneficial.
  • The management of antiplatelet therapy in patients requiring anticoagulation depends on balancing thrombotic and bleeding risks, necessitating individualized clinical decision-making.

The commentary below dives more deeply into topics and questions posed by a live audience of healthcare professionals (HCPs) during a symposium on antiplatelet reversal and bleeding management strategies, including practical steps to implement the evidence into practice on managing acute stroke. This event was held in Los Angeles, California, in February 2025. 

What is the potential risk of stent thrombosis in patients who have had a coronary stent placed within the past 30 days and receive bentracimab?
Based on the mechanism of action of bentracimab and data on its biology, I would not expect it to cause a prothrombotic state or rebound in platelet activity. Furthermore, the therapeutic benefit of ticagrelor will be lost until treatment is resumed. In patients with recent stent placement, if HCPs need to reverse the effects of ticagrelor because of an intracranial hemorrhage or emergency surgery, I think it would be appropriate to administer bentracimab and resume the ticagrelor and/or aspirin as quickly as possible.

In general, patients who are bleeding tend to have higher rates of thrombotic and ischemic events, and those pathways are somewhat interrelated and complex. In this scenario, withholding antiplatelet agents increases the risk of stent thrombosis and other thrombotic events, because the patient is no longer benefiting from their protective effects. In addition, other medications may also be temporarily discontinued during bleeding episodes. For example, β-blockers are sometimes held because of concerns that they may mask compensatory tachycardia or for hypotension. Similarly, statins may be paused during active bleeding and should be resumed by the time of hospital discharge, but are often not. Therefore, many factors lead to prothrombotic states and ischemic events. During a bleeding event, the body’s natural response to stop bleeding can inadvertently create a more prothrombotic state. This poses a particular risk for individuals with arterial plaque, because the heightened prothrombotic effect may increase the likelihood of ischemic events. This is why HCPs should always be mindful of that potential.

What are the practical considerations for implementing bentracimab in clinical practice?
One challenge we face with this agent, as we have with other reversal agents, is low-frequency, high-impact events. Bentracimab works best if used right away. Therefore, this is one setting in which the electronic health record can help a great deal with alerts and such—for example, for patients who are treated with ticagrelor. It is also useful to have a monthly refresher of the low-frequency, high-impact events that HCPs will see in the emergency department, so there is continuous refresher of this information.

Contingent on bentracimab receiving FDA approval, I think it will need to be made available in every emergency department and ICU. Even a small, rural emergency department or ICU would need to carry it. Furthermore, HCPs may not remember exactly how to use the agent, but as long as they recall that bentracimab is the reversal agent for ticagrelor, that is sufficient.

In terms of practicalities, if the agent is also approved for surgical procedures, in general, that will make its use more frequent. Patients treated with ticagrelor often face a 3- to 5-day delay while awaiting surgery. During this time, they experience prolonged hospitalization, which can lead to dissatisfaction for both the patients and their families because of the delay to their surgical procedure. Furthermore, patients’ ischemic risk is elevated because HCPs are waiting for the ticagrelor to wash out. This is a case example where bentracimab could play a role in reversing ticagrelor, thereby negating the need for a washout period. If bentracimab is used in this way, then it will be in very common use and there will be a great deal of familiarity with it. Of note, this will be dependent on the approved labeling for its use and the cost of the agent.

Is there a role for monitoring a P2Y12 functional goal in testing when using bentracimab?
We did plenty of fancy platelet function tests for the sake of science and the trial. In clinical practice, I do not think it is necessary. If bentracimab receives FDA approval, I would administer the agent with the expectation that it is working effectively, because the trial data indicated that there were no nonresponders. Although there is some variability to every antiplatelet agent, ticagrelor is not like clopidogrel—to which there is a fair amount of variability in response. Ticagrelor tends to provide a more consistent level of antiplatelet effect. Therefore, I would not feel obligated to check a VerifyNow-P2Y12 assay with bentracimab.

Are there plans to study cangrelor in patients with a recent stroke or coronary event who require urgent (but not emergent) cardiac or noncardiac procedures during the bridging period after discontinuing their oral antiplatelet agent?
With respect to cangrelor, I was a co-principal investigator on the phase III trial that led to its approval. That trial enrolled approximately 11,000 patients who underwent percutaneous coronary intervention for a variety of indications. Our findings showed that cangrelor significantly reduced rates of stent thrombosis and other ischemic events. So it is very useful in a cardiac catheterization laboratory, especially in higher-risk patients.

There was a smaller study called BRIDGE that enrolled 200 patients who underwent elective coronary artery bypass graft surgery. This study found that using cangrelor for bridging at a lower infusion dose provides an antiplatelet effect similar to that of long-term oral antiplatelet use. If patients are admitted to the hospital while being treated with clopidogrel, HCPs can stop the clopidogrel and start a cangrelor infusion. As a prelude to a surgical procedure, I have certainly used cangrelor as a bridging strategy. Of note, cangrelor is not approved by the FDA for this. It also gets expensive if you have someone receiving cangrelor for a long time; the costs of a 24-hour infusion for several days can really add up. For example, you could have a patient who had a left main stent and now needs a left ventricular assist device or transplant. That patient could go to the operating room any day, so there is an advantage to bridging with cangrelor instead of using aspirin and clopidogrel. But the patient could be waiting for more than 1 month for a transplant, so the cangrelor cost would be very high. Putting that point aside, it is a safe and effective way of substituting an oral antiplatelet agent.

For a patient receiving antiplatelet therapy for a cardiac indication who develops a thromboembolism and requires anticoagulation, would you recommend discontinuing the antiplatelet agent or managing both therapies concurrently?
First, I would ask: “Does the patient really need anticoagulation if they have deep vein thrombosis, pulmonary embolism, or atrial fibrillation?” The answer is yes. Barring a contraindication, there should be an anticoagulant with a dosage adjustment, if needed, based on the specific agent and other factors. Now, what do you do with antiplatelet therapy? I would look closely to determine whether it is needed. If a patient is being treated with aspirin for primary prevention, I would not continue the antiplatelet therapy because the data for using aspirin for primary prevention are rather weak. By adding an anticoagulant, this regimen would go from being weak to being a bad idea; therefore, I recommend stopping the antiplatelet therapy.

If a patient has just received a left main stent, I would feel uncomfortable with stopping the dual antiplatelet therapy. Although there are no randomized trial data of direct comparisons to answer the question of whether it is necessary to start using a new agent for a new disease state such as deep vein thrombosis or atrial fibrillation, the existing data support the strategy of double antithrombotic therapy—a full dose of an anticoagulant and an antiplatelet agent. Assuming that a patient is placed on therapy with an appropriate full-dose anticoagulant, I add 1 antiplatelet agent, which is most often clopidogrel because it has a low bleeding risk and has been studied in combination with anticoagulants. If a patient has a low bleeding risk but a high ischemia risk, HCPs may combine using ticagrelor with the anticoagulant. Of note, I avoid sustained triple antithrombotic therapy (aspirin plus a P2Y12 receptor plus an anticoagulant), which is a recipe for bleeding.

Your Thoughts
In your practice, how often does a patient’s bleeding risk determine your choice of an antiplatelet agent? You can get involved in the discussion by answering the poll and posting a comment below.

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