Management of Anticoagulation and Antiplatelet Therapy After Stroke in the Setting of Recurrent Gastrointestinal Bleeding: A Dynamic Shared Decision-Making Approach

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EP LAB DIGEST. 2026;26(8):24-25.

Demetra Menoudakos, BS¹; Matthew Duazo, BS¹; Ruchitha Arvapally, BS¹; Bilal Niazi, BS¹; Ermin Tale, DO²; Todd J Cohen, MD¹
¹New York Institute of Technology College of Osteopathic Medicine, Old Westbury, New York 
²Jacobi Medical Center/Albert Einstein College of Medicine, Bronx, New York

Introduction
The etiology of ischemic stroke is often multifactorial and not always clearly defined. When multiple potential embolic sources are present, risk assessment can be challenging. These patients are considered at high risk for sequelae and recurrent stroke and therefore warrant close monitoring. Although indications for antithrombotic therapy are generally well established, management is less clear in special populations, particularly among patients at increased risk for bleeding. Presented here is a case of an elderly patient with recurrent, life-threatening gastrointestinal (GI) bleeding and a history of iatrogenic ischemic stroke in the setting of multiple cardioembolic risk factors. This case highlights the importance of shared decision-making and its evolving nature over time when determining whether to continue anticoagulation and/or antiplatelet therapy after recurrent life-threatening GI bleeding.

Case Presentation
An 82-year-old man with a history of myocardial infarction, coronary artery disease, hypertension, and paroxysmal atrial fibrillation (PAF) had been followed in the cardiology clinic for routine care for the past 7 years. Prior to establishing care at the clinic, the patient underwent implantable loop recorder (ILR) placement for long-standing palpitations, which demonstrated infrequent but highly symptomatic episodes of PAF with rapid ventricular response rates up to 180 beats per minute. His condition was managed with rivaroxaban, 20 mg daily, and diltiazem, 240 mg daily. Additional medications included aspirin, 81 mg daily, and atorvastatin calcium, 20 mg daily. Other causes of palpitations, including electrolyte abnormalities, thyroid disease, ischemia, and Lyme disease, were excluded.
Nearly all of the patient’s PAF episodes were precipitated by alcohol consumption. His early clinical course was previously described in an EP Lab Digest case report, which highlighted the utility of administering beta-blockers immediately before alcohol intake as a preventive strategy for AF.¹ This approach remained effective for approximately 18 months, after which the frequency of AF episodes increased, ultimately leading to discontinuation of beta-blocker therapy.

Upon establishing care at the clinic, the patient’s symptoms were well controlled; however, interrogation of the ILR demonstrated brief, infrequent episodes of AF and low battery status. In March 2019, the ILR was removed and replaced. He was counseled on lifestyle modifications, including diet, exercise, and moderation of alcohol intake. The patient initially adhered to rivaroxaban therapy but reported bruising and excessive bleeding from minor cuts, leading him to self-administer the medication only during episodes of AF. These episodes were consistently symptomatic and confirmed by ILR recordings.

Three months later, the patient experienced a nonhemorrhagic stroke. Interrogation of the ILR revealed no episodes of AF surrounding the event. Transthoracic echocardiography demonstrated a preserved ejection fraction (EF), a laminated ascending aortic plaque, and a patent foramen ovale (PFO) identified on bubble study, either of which may have contributed to the stroke. Rivaroxaban therapy was subsequently resumed on a daily basis.

One year later, the patient experienced a diverticular GI bleed that resolved without intervention; no definitive source was identified. In 2021, he underwent pulmonary vein isolation and cavotricuspid isthmus ablation for AF. The procedure was complicated by transient hypotension secondary to a large periprocedural pericardial effusion with tamponade physiology, which was successfully treated without recurrence. Thereafter, he experienced only brief, infrequent episodes of PAF and remained free of GI bleeding for the next 2 years.

In 2023, he underwent knee arthroplasty, requiring temporary interruption of direct oral anticoagulant (DOAC) therapy. After resuming anticoagulation, he took ketorolac for postoperative pain control and subsequently experienced a second, self-limited GI bleed. Later that summer, following shoulder arthroplasty and reinitiation of DOAC therapy, he again received ketorolac, which precipitated a third GI hemorrhage. This episode required hospitalization, temporary cessation of anticoagulation, and blood transfusion for a hemoglobin level of 6 g/dL. GI evaluation revealed possible angiodysplasia but no definitive bleeding source. The gastroenterology team recommended a conservative “watch-and-wait” approach, with cardiology follow-up to guide ongoing antiplatelet and anticoagulation management.

At posthospitalization cardiology follow-up, the patient appeared fatigued and dehydrated following transfusion and had labile blood pressure readings. Echocardiography demonstrated an unchanged EF, stable aortic plaque, and no PFO on repeat bubble study. Interrogation of the ILR revealed no recent episodes of AF. His stroke risk associated with AF, as estimated by the CHA₂DS₂-VASc score, was 6, corresponding to an annual stroke risk of 9.7%.² His bleeding risk while receiving anticoagulation, as estimated by the HAS-BLED score, was 4, corresponding to an annual bleeding risk of 8.7%.³

Following extensive discussions among the patient, his cardiologist, and consultants in neurology and gastroenterology, a treatment plan was developed to balance bleeding risk while minimizing the likelihood of recurrent stroke. The plan included aspirin, 81 mg daily, without DOAC therapy unless symptomatic AF recurred, given that the patient reliably perceived each episode and remained monitored with an ILR. He was counseled to avoid ketorolac while taking a DOAC and was scheduled for 6-month follow-up.

Subsequently, in November 2025, the patient notified his cardiologist of a fourth GI bleed that occurred while taking only baby aspirin. After further shared decision-making, aspirin therapy was discontinued, and the gastroenterology team again recommended observation without intervention. He has remained free of recurrent GI bleeding for the past 6 months.

Discussion
This case highlights the challenge of balancing high thromboembolic risk, reflected by a CHA₂DS₂-VASc score of 6, against substantial bleeding risk, reflected by a HAS-BLED score of 4. Three potential etiologies contributing to this patient’s stroke risk were identified: (1) PAF, which demonstrated only rare, brief episodes on long-term monitoring following ablation; (2) a history of PFO, although repeat evaluation with bubble study showed no evident or provocable PFO and therefore no clear ongoing risk of paradoxical embolism; and (3) a long-standing laminated ascending aortic plaque, for which the true embolic risk was considered low but difficult to quantify. Notably, the patient’s second and third GI bleeds occurred in the setting of concurrent nonsteroidal anti-inflammatory drug (NSAID) use after resumption of DOAC therapy. He was therefore advised to avoid future NSAID use to reduce the risk of recurrent GI bleeding.

According to expert consensus from the American College of Cardiology, current guidelines recommend delaying initiation of oral anticoagulation in patients with stroke and recent GI bleeding.⁴ Following the patient’s third GI bleed, cardiology recommended withholding DOAC therapy unless symptomatic AF recurred. After multidisciplinary discussion involving neurology, the cardiologist, and the patient, a shared decision was made to continue low-dose aspirin for secondary stroke prevention. Given the infrequency and short duration of AF episodes, none of which occurred around the time of his prior stroke, left atrial appendage occlusion was not pursued. The patient was amenable to short-term DOAC therapy should symptomatic AF occur, as he reliably perceived each episode, analogous to a “pill-in-the-pocket” strategy. Data evaluating this approach remain limited; however, 2 single-arm pilot studies involving a combined total of 96 patients with AF reported no strokes, supporting the need for further investigation.⁵ Following the patient’s fourth GI bleed, aspirin therapy was also discontinued after a shared decision-making discussion.

DOACs remain the preferred anticoagulation therapy for stroke prevention in patients with AF because of their favorable pharmacokinetic profile and lack of routine monitoring requirements. However, their use becomes more challenging in patients at high risk for GI bleeding, particularly those aged 75 years or older.⁶ Previous case reports have described similar clinical dilemmas involving significant GI bleeding in patients with AF receiving DOAC therapy. In some cases, clinicians have favored warfarin because of INR-based monitoring and evidence suggesting a higher incidence of GI bleeding with DOACs compared with warfarin among older adults.⁷, ⁸ Overall, even in patients at elevated bleeding risk, DOAC therapy has been associated with improved outcomes and reduced stroke incidence; however, it should only be used with caution.⁹ Future research should assess shared decision-making models in patients with competing thrombotic and bleeding risks, particularly those requiring antiplatelet and/or anticoagulation therapy. Additionally, studies should focus on developing patient-centered risk stratification tools to guide antithrombotic therapy in patients with a history of bleeding.

Summary
This case illustrates the complexity of managing patients with both high thromboembolic risk and substantial bleeding risk. It also highlights the importance of joint decision-making among subspecialists and the patient, as the relative contributions of AF, PFO, and aortic plaque to stroke risk may evolve over time. Shared decision-making can be dynamic and requires ongoing reassessment as stroke and bleeding risks change. This approach can help reconcile differing multidisciplinary recommendations while underscoring the central role of the patient in developing an individualized and optimal management strategy. 

Acknowledgement. Presented as a poster finalist at the American College of Physicians National Medical Student Clinical Vignette Competition on April 18, 2026, in San Francisco, California.

Disclosures: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest, and have no conflicts of interest to report. 

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