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Acute stroke is one of the leading causes of mortality worldwide, with venous thromboembolism (VTE) representing a significant yet under-recognized complication. The risk of VTE is highest in the early post-stroke period, driven by factors encapsulated by Virchow’s triad. However, the risk of haemorrhagic transformation following ischaemic stroke, and haematoma development and expansion after haemorrhagic stroke complicate the routine use of pharmacological VTE prophylaxis. In this review, we discuss the epidemiology and aetiology of VTE post-stroke, haemorrhagic transformation after acute ischaemic events, and the available evidence supporting mechanical and pharmacological approaches to VTE prophylaxis in these patients. Finally, we discuss the recommendations provided by the current international consensus guidelines and reasons underpinning the heterogenous management of patients in routine clinical practice, including the need for well-designed, large-scale clinical trials to better define thromboprophylaxis strategies for patients following acute stroke. [Display omitted]

In this audio interview, Editor-in-Chief Eric Rubin and Deputy Editor Jane Leopold discuss research being presented at the 2024 European Society of Cardiology annual meeting. . . .

In patients with subdural hematoma and an indication for surgical evacuation, middle meningeal artery embolization plus surgery led to a lower risk of reoperation for recurrence or progression within 90 days than surgery alone.

Venous thromboembolism (VTE) is a serious and often fatal medical condition with an increasing incidence. The treatment of VTE is undergoing tremendous changes with the introduction of the new direct oral anticoagulants and clinicians need to understand new treatment paradigms. This article, initiated by the Anticoagulation Forum, provides clinical guidance based on existing guidelines and consensus expert opinion where guidelines are lacking. Well-managed warfarin therapy remains an important anticoagulant option and it is hoped that anticoagulation providers will find the guidance contained in this article increases their ability to achieve optimal outcomes for their patients with VTE Pivotal practical questions pertaining to this topic were developed by consensus of the authors and were derived from evidence-based consensus statements whenever possible. The medical literature was reviewed and summarized using guidance statements that reflect the consensus opinion(s) of all authors and the endorsement of the Anticoagulation Forum’s Board of Directors. In an effort to provide practical and implementable information about VTE and its treatment, guidance statements pertaining to choosing good candidates for warfarin therapy, warfarin initiation, optimizing warfarin control, invasive procedure management, excessive anticoagulation, subtherapeutic anticoagulation, drug interactions, switching between anticoagulants, and care transitions are provided.

In a large trial, the estimated incidence of stroke, systemic embolism, hemorrhage, or death was 2.8 percentage points lower to 0.5 percentage points higher with early than with later use of direct oral anticoagulants.

A randomized trial of the factor XIa inhibitor asundexian was stopped early owing to a higher incidence of stroke or systemic embolism than with apixaban therapy among patients with atrial fibrillation.

VITT is caused by antibodies to PF4 that recognize the heparin-binding site. Thrombocytopenia and thrombosis associated with VITT-like antibody specificity developed in a child and an adult after adenovirus infection.

In a trial in patients with pelvic or acetabular fractures or extremity fractures that were treated operatively, aspirin thromboprophylaxis was noninferior to low-molecular-weight heparin in preventing death at 90 days.

Abelacimab is a fully human monoclonal antibody that binds to the inactive form of factor XI and blocks its activation. The safety of abelacimab as compared with a direct oral anticoagulant in patients with atrial fibrillation is unknown. Patients with atrial fibrillation and a moderate-to-high risk of stroke were randomly assigned, in a 1:1:1 ratio, to receive subcutaneous injection of abelacimab (150 mg or 90 mg once monthly) administered in a blinded fashion or oral rivaroxaban (20 mg once daily) administered in an open-label fashion. The primary end point was major or clinically relevant nonmajor bleeding. A total of 1287 patients underwent randomization; the median age was 74 years, and 44% were women. At 3 months, the median reduction in free factor XI levels with abelacimab at a dose of 150 mg was 99% (interquartile range, 98 to 99) and with abelacimab at a dose of 90 mg was 97% (interquartile range, 51 to 99). The trial was stopped early on the recommendation of the independent data monitoring committee because of a greater-than-anticipated reduction in bleeding events with abelacimab. The incidence rate of major or clinically relevant nonmajor bleeding was 3.2 events per 100 person-years with 150-mg abelacimab and 2.6 events per 100 person-years with 90-mg abelacimab, as compared with 8.4 events per 100 person-years with rivaroxaban (hazard ratio for 150-mg abelacimab vs. rivaroxaban, 0.38 [95% confidence interval {CI}, 0.24 to 0.60]; hazard ratio for 90-mg abelacimab vs. rivaroxaban, 0.31 [95% CI, 0.19 to 0.51]; P<0.001 for both comparisons). The incidence and severity of adverse events appeared to be similar in the three groups. Among patients with atrial fibrillation who were at moderate-to-high risk for stroke, treatment with abelacimab resulted in markedly lower levels of free factor XI and fewer bleeding events than treatment with rivaroxaban. (Funded by Anthos Therapeutics; AZALEA-TIMI 71 ClinicalTrials.gov number, NCT04755283.).

In this audio interview, Editor-in-Chief Eric Rubin and Deputy Editor Jane Leopold discuss research being presented at the 2024 European Society of Cardiology annual meeting. . . .