Arrhythmias & electrophysiologyResearch article
Involvement of Btk in Cardiovascular Disease and Its Therapeutic Targeting
- Narrative review
- state-of-the-art review
Authors' conclusion
This review conceptualizes and underscores Btk's pivotal role at immune-thrombosis interfaces in atherothrombosis, advocating for precision medicine approaches and innovative platforms to unlock its full therapeutic potential in cardiovascular disease management.
Main finding
As reported in the abstract
Btk's role in thrombosis and CVD and the therapeutic potential of BTKi (narrative review)
- Patients with X-linked agammaglobulinemia who lack Btk do not have a bleeding diathesis
- In platelets, Btk drives atherothrombosis, venous thrombosis and immunothrombosis without affecting hemostatic platelet functions
- In myeloid cells, Btk amplifies inflammation via NLRP3 inflammasome activation and neutrophil extracellular trap formation
- First-generation Btk inhibitors (BTKi) (ibrutinib) show antithrombotic efficacy but off-target bleeding and AF
- Second- and third-generation inhibitors show enhanced selectivity, reducing CV toxicity in B-cell malignancies
- Highly selective BTKi (fenebrutinib, remibrutinib) show no bleeding in trials of autoimmune disorders
Original publication
Involvement of Btk in Cardiovascular Disease and Its Therapeutic Targeting. Circulation. Published 9 February 2026. doi:10.1161/circulationaha.125.076186
Summarised from the published abstract; every number is checked against it