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Clinical Trial
. 2023 Mar 17;119(1):e111-e114.
doi: 10.1093/cvr/cvac196.

Factor XIa inhibition in atrial fibrillation: insights and knowledge gaps emerging from the PACIFIC-AF trial

Sandro Ninni  1   2 , Stanley Nattel  1   3   4   5
Affiliations
Clinical Trial

Factor XIa inhibition in atrial fibrillation: insights and knowledge gaps emerging from the PACIFIC-AF trial

Sandro Ninni et al. Cardiovasc Res. .
No abstract available

Keywords: Anticoagulants; Atrial fibrillation; Blood coagulation; Factor XI; Stroke.

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Conflict of interest statement

Conflict of interest: Sa.Ni. is a speaker for BMS/Pfizer and Bayer. St.Na. is a consultant for LQT Therapeutics and Glasco Smith Klein.

Figures

Figure 1
Figure 1
A schematic representation of haemostasis and thrombosis processes in relation to current knowledge regarding anticoagulant drugs in patients with AF. Endothelial injury leads to haemostasis activation involving the extrinsic pathway, following tissue factor release and Factor VII activation. Thrombin and various molecular patterns (DNA, neutrophil extracellular traps, and collagen or polyphosphate groups) lead to the activation of the intrinsic pathway. FXIa is an important component of the intrinsic pathway. FXIa also leads to the generation of chemerin, potentially involved in the inflammatory response. Large-scale studies have demonstrated at least equivalent efficiency for stroke prevention and reduced bleeding risk with DOACs, compared with VKA. Early stage clinical trial studies suggest that FXIa inhibitors have lower bleeding risks than DOACs. The impact of FXIa inhibition on stroke prevention is currently under investigation. DOACs, direct-acting oral anticoagulants; FXI-LICA, Factor XI ligand-conjugated antisense; VKA, vitamin K antagonists.
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