Session: 330. Vascular Biology, Thrombosis, and Thrombotic Microangiopathies: Basic and Translational: Poster I
Hematology Disease Topics & Pathways:
Research, Adult, Translational Research, Study Population, Human
Methods: In this sub-study of RACE V (Reappraisal of Atrial Fibrillation: Interaction between HyperCoagulability, Electrical Remodelling, and Vascular Destabilisation in the Progression of Atrial Fibrillation, NCT02726698) study, 417 patients with PAF were included. At baseline extensive phenotyping was performed including blood samples drawn. During follow-up continuous monitoring for AF progression defined as either development of persistent or permanent AF during follow-up or an increase of >3% AF burden over the first 6 months or total follow-up, was performed for at least one year. Hypercoagulability was monitored through activated coagulation factors (FXIIa, FXIa, FIXa, FXa, pKa and thrombin) in complex with their natural inhibitors (antithrombin (AT), C1-esterase inhibitor (C1Inh), or alpha-1-antitrypsin (a1AT)) utilizing ELISA. Multivariable logistic regression analysis was used for the association of coagulation markers with AF progression.
Results: 51 out of 417 study subjects showed AF progression within the follow-up time period. Patients with AF progression showed significantly lower FXIIa complexes in comparison to patients without AF progression (759 pM [660-879] vs. 886 pM [765-1007]. The activation state of the other coagulation factors showed no statistically significant differences. Multivariate analysis identified that FXIIa complexes (odds ratio [OR] 0.998, 95% confidence intervals [CI] 0.997-0.999, p<.001.) are associated with AF progression. FXIa (OR 0.734, 95%CI 0.521-1.033, p=0.76), FXa (OR 0.532, 95%CI 0.201-1.405, p=0.203), FIXa (OR 1.101, 95%CI 0.789-1.538, p=0.572), thrombin (OR 1.022, 95%CI 0.997-1.048, p=0.086) and kallikrein (OR 0.969, 95%CI 0.903-1.039, p=0.372) showed no relationship with AF-progression.
Conclusion: In patients with PAF FXIIa was inversely related to AF progression. Downstream activation of the intrinsic cascade, however, was not related to AF progression. Whether this means that FXII is over-proportionally auto-activated or has a protective role or in AF-progression needs to be further investigated.
Disclosures: Van Gelder: Dutch Heart foundation, EU Horizon (EHRA-PATHs): Research Funding; Bayer AG, Boston Scientific, Medtronic, Pfizer, Roche Diagnostics: Other, Research Funding; Heart (BMJ group): Other: Associate Editor. Rienstra: Bayer: Consultancy; InCarda Therpeutics: Consultancy.
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