Abstract:

Objective To study the relationship between anticoagulant therapy and concentration changesof T⁃tau protein and Aβ1⁃42 in plasma neurogenic exosomes in patients with permanent atrial fibrillation（AF），and then to evaluate the effect of anticoagulant therapy on cognitive function in AF patients. Methods A total of140 permanent AF patients aged 50 ~ 75 without previous cerebrovascular events were enrolled in this study. Theywere divided into two groups according to whether anticoagulant therapy was performed，40 patients in anticoagulantgroup and 100 patients in non⁃anticoagulant group. We used Mini Mental State Examination（MMSE）to assess thecognitive function of all participants. Logistic regression analysis was used to explore the effect of anticoagulanttherapy on cognitive function in patients with AF. We collected fasting venous blood from all subjects and enrichedneuronal⁃derived exosomes by immunoprecipitation，then confirmed exosomes by transmission electron microscopeand western blot. Quantitative analysis of T⁃tau protein and Aβ1⁃42 in exosomes was conducted by ELISA. Thedifference of protein concentration in neurogenic exosomes between the two groups was tested. Results Afteradjustment for demographic characteristics and comorbid conditions，non⁃anticoagulant therapy in patients with AFwas significantly associated with CI（OR = 5.024，95%CI：1.584 ~ 15.936，P < 0.01）. The cognitive impairment ofpatients with AF in non⁃anticoagulant group was significantly severer than that in anticoagulant group（P < 0.001）.The concentration of T⁃tau protein and Aβ1⁃42 in plasma neuronal⁃derived exosomes in non⁃anticoagulant group（221.75 ± 54.34 pg/mL and 3.97 ± 1.20 pg/mL）was significantly higher than that in anticoagulant group（183.02± 46.84 pg/mL and 3.09 ± 0.79 pg/mL）（P < 0.001）. Conclusion Anticoagulant therapy is a protective factor forcognitive function in patients with permanent AF and delays the growth of markers related to cognitive impairment.

Key words:

permanent atrial fibrillation, neuronal?derived exosomes, cognitive impairment, antico?agulant therapy, T?tau, Aβ1?42