Heart rhythm · 2026
Concussion AF trial: Longitudinal assessment of brain injury biomarkers and cognitive decline in elderly patients with atrial fibrillation.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Bunch T Jared, May Heidi T, Muhlestein Joseph B, Anderson Jeffrey L, Le Viet, Woller Scott C, Cutler Michael J, Mahajan Rajiv, Targueta Gabriel P, Gurol M Edip, Knowlton Kirk
Аннотация
BACKGROUND: Atrial fibrillation (AF) is associated with cognitive impairment. Serum biomarkers to detect subclinical brain injury or predict dementia in patients with anticoagulated AF are understudied.
OBJECTIVE: This study aimed to quantify neural injury biomarkers and assess their ability to predict incident dementia or moderate cognitive decline in patients with AF.
METHODS: Prospective longitudinal study of 120 patients with AF (mean age 71.1 ± 10.7 years; 62.5% male) without baseline dementia. Assessments at baseline and at 6, 12, and 24 months (60% completed all visits). Cognitive and functional measures included the Mini-Mental State Examination (MMSE), the 11-item cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog11), the Disability Assessment for Dementia, and quality-of-life measures. Serum biomarkers measured were glial fibrillary acidic protein, neuron-specific enolase (NSE), tau, S100 calcium-binding protein B (S100B), and spectrin N-terminal fragment (SNT145). The primary endpoint was incident dementia (MMSE score <24 with memory-related quality-of-life impact). The secondary endpoint was moderate cognitive decline defined as >30% worsening in ADAS-cog11 or >30% decline in the Disability Assessment for Dementia.
RESULTS: Comorbidities were common: hypertension 64.2%, heart failure 23%, diabetes 16%, and sleep apnea 30.8%; 2 had previous stroke. No participants met the criteria for incident dementia; 3 had an MMSE score of <24 without quality-of-life impact. At 24 months, 9 of 72 (12.5%) exhibited moderate cognitive decline by ADAS-cog11. Biomarkers indicated chronic subclinical stress rather than acute injury: S100B was persistently elevated (baseline 0.18 ± 0.23; 24 months 0.18 ± 0.19 pg/mL). SNT145 was elevated (baseline 2.85 ± 3.73; 24 months 2.36 ± 1.86 ng/mL). NSE and tau remained within normal ranges; inflammatory markers were persistently elevated. Changes in biomarker levels did not correlate with cognitive decline.
CONCLUSION: Over 2 years, dementia incidence was low but 12.5% experienced moderate cognitive decline. Persistent elevations of S100B and SNT145 suggest ongoing subclinical brain injury in patients with anticoagulated AF without acute spikes in traditional stroke markers such as NSE.
OBJECTIVE: This study aimed to quantify neural injury biomarkers and assess their ability to predict incident dementia or moderate cognitive decline in patients with AF.
METHODS: Prospective longitudinal study of 120 patients with AF (mean age 71.1 ± 10.7 years; 62.5% male) without baseline dementia. Assessments at baseline and at 6, 12, and 24 months (60% completed all visits). Cognitive and functional measures included the Mini-Mental State Examination (MMSE), the 11-item cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog11), the Disability Assessment for Dementia, and quality-of-life measures. Serum biomarkers measured were glial fibrillary acidic protein, neuron-specific enolase (NSE), tau, S100 calcium-binding protein B (S100B), and spectrin N-terminal fragment (SNT145). The primary endpoint was incident dementia (MMSE score <24 with memory-related quality-of-life impact). The secondary endpoint was moderate cognitive decline defined as >30% worsening in ADAS-cog11 or >30% decline in the Disability Assessment for Dementia.
RESULTS: Comorbidities were common: hypertension 64.2%, heart failure 23%, diabetes 16%, and sleep apnea 30.8%; 2 had previous stroke. No participants met the criteria for incident dementia; 3 had an MMSE score of <24 without quality-of-life impact. At 24 months, 9 of 72 (12.5%) exhibited moderate cognitive decline by ADAS-cog11. Biomarkers indicated chronic subclinical stress rather than acute injury: S100B was persistently elevated (baseline 0.18 ± 0.23; 24 months 0.18 ± 0.19 pg/mL). SNT145 was elevated (baseline 2.85 ± 3.73; 24 months 2.36 ± 1.86 ng/mL). NSE and tau remained within normal ranges; inflammatory markers were persistently elevated. Changes in biomarker levels did not correlate with cognitive decline.
CONCLUSION: Over 2 years, dementia incidence was low but 12.5% experienced moderate cognitive decline. Persistent elevations of S100B and SNT145 suggest ongoing subclinical brain injury in patients with anticoagulated AF without acute spikes in traditional stroke markers such as NSE.