The Johns Hopkins University School of Medicine Baltimore MD.
University of Mississippi Medical Center Jackson MS.
J Am Heart Assoc. 2020 Dec 15;9(24):e018399. doi: 10.1161/JAHA.120.018399. Epub 2020 Dec 8.
Background Atrial fibrillation (AF) is a risk factor for cognitive decline, possibly from silent brain infarction. Left atrial changes in structure or function (atrial cardiopathy) can lead to AF but may impact cognition independently. It is unknown if AF or atrial cardiopathy also acts on Alzheimer disease-specific mechanisms, such as deposition of β-amyloid. Methods and Results A total of 316 dementia-free participants from the ARIC (Atherosclerosis Risk in Communities) study underwent florbetapir positron emission tomography, electrocardiography, and 2-dimensional echocardiography. Atrial cardiopathy was defined as ≥1: (1) left atrial volume index >34 mL/m; (2) P-wave terminal force >5000 µV×ms; and (3) serum NT-proBNP (N-terminal pro-B-type natriuretic peptide) >250 pg/mL. Cross-sectional associations between global cortical β-amyloid (>1.2 standardized uptake value ratio) and adjudicated history of AF and atrial cardiopathy, each, were evaluated using multivariable logistic regression. Participants (mean age, 76 years) were 56% women and 42% Black individuals. Odds of elevated florbetapir standardized uptake value ratio were significantly increased among those with atrial cardiopathy (odds ratio, 1.81; 95% CI, 1.02-3.22) and doubled for those with enlarged left atrial volume index after adjustment for demographics/risk factors (95% CI, 1.04-4.61). There was no association between P-wave terminal force or NT-proBNP and elevated florbetapir standardized uptake value ratio, nor between AF and elevated standardized uptake value ratio. Conclusions Among healthy, nondemented community-dwelling older individuals, we report an association between atrial cardiopathy, left atrial volume index, and elevated brain amyloid, by positron emission tomography, without a similar association in individuals with AF. Potential limitations include reverse causation and survival bias. Ongoing work will help determine if changes in cardiac structure and function precede or occur simultaneously with amyloid deposition.
心房颤动（AF）是认知能力下降的一个危险因素，可能是由于无症状性脑梗死引起的。左心房结构或功能的改变（心房心肌病）可导致 AF，但也可能独立影响认知。目前尚不清楚 AF 或心房心肌病是否也作用于阿尔茨海默病特有的机制，如β-淀粉样蛋白的沉积。
共有 316 名来自 ARIC（社区动脉粥样硬化风险）研究的无痴呆参与者接受了氟代多巴正电子发射断层扫描、心电图和二维超声心动图检查。心房心肌病定义为≥1：（1）左心房容积指数>34 mL/m；（2）P 波终末电势>5000 µV×ms；（3）血清 NT-proBNP（N 端脑利钠肽前体）>250 pg/mL。使用多变量逻辑回归评估全局皮质β-淀粉样蛋白（>1.2 标准化摄取值比）与经裁决的 AF 和心房心肌病病史之间的横断面相关性。参与者（平均年龄 76 岁）中 56%为女性，42%为黑人。在调整了人口统计学/危险因素后，与心房心肌病（优势比，1.81；95%CI，1.02-3.22）和左心房容积指数增大（95%CI，1.04-4.61）相关的高氟代多巴标准化摄取值比的几率显著增加。P 波终末电势或 NT-proBNP 与高氟代多巴标准化摄取值比之间没有关联，AF 与高标准化摄取值比之间也没有关联。
在健康、无痴呆的社区居住的老年人中，我们报告了心房心肌病、左心房容积指数与正电子发射断层扫描显示的脑淀粉样蛋白升高之间的关联，而在 AF 患者中没有发现这种关联。潜在的局限性包括反向因果关系和生存偏差。正在进行的研究将有助于确定心脏结构和功能的变化是先于还是同时发生淀粉样蛋白沉积。
