Kidney Research Institute Department of Medicine University of Washington Seattle WA.
Division of Cardiology Department of Medicine University of Washington Seattle WA.
J Am Heart Assoc. 2019 Aug 6;8(15):e012200. doi: 10.1161/JAHA.119.012200. Epub 2019 Aug 5.
Background We tested associations of cardiac biomarkers of myocardial stretch, injury, inflammation, and fibrosis with the risk of incident atrial fibrillation (AF) in a prospective study of chronic kidney disease patients. Methods and Results The study sample was 3053 participants with chronic kidney disease in the multicenter CRIC (Chronic Renal Insufficiency Cohort) study who were not identified as having AF at baseline. Cardiac biomarkers, measured at baseline, were NT-proBNP (N-terminal pro-B-type natriuretic peptide), high-sensitivity troponin T, galectin-3, growth differentiation factor-15, and soluble ST-2. Incident AF ("AF event") was defined as a hospitalization for AF. During a median follow-up of 8 years, 279 (9%) participants developed a new AF event. In adjusted models, higher baseline log-transformed NT-proBNP (N-terminal pro-B-type natriuretic peptide) was associated with incident AF (adjusted hazard ratio [HR] per SD higher concentration: 2.11; 95% CI, 1.75, 2.55), as was log-high-sensitivity troponin T (HR 1.42; 95% CI, 1.20, 1.68). These associations showed a dose-response relationship in categorical analyses. Although log-soluble ST-2 was associated with AF risk in continuous models (HR per SD higher concentration 1.35; 95% CI, 1.16, 1.58), this association was not consistent in categorical analyses. Log-galectin-3 (HR 1.05; 95% CI, 0.91, 1.22) and log-growth differentiation factor-15 (HR 1.16; 95% CI, 0.96, 1.40) were not significantly associated with incident AF. Conclusions We found strong associations between higher NT-proBNP (N-terminal pro-B-type natriuretic peptide) and high-sensitivity troponin T concentrations, and the risk of incident AF in a large cohort of participants with chronic kidney disease. Increased atrial myocardial stretch and myocardial cell injury may be implicated in the high burden of AF in patients with chronic kidney disease.
我们在一项针对慢性肾脏病患者的前瞻性研究中,检测了心肌拉伸、损伤、炎症和纤维化的心脏生物标志物与新发心房颤动(AF)风险之间的关联。
研究样本为 CRIC(慢性肾功能不全队列)研究中的 3053 名慢性肾脏病患者,他们在基线时未被诊断为 AF。基线时测量的心脏生物标志物包括 NT-proBNP(氨基末端 B 型利钠肽前体)、高敏肌钙蛋白 T、半乳糖凝集素-3、生长分化因子-15 和可溶性 ST-2。新发 AF(“AF 事件”)定义为 AF 住院。在中位随访 8 年后,279(9%)名参与者发生新的 AF 事件。在调整后的模型中,较高的基线 log 转化 NT-proBNP(氨基末端 B 型利钠肽前体)与新发 AF 相关(每增加一个标准差的调整后 HR:2.11;95%CI,1.75,2.55),log 高敏肌钙蛋白 T 也是如此(HR 1.42;95%CI,1.20,1.68)。在分类分析中,这些关联呈剂量-反应关系。尽管可溶性 ST-2 在连续模型中与 AF 风险相关(每增加一个标准差的 HR:1.35;95%CI,1.16,1.58),但在分类分析中并不一致。log 半乳糖凝集素-3(HR 1.05;95%CI,0.91,1.22)和 log 生长分化因子-15(HR 1.16;95%CI,0.96,1.40)与新发 AF 无显著相关性。
在一个大型慢性肾脏病患者队列中,我们发现较高的 NT-proBNP(氨基末端 B 型利钠肽前体)和高敏肌钙蛋白 T 浓度与新发 AF 风险之间存在很强的关联。增加的心房心肌拉伸和心肌细胞损伤可能与慢性肾脏病患者 AF 负担增加有关。