Hooman Kamel, Mitchell Sv Elkind, Richard A Kronmal, W T Longstreth, Pamela Plummer, Rebeca Aragon Garcia, Joseph P Broderick, Qi Pauls, Jordan J Elm, Fadi Nahab, L Scott Janis, Marco R Di Tullio, Elsayed Z Soliman, Jeff S Healey, David L Tirschwell
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We examined the relationship between biomarker levels and subsequent detection of AF, the hallmark of atrial cardiopathy.</p><p><strong>Methods: </strong>Patients were randomized if they met criteria for atrial cardiopathy, defined as P-wave terminal force >5000 μV*ms in ECG lead V<sub>1</sub> (PTFV<sub>1</sub>), NT-proBNP >250 pg/mL, or left atrial diameter index (LADI) ⩾3 cm/m<sup>2</sup>. For this analysis, the outcome was AF detected per routine care.</p><p><strong>Results: </strong>Of 3745 patients who consented to screening for atrial cardiopathy, 254 were subsequently diagnosed with AF; 96 before they could be randomized and 158 after randomization. In unadjusted analyses, ln(NT-proBNP) (RR per SD, 1.99; 95% CI, 1.85-2.13), PTFV<sub>1</sub> (RR per SD, 1.15; 95% CI, 1.03-1.28) and LADI (RR per SD, 1.34; 95% CI, 1.20-1.50) were associated with AF. In a model containing all 3 biomarkers, demographics, and AF risk factors, age (RR per 10 years, 1.24; 95% CI, 1.09-1.41), ln(NT-proBNP) (RR per SD, 1.88; 95% CI, 1.67-2.11) and LADI (RR per SD, 1.25; 95% CI, 1.14-1.37) were associated with AF. These three variables together had a c-statistic of 0.82 (95% CI, 0.79-0.85) but only modest calibration. 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引用次数: 0
摘要
背景ARCADIA 比较了阿哌沙班和阿司匹林对隐源性卒中和心房性心脏病患者进行卒中二级预防的效果。中性结果的一个可能原因是所使用的生物标志物不能最佳地识别心房性心脏病。我们研究了生物标志物水平与随后发现房颤（心房颤动的标志）之间的关系：如果患者符合心房性心脏病的标准，即心电图 V1 导联（PTFV1）P 波终末力>5000 μV*ms、NT-proBNP>250 pg/mL，或左心房直径指数（LADI）⩾3 cm/m2，则对其进行随机分组。本次分析的结果是在常规护理中发现房颤：在 3745 名同意接受心房病变筛查的患者中，有 254 人随后被确诊为房颤；其中 96 人在接受随机化之前，158 人在接受随机化之后。在未经调整的分析中，ln(NT-proBNP) (RR per SD, 1.99; 95% CI, 1.85-2.13)、PTFV1 (RR per SD, 1.15; 95% CI, 1.03-1.28)和 LADI (RR per SD, 1.34; 95% CI, 1.20-1.50)与房颤相关。在包含所有三种生物标志物、人口统计学特征和房颤风险因素的模型中，年龄（每 10 年的 RR 值为 1.24；95% CI 为 1.09-1.41）、ln（NT-proBNP）（每 SD 的 RR 值为 1.88；95% CI 为 1.67-2.11）和 LADI（每 SD 的 RR 值为 1.25；95% CI 为 1.14-1.37）与房颤相关。这三个变量加在一起的 c 统计量为 0.82（95% CI，0.79-0.85），但校准度不高。在对符合随机化条件的患者进行的敏感性分析中，对房颤进行更密切随访的识别率有所降低：结论：在 ARCADIA 中用于识别房颤的生物标志物对后续房颤有一定的预测作用。
Atrial cardiopathy biomarkers and atrial fibrillation in the ARCADIA trial.
Background: ARCADIA compared apixaban to aspirin for secondary stroke prevention in patients with cryptogenic stroke and atrial cardiopathy. One possible explanation for the neutral result is that biomarkers used did not optimally identify atrial cardiopathy. We examined the relationship between biomarker levels and subsequent detection of AF, the hallmark of atrial cardiopathy.
Methods: Patients were randomized if they met criteria for atrial cardiopathy, defined as P-wave terminal force >5000 μV*ms in ECG lead V1 (PTFV1), NT-proBNP >250 pg/mL, or left atrial diameter index (LADI) ⩾3 cm/m2. For this analysis, the outcome was AF detected per routine care.
Results: Of 3745 patients who consented to screening for atrial cardiopathy, 254 were subsequently diagnosed with AF; 96 before they could be randomized and 158 after randomization. In unadjusted analyses, ln(NT-proBNP) (RR per SD, 1.99; 95% CI, 1.85-2.13), PTFV1 (RR per SD, 1.15; 95% CI, 1.03-1.28) and LADI (RR per SD, 1.34; 95% CI, 1.20-1.50) were associated with AF. In a model containing all 3 biomarkers, demographics, and AF risk factors, age (RR per 10 years, 1.24; 95% CI, 1.09-1.41), ln(NT-proBNP) (RR per SD, 1.88; 95% CI, 1.67-2.11) and LADI (RR per SD, 1.25; 95% CI, 1.14-1.37) were associated with AF. These three variables together had a c-statistic of 0.82 (95% CI, 0.79-0.85) but only modest calibration. Discrimination was attenuated in sensitivity analyses of patients eligible for randomization who may have been more closely followed for AF.
Conclusions: Biomarkers used to identify atrial cardiopathy in ARCADIA were moderately predictive of subsequent AF.
期刊介绍：
Launched in 2016 the European Stroke Journal (ESJ) is the official journal of the European Stroke Organisation (ESO), a professional non-profit organization with over 1,400 individual members, and affiliations to numerous related national and international societies. ESJ covers clinical stroke research from all fields, including clinical trials, epidemiology, primary and secondary prevention, diagnosis, acute and post-acute management, guidelines, translation of experimental findings into clinical practice, rehabilitation, organisation of stroke care, and societal impact. It is open to authors from all relevant medical and health professions. Article types include review articles, original research, protocols, guidelines, editorials and letters to the Editor. Through ESJ, authors and researchers have gained a new platform for the rapid and professional publication of peer reviewed scientific material of the highest standards; publication in ESJ is highly competitive. The journal and its editorial team has developed excellent cooperation with sister organisations such as the World Stroke Organisation and the International Journal of Stroke, and the American Heart Organization/American Stroke Association and the journal Stroke. ESJ is fully peer-reviewed and is a member of the Committee on Publication Ethics (COPE). Issues are published 4 times a year (March, June, September and December) and articles are published OnlineFirst prior to issue publication.
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