Biomarker Profiles in Heart Failure Patients With Preserved and Reduced Ejection Fraction.
Biomarker Profiles in Heart Failure Patients With Preserved and Reduced Ejection Fraction.
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心力衰竭患者的生物标志物谱保留和减少射血分数。
DOI：
10.1161/jaha.116.003989
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发表时间：
2017-03-30
影响因子：
5.4
通讯作者：
Voors AA
中科院分区：
文献类型：
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作者：
Tromp J;Khan MA;Klip IT;Meyer S;de Boer RA;Jaarsma T;Hillege H;van Veldhuisen DJ;van der Meer P;Voors AA
生物标志物可以帮助我们阐明射血分数降低（HFrEF）和射血分数保持（HFpEF）的心力衰竭（HF）患者之间的潜在病理生理学差异。因此，我们比较了生物标志物谱，以表征HFrEF和HFpEF患者之间的病理生理学差异。我们回顾性分析了460例HF患者（21%HFpEF，左心室射血分数≥45%）因急性HF住院后出院时测量的33种不同病理生理学领域（炎症、氧化应激、重塑、心脏牵张、血管生成、动脉硬化和肾功能）的生物标志物。在HFrEF和HFpEF患者之间比较了这些标志物与18个月时全因死亡和/或HF相关再住院发生率之间的相关性。患者年龄为70.6±11.4岁，37.4%为女性。HFpEF患者年龄较大，多为女性，收缩压较高。HFpEF患者的超敏C反应蛋白水平显著较高，而HFrEF患者的心房型利钠肽前体和N末端脑利钠肽前体水平较高。线性回归和网络分析显示HFpEF中存在显著的炎症和血管生成相关相互作用，HFrEF中主要存在心脏牵张相关相互作用。血管生成特异性标志物神经纤毛蛋白和重塑特异性标志物骨桥蛋白可预测HFpEF患者18个月时的全因死亡率和/或HF相关再住院率，但在HFrEF患者中不可预测（相互作用P <0.05）。在HFpEF中，主要观察到炎症和血管生成介导的相互作用，而在HFrEF中发现拉伸介导的相互作用。重塑标志物骨桥蛋白和血管生成标志物神经毡蛋白可预测HFpEF的结果，但不能预测HFrEF的结果。
Biomarkers may help us to unravel differences in the underlying pathophysiology between heart failure (HF) patients with a reduced ejection fraction (HFrEF) and a preserved ejection fraction (HFpEF). Therefore, we compared biomarker profiles to characterize pathophysiological differences between patients with HFrEF and HFpEF. We retrospectively analyzed 33 biomarkers from different pathophysiological domains (inflammation, oxidative stress, remodeling, cardiac stretch, angiogenesis, arteriosclerosis, and renal function) in 460 HF patients (21% HFpEF, left ventricular ejection fraction ≥45%) measured at discharge after hospitalization for acute HF. The association between these markers and the occurrence of all‐cause mortality and/or HF‐related rehospitalizations at 18 months was compared between patients with HFrEF and HFpEF. Patients were 70.6±11.4 years old and 37.4% were female. Patients with HFpEF were older, more often female, and had a higher systolic blood pressure. Levels of high‐sensitive C‐reactive protein were significantly higher in HFpEF, while levels of pro‐atrial‐type natriuretic peptide and N‐terminal pro‐brain natriuretic peptide were higher in HFrEF. Linear regression followed by network analyses revealed prominent inflammation and angiogenesis‐associated interactions in HFpEF and mainly cardiac stretch–associated interactions in HFrEF. The angiogenesis‐specific marker, neuropilin and the remodeling‐specific marker, osteopontin were predictive for all‐cause mortality and/or HF‐related rehospitalizations at 18 months in HFpEF, but not in HFrEF (P for interaction <0.05). In HFpEF, inflammation and angiogenesis‐mediated interactions are predominantly observed, while stretch‐mediated interactions are found in HFrEF. The remodeling marker osteopontin and the angiogenesis marker neuropilin predicted outcome in HFpEF, but not in HFrEF.