INSERM, Centre d'Investigations Cliniques Plurithématique 1433, F-CRIN INI-CRCT, INSERM U1116, Université de Lorraine, CHRU de Nancy, Nancy, France.
Cardiovascular Research and Development Unit, Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal.
Clin Res Cardiol. 2018 Jan;107(1):49-59. doi: 10.1007/s00392-017-1157-3. Epub 2017 Aug 29.
Aldosterone stimulates cardiac collagen synthesis. Circulating biomarkers of collagen turnover provide a useful tool for the assessment of cardiac remodeling in patients with an acute myocardial infarction (MI).
The REMINDER trial assessed the effect of eplerenone in patients with an acute ST-elevation Myocardial Infarction (STEMI) without known heart failure (HF), when initiated within 24 h of symptom onset. The primary outcome was almost totally (>90%) driven by natriuretic peptide (NP) thresholds after 1-month post-MI (it also included a composite of cardiovascular death or re-hospitalization or new onset HF or sustained ventricular tachycardia or fibrillation or LVEF ≤40% after 1-month post-MI). This secondary analysis aims to assess the extracellular matrix marker (ECMM) levels with regards to: (1) patients` characteristics; (2) determinants; (3) and eplerenone effect.
Serum levels of ECMM were measured in 526 (52%) of the 1012 patients enrolled in the REMINDER trial. Patients with procollagen type III N-terminal propeptide (PIIINP) above the median were older and had worse renal function (p < 0.05). Worse renal function was associated with increased levels of PIIINP (standardized β ≈ 0.20, p < 0.05). Eplerenone reduced PIIINP when the levels of this biomarker were above the median of 3.9 ng/mL (0.13 ± 1.48 vs. -0.37 ± 1.56 ng/mL, p = 0.008). Higher levels of PIIINP were independently associated with higher proportion of NP above the prespecified thresholds (HR = 1.95, 95% CI 1.16-3.29, p = 0.012).
Eplerenone effectively reduces PIIINP levels when baseline values were above the median. Eplerenone may limit ECMM formation in post-MI without HF.
醛固酮可刺激心肌胶原合成。胶原代谢的循环生物标志物为评估急性心肌梗死(MI)患者的心脏重构提供了有用的工具。
REMDINER 试验评估了依普利酮在急性 ST 段抬高型心肌梗死(STEMI)且无已知心力衰竭(HF)患者中的作用,这些患者在症状发作后 24 小时内开始接受治疗。主要终点几乎完全(>90%)由 MI 后 1 个月时的利钠肽(NP)阈值驱动(该终点也包括 MI 后 1 个月时心血管死亡或再住院或新发 HF 或持续性室性心动过速或心室颤动或 LVEF≤40%的复合终点)。这项次要分析旨在评估细胞外基质标志物(ECMM)水平与以下方面的关系:(1)患者特征;(2)决定因素;(3)依普利酮的作用。
在 REMDINER 试验中,共纳入了 1012 例患者,其中 526 例(52%)患者检测了血清 ECMM 水平。与中位数以上的患者相比,前胶原 III 型 N 端前肽(PIIINP)水平较高的患者年龄较大且肾功能更差(p<0.05)。肾功能更差与 PIIINP 水平升高相关(标准化β≈0.20,p<0.05)。当该生物标志物水平高于 3.9ng/ml 的中位数时,依普利酮降低了 PIIINP(0.13±1.48 vs.-0.37±1.56ng/ml,p=0.008)。较高的 PIIINP 水平与 NP 高于预设阈值的比例更高独立相关(HR=1.95,95%CI 1.16-3.29,p=0.012)。
当基线值高于中位数时,依普利酮可有效降低 PIIINP 水平。在无 HF 的 MI 后,依普利酮可能限制 ECMM 的形成。