Wyderka Rafał, Ołpińska Bogusława, Diakowska Dorota, Leśków Anna, Osuch Łukasz, Borger Michał, Brzezińska Barbara, Łoboz-Rudnicka Maria, Jaroch Joanna
Department of Cardiology, Tadeusz Marciniak Lower Silesia Specialist Hospital-Emergency Medicine Center, Wroclaw, Poland.
Faculty of Medicine, Wroclaw University of Science and Technology, Wroclaw, Poland.
Vasc Health Risk Manag. 2025 Apr 24;21:279-291. doi: 10.2147/VHRM.S507783. eCollection 2025.
Despite a growing evidence from the animal models of the cardioprotective function of the apelinergic system in the setting of myocardial infarction, little is known on the role of apelinergic system in the development of post- infarction adverse left ventricle remodeling in humans.
The study group consisted of 49 patients with first-time ST-segment elevation myocardial infarction of anterior wall treated invasively. Echocardiography was performed on index hospitalization and on one-year check-up, with categorizing the study population into group with adverse LV remodeling defined as an increase of LV end diastolic volume by >20% (n = 12) and the group without adverse remodeling (n = 29). ELA, AP-17, AP-13 and APJ receptor levels were measured on one-year follow-up.
Patients with adverse LV remodeling presented significantly higher plasma level of apelin-13 (85.63 [75.43-96.13] vs 65.43 [57.35-69.35], p = 0.001) and apelin-17 (69.36 [42.61-77.04] vs 30.04 [25.97-41.95], p = 0.004). In a univariable logistic regression analysis, higher LVEDV and LVEDV1, higher LVESV and LVESVi, lower LVEF, higher WMSI score, higher SYNTAX score, higher levels of hs-CRP during index hospitalization and higher levels of AP-13 and AP-17 on the one-year check-up were associated with adverse LV remodeling. In multivariable logistic regression analysis, only AP-17 level was independently associated with adverse LV remodeling (p = 0.050).
Apelinergic system may be involved in the development of post- infarction adverse left ventricle remodeling.
尽管动物模型中越来越多的证据表明阿片肽系统在心肌梗死情况下具有心脏保护功能，但关于阿片肽系统在人类心肌梗死后不良左心室重构发展中的作用知之甚少。
研究组由49例接受侵入性治疗的首次前壁ST段抬高型心肌梗死患者组成。在入院时和一年随访时进行超声心动图检查，将研究人群分为不良左心室重构组（定义为左心室舒张末期容积增加>20%，n = 12）和无不良重构组（n = 29）。在一年随访时测量ELA、AP-17、AP-13和APJ受体水平。
不良左心室重构患者的血浆阿片肽-13水平（85.63 [75.43 - 96.13] 对 65.43 [57.35 - 69.35]，p = 0.001）和阿片肽-17水平（69.36 [42.61 - 77.04] 对 30.04 [25.97 - 41.95]，p = 0.004）显著更高。在单变量逻辑回归分析中，较高的左心室舒张末期容积和左心室舒张末期容积指数、较高的左心室收缩末期容积和左心室收缩末期容积指数、较低的左心室射血分数、较高的室壁运动记分指数、较高的SYNTAX评分、入院时较高的hs-CRP水平以及一年随访时较高的AP-13和AP-17水平与不良左心室重构相关。在多变量逻辑回归分析中，只有AP-17水平与不良左心室重构独立相关（p = 0.050）。
阿片肽系统可能参与心肌梗死后不良左心室重构的发展。
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