Eyyupkoca Ferhat, Sabanoglu Cengiz, Altintas Mehmet Sait, Kocak Ajar, Ercan Karabekir, Eyerci Nilnur, Okutucu Sercan
Department of Cardiology, Dr. Nafiz Korez Sincan State Hospital, Ankara, Turkey.
Department of Cardiology, Kirikkale High Specialization Hospital, Kirikkale, Turkey.
Postepy Kardiol Interwencyjnej. 2021 Dec;17(4):356-365. doi: 10.5114/aic.2021.111967. Epub 2021 Dec 28.
It is known that the levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK/TNFSF12) increase after myocardial infarction (MI) and that it interacts with sCD163. It has also been argued that TWEAK can induce matrix metalloproteinases (MMPs) in macrophages.
To investigate the roles of TWEAK, sCD163, and MMPs in left ventricular (LV) adverse remodeling (AR) in the early post-MI period.
Forty-six patients with ST-elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention were enrolled in the study. Post-MI LV functions and volumes were assessed by cardiac magnetic resonance imaging at 2 weeks and 6 months. Cytokines and MMPs were measured using a bead-based multiplex immunoassay system at 1 day (baseline) and 2 weeks post-MI. AR was defined as an increase in LV end-diastolic volume of ≥ 10% at the 6-month follow up.
The TWEAK, MMP-2, and MMP-3 baseline levels were higher in the patients with AR than those without AR. At 2 weeks post-MI, these expression levels were similar in patients with and without AR, but sCD163 expression was increased in patients without AR. The TWEAK and MMP levels were positively correlated in the early period post-MI. At first day post-MI, higher levels of TWEAK and MMP-3 were predictors of AR (OR = 1.03, = 0.006; OR = 1.08, = 0.015; respectively).
TWEAK can induce MMPs in the early period post-MI, and these higher levels contribute to development of AR. Increased sCD163 levels at 2 weeks post-MI seem to be associated with the healing process through neutralizing the excessive inflammatory effects of TWEAK.
已知心肌梗死（MI）后肿瘤坏死因子样凋亡弱诱导因子（TWEAK/TNFSF12）水平会升高，且它与可溶性CD163（sCD163）相互作用。也有人认为TWEAK可诱导巨噬细胞中的基质金属蛋白酶（MMPs）。
研究TWEAK、sCD163和MMPs在心肌梗死后早期左心室（LV）不良重构（AR）中的作用。
46例行直接经皮冠状动脉介入治疗的ST段抬高型心肌梗死（STEMI）患者纳入本研究。在2周和6个月时通过心脏磁共振成像评估心肌梗死后左心室功能和容积。在心肌梗死后1天（基线）和2周时使用基于微珠的多重免疫分析系统测量细胞因子和MMPs。AR定义为在6个月随访时左心室舒张末期容积增加≥10%。
发生AR的患者中TWEAK、MMP-2和MMP-3的基线水平高于未发生AR的患者。在心肌梗死后2周，发生AR和未发生AR的患者中这些表达水平相似，但未发生AR的患者中sCD163表达增加。在心肌梗死后早期，TWEAK和MMP水平呈正相关。在心肌梗死后第1天，较高水平的TWEAK和MMP-3是AR的预测指标（分别为OR = 1.03，P = 0.006；OR = 1.08，P = 0.015）。
TWEAK可在心肌梗死后早期诱导MMPs，这些较高水平促成AR的发展。心肌梗死后2周sCD163水平升高似乎与通过中和TWEAK的过度炎症作用的愈合过程相关。
