A Synthetic Non-degradable Polyethylene Glycol Hydrogel Retards Adverse Post-infarct Left Ventricular Remodeling

A Synthetic Non-degradable Polyethylene Glycol Hydrogel Retards Adverse Post-infarct Left Ventricular Remodeling
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DOI:
10.1016/j.cardfail.2009.03.003
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发表时间:
2009-09-01
影响因子:
6
通讯作者:
Davies, Neil
Davies, Neil
中科院分区:
医学2区
文献类型:
--
作者:
Dobner, Stephan;Bezuidenhout, Deon;Davies, Neil

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背景资料:心肌梗死后左室重构是心力衰竭的重要组成部分,长期以来一直认为其可能是室壁应力增加所致。最近有人提出,一种可注射的、不可降解的聚合物可以以类似于心脏支持装置的方式限制病理性重塑。我们已经测试了一种不可降解的聚乙二醇(PEG)凝胶在大鼠infarction model.Methods和结果:永久结扎后,左前降支动脉在雄性Wistar大鼠,PEG凝胶试剂被注射到梗死区域和聚合原位。在4周时,相对于注射生理盐水的对照组,缩短分数和梗死体积没有变化,但梗死诱导的左心室舒张末期直径(LVEDD)增加显著减少(43%,P <0.05),壁变薄被完全阻止。在13周时,注射生理盐水和PEG的心脏的LVEDD相似。不可降解的聚乙二醇凝胶引起巨噬细胞为基础的炎症反应。结论:注射不可降解的合成凝胶是有效的改善病理性重塑在梗死后立即愈合阶段,但无法防止扩张发生在愈合的心脏的后期阶段。(J Cardiac Fail 2009;15:629-636)
Background: Left ventricular remodeling after myocardial infarction is a key component of heart failure and it has long been postulated that it may result from increased wall stress. It has recently been suggested that an injectable, non-degradable polymer may limit pathological remodeling in a manner analogous to that of cardiac support devices. We have tested a non-degradable polyethylene glycol (PEG) gel in a rat infarction model.Methods and Results: After permanent ligation of the left anterior descending artery in male Wistar rats, PEG gel reagents were injected into the infarcted region and polymerized in situ. At 4 weeks, fractional shortening and infarct volume were unchanged relative to a saline injected control, but the infarct-induced left ventricular end-diastolic diameter (LVEDD) increase was substantially reduced (43%, P < .05) and wall thinning was completely prevented. At 13 weeks, the LVEDD were similar for both saline- and PEG-injected hearts. The non-degradable PEG gels did elicit a macrophage-based inflammatory reaction.Conclusions: The injection of non-degradable synthetic gel was effective in ameliorating pathological remodeling in the immediate postinfarction healing phase, but was unable to prevent the dilation that occurred at later stages in the healed heart. (J Cardiac Fail 2009;15:629-636)