Fujimoto Kazuro L, Tobita Kimimasa, Merryman W David, Guan Jianjun, Momoi Nobuo, Stolz Donna B, Sacks Michael S, Keller Bradley B, Wagner William R
Department of Surgery, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA.
J Am Coll Cardiol. 2007 Jun 12;49(23):2292-300. doi: 10.1016/j.jacc.2007.02.050. Epub 2007 May 25.
Our objective in this study was to apply an elastic, biodegradable polyester urethane urea (PEUU) cardiac patch onto subacute infarcts and to examine the resulting cardiac ventricular remodeling and performance.
Myocardial infarction induces loss of contractile mass and scar formation resulting in adverse left ventricular (LV) remodeling and subsequent severe dysfunction.
Lewis rats underwent proximal left coronary ligation. Two weeks after coronary ligation, a 6-mm diameter microporous PEUU patch was implanted directly on the infarcted LV wall surface (PEUU patch group, n = 14). Sham surgery was performed as an infarction control (n = 12). The LV contractile function, regional myocardial wall compliance, and tissue histology were assessed 8 weeks after patch implantation.
The end-diastolic LV cavity area (EDA) did not change, and the fractional area change (FAC) increased in the PEUU patch group (p < 0.05 vs. week 0), while EDA increased and FAC decreased in the infarction control group (p < 0.05). The PEUU patch was largely resorbed 8 weeks after implantation and the LV wall was thicker than infarction control (p < 0.05 vs. control group). Abundant smooth muscle bundles with mature contractile phenotype were found in the infarcted myocardium of the PEUU group. The myocardial compliance of the PEUU group was distributed between normal myocardium and infarction control (p < 0.001).
Implantation of a novel biodegradable PEUU patch onto a subacute myocardial infarction promoted contractile phenotype smooth muscle tissue formation and improved cardiac remodeling and contractile function at the chronic stage. Our findings suggest a new therapeutic option against post-infarct cardiac failure.
本研究的目的是将一种弹性、可生物降解的聚酯聚氨酯脲(PEUU)心脏补片应用于亚急性梗死灶,并检查由此产生的心室重塑和心脏功能。
心肌梗死导致收缩性心肌质量丧失和瘢痕形成,从而导致不良的左心室(LV)重塑和随后的严重功能障碍。
对Lewis大鼠进行左冠状动脉近端结扎。冠状动脉结扎两周后,将直径6毫米的微孔PEUU补片直接植入梗死的左心室壁表面(PEUU补片组,n = 14)。进行假手术作为梗死对照(n = 12)。在补片植入8周后评估左心室收缩功能、局部心肌壁顺应性和组织组织学。
PEUU补片组左心室舒张末期腔面积(EDA)无变化,面积变化分数(FAC)增加(与第0周相比,p < 0.05),而梗死对照组EDA增加,FAC降低(p < 0.05)。PEUU补片在植入8周后大部分被吸收,左心室壁比梗死对照组厚(与对照组相比,p < 0.05)。在PEUU组梗死心肌中发现大量具有成熟收缩表型的平滑肌束。PEUU组的心肌顺应性分布在正常心肌和梗死对照组之间(p < 0.001)。
将新型可生物降解的PEUU补片植入亚急性心肌梗死可促进收缩表型平滑肌组织形成,并在慢性期改善心脏重塑和收缩功能。我们的研究结果提示了一种针对梗死后心力衰竭的新治疗选择。