Gorman Cardiovascular Research Group, Department of Surgery, University of Pennsylvania, Philadelphia, PA, USA.
Ann Thorac Surg. 2011 Aug;92(2):617-24. doi: 10.1016/j.athoracsur.2011.04.051.
Infarct expansion after myocardial infarction (MI) is an important phenomenon that initiates and sustains adverse left ventricular (LV) remodeling. We tested the hypothesis that infarct modification by material-induced infarct stiffening and thickening limits infarct expansion and LV remodeling.
Anteroapical infarction was induced in 21 sheep. Sheep were randomized to injection of saline (2.6 mL) or tissue filler material (2.6 mL) into the infarct within 3 hours of MI. Animals were monitored for 8 weeks with echocardiography to assess infarct expansion and global LV remodeling. Morphometric measurements were performed of excised hearts to quantify infarct thickness. Regional blood flow was assessed with colored microspheres. Infarct material properties were measured using biaxial tensile testing.
Compared with controls at 8 weeks, treatment animals had less infarct expansion, reduced LV dilatation (LV systolic volumes: 60.8±4.3 vs 80.3±6.9 mL; p<0.05), greater ejection fraction (0.310±0.026 vs 0.276±0.013; p<0.05), thicker infarcts (5.5±0.2 vs 2.2±0.3 mm; p<0.05), and greater infarct blood flow (0.22±0.04 vs 0.11±0.03 mL/min/g; p<0.05). The longitudinal peak strain in the treatment group was less (0.05014±0.0141) than the control group (0.1024±0.0101), indicating increased stiffness of the treated infarcts.
Durable infarct thickening and stiffening can be achieved by infarct biomaterial injection, resulting in the amelioration of infarct expansion and global LV remodeling. Further material optimization will allow for clinical translation of this novel treatment paradigm.
心肌梗死后梗死扩展是引发和持续不良左心室（LV）重构的重要现象。我们检验了这样一个假设，即通过材料诱导的梗死变硬和增厚来修饰梗死，从而限制梗死扩展和 LV 重构。
在 21 只绵羊中诱发前侧壁梗死。绵羊在 MI 后 3 小时内随机接受生理盐水（2.6 mL）或组织填充材料（2.6 mL）注射。用超声心动图监测动物 8 周，以评估梗死扩展和整体 LV 重构。对切除的心脏进行形态测量以量化梗死厚度。使用双色微球评估局部血流。使用双轴拉伸试验测量梗死材料特性。
与 8 周时的对照组相比，治疗组的梗死扩展减少，LV 扩张减少（LV 收缩容积：60.8±4.3 vs 80.3±6.9 mL；p<0.05），射血分数更高（0.310±0.026 vs 0.276±0.013；p<0.05），梗死更厚（5.5±0.2 vs 2.2±0.3 mm；p<0.05），梗死区血流更多（0.22±0.04 vs 0.11±0.03 mL/min/g；p<0.05）。治疗组的纵向峰值应变较低（0.05014±0.0141），低于对照组（0.1024±0.0101），表明治疗性梗死的硬度增加。
通过梗死生物材料注射可以实现持久的梗死增厚和变硬，从而改善梗死扩展和整体 LV 重构。进一步的材料优化将使这一新的治疗模式能够在临床上转化。
