Ryan Liam P, Matsuzaki Kanji, Noma Mio, Jackson Benjamin M, Eperjesi Thomas J, Plappert Theodore J, St John-Sutton Martin G, Gorman Joseph H, Gorman Robert C
Department of Surgery, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Ann Thorac Surg. 2009 Jan;87(1):148-55. doi: 10.1016/j.athoracsur.2008.09.028.
Early infarct expansion after coronary occlusion compromises contractile function in perfused myocardial regions and promotes adverse long-term left ventricular (LV) remodeling. We hypothesized that injection of a tissue-expanding dermal filler material into a myocardial infarction (MI) would attenuate infarct expansion and limit LV remodeling.
Fifteen sheep were subjected to an anteroapical MI involving approximately 20% of the LV followed by the injection of 1.3 mL of a calcium hydroxyapatite-based dermal filler into the infarct. Real-time three-dimensional echocardiography was performed at baseline, 30 minutes after MI, and 15 minutes after injection to assess infarct expansion. Sixteen additional sheep were subjected to the same infarction and followed echocardiographically and hemodynamically for 4 weeks after MI to assess chronic remodeling. Eight animals had injection with dermal filler as described above immediately after MI, and 8 animals were injected with an equal amount of saline solution.
All animals exhibited infarct expansion soon after coronary occlusion. The regional ejection fraction of the apex became negative after infarction, consistent with systolic dyskinesia. Injection of the dermal filler converted the apical wall motion from dyskinetic to akinetic and resulted immediately in significant decreases in global, regional, and segmental LV volumes. Chronically, relative to saline control, dermal filler injection significantly reduced LV end-systolic volume (62.2 +/- 3.6 mL versus 44.5 +/- 3.9 mL; p < 0.05) and improved global ejection fraction (0.295 +/- 0.016 versus 0.373 +/- 0.017; p < 0.05) at 4 weeks after infarction.
Injection of an acellular dermal filler into an MI immediately after coronary occlusion reduces early infarct expansion and limits chronic LV remodeling.
冠状动脉闭塞后的早期梗死扩展会损害灌注心肌区域的收缩功能，并促进不良的长期左心室（LV）重塑。我们假设向心肌梗死（MI）部位注射一种组织扩张性真皮填充材料会减弱梗死扩展并限制左心室重塑。
15只绵羊接受了累及约20%左心室的前尖部心肌梗死，随后向梗死部位注射1.3 mL基于羟基磷灰石的真皮填充剂。在基线、心肌梗死后30分钟和注射后15分钟进行实时三维超声心动图检查以评估梗死扩展。另外16只绵羊接受相同的梗死，并在心肌梗死后进行4周的超声心动图和血流动力学随访以评估慢性重塑。8只动物在心肌梗死后立即按上述方法注射真皮填充剂，8只动物注射等量的盐溶液。
所有动物在冠状动脉闭塞后不久均出现梗死扩展。梗死后心尖部的区域射血分数变为负值，与收缩期运动障碍一致。注射真皮填充剂使心尖壁运动从运动障碍转变为运动不能，并立即导致左心室整体、区域和节段容积显著减小。长期来看，相对于盐水对照，注射真皮填充剂在梗死后4周时显著降低了左心室收缩末期容积（62.2±3.6 mL对44.5±3.9 mL；p<0.05）并改善了整体射血分数（0.295±0.016对0.373±0.017；p<0.05）。
冠状动脉闭塞后立即向心肌梗死部位注射无细胞真皮填充剂可减少早期梗死扩展并限制慢性左心室重塑。
