Modification of Infarct Material Properties Limits Adverse Ventricular Remodeling

• Published in: The Annals of thoracic surgery Vol. 92; no. 2; pp. 617 - 624
• Main Authors: Morita, Masato, MD, Eckert, Chad E., PhD, Matsuzaki, Kanji, MD, PhD, Noma, Mio, MD, Ryan, Liam P., MD, Burdick, Jason A., PhD, Jackson, Benjamin M., MD, Gorman, Joseph H., MD, Sacks, Michael S., PhD, Gorman, Robert C., MD
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.08.2011; Elsevier
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biocompatible Materials; Biological and medical sciences; Biomechanical Phenomena; Cardiology. Vascular system; Cardiothoracic Surgery; Collagen - metabolism; Coronary Circulation - physiology; Disease Models, Animal; Durapatite; Echocardiography; Echocardiography, Three-Dimensional; Fibroblasts - pathology; Fibroblasts - physiology; Finite Element Analysis; Hemodynamics - physiology; Injections; Medical sciences; Microspheres; Myocardial Contraction - physiology; Myocardial Infarction - pathology; Myocardial Infarction - physiopathology; Myocardium - pathology; Pneumology; Sheep; Stress, Mechanical; Surgery; Tensile Strength; Ventricular Dysfunction, Left - pathology; Ventricular Dysfunction, Left - physiopathology; Ventricular Remodeling - physiology; 30; Vascular remodeling; Modification; Infarct; Materials; Anesthesia; Circulatory system; Limit; Cardiology; Properties
• ISSN: 0003-4975; 1552-6259
• DOI: 10.1016/j.athoracsur.2011.04.051

Background 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. Methods 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. Results 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. Conclusions 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.