N Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PabUniversityof Pittsburgh

N Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PabUniversityof Pittsburgh Medical Center, Cardiovascular Institute, Pittsburgh, Pa of Developmental Biology, University of Pittsburgh, Pittsburgh, Pa of Bioengineering and Chemical Engineering, University of Pittsburgh, Pittsburgh,cDepartmentdDepartmentsPaAbstractObjective–Myocardial infarction (MI) can lead to irreversible adverse left ventricular remodeling resulting in subsequent severe dysfunction. The objective of this study was to investigate the potential for biodegradable, elastomeric patch implantation to positively alter the remodeling process after MI in a porcine model. Methods–Yorkshire pigs underwent a 60-minute catheter balloon occlusion of the left circumflex artery. Two weeks after MI animals underwent epicardial placement of a biodegradable, porous polyurethane (poly(ester urethane)urea; PEUU) patch (MI+PEUU, n = 7) or sham surgery (MI+sham, n = 8). Echocardiography before surgery and at 4 and 8 weeks after surgery measured the end-diastolic area (EDA) and fractional area change ( FAC). All animals were humanely killed 8 weeks after surgery and hearts were histologically assessed. Results–At 8 weeks, echocardiography revealed greater EDA values in the MI+sham group (23.6 6.6 cm2 , mean standard deviaation) than in the MI+PEUU group (15.9 2.5 cm2) (P . 05) and a lower FAC in the MI+sham group (24.8 7.6) than in the MI+PEUU group (35.9 7.8) (P .05). The infarcted ventricular wall was thicker in the MI+PEUU group (1.56 0.5 cm) than in the MI+sham group (0.91 0.24 cm) (P .01). Conclusions–Biodegradable elastomeric PEUU patch implantation onto the porcine heart 2 weeks post-MI attenuated left ventricular adverse remodeling and functional deterioration and was accompanied by increased neovascularization. These findings, although limited to a 2-month follow-up, may suggest an attractive clinical option to moderate post-MI cardiac failure.Copyright 2012 by The American Association for Thoracic Surgery Address for reprints: William R. Wagner, PhD, Bridgeside Point II, 450 Technology Dr, Suite 300 Pittsburgh, PA 15219 ([email protected]).. Present addresses: R.H: Department of Pathology and Matrix Biology, Mie University Graduate School of Medicine, Tsu, Mie, Japan; J.G: Department of Materials Science and Engineering, The Ohio State University, Columbus, Ohio. R.H. and K.L.F contributed equally to this work. Disclosures: Authors have nothing to disclose with regard to commercial support.Hashizume et al.PageMyocardial infarction (MI) is the most frequently identified specific cause of dilated cardiomyopathy, leading to symptomatic congestive heart failure over time.IL-6 Protein, Mouse Regional structural changes in left ventricular (LV) remodeling after MI can lead to global LV geometric change, which contributes to an increase in LV wall stress1 and mitral regurgitation.SS-208 2 Epidemiologically, survival after MI is related to the magnitude of LV dilatation.PMID:25429455 3 Thus, therapies designed to attenuate postinfarct LV dilatation, by pharmacologic or surgical means, have been pursued to alleviate postinfarction morbidity and mortality in adverse remodeling after MI. A spectrum of surgical procedures, cardiac resynchronization therapy (biventricular pacing),4 or pharmacologic therapy (eg, angiotensin-converting enzyme inhibitors and betablockers)5 have been applied in the clinical setting after MI in an effort to limit adverse LV remodeling. Surgical approachesinclude surgic.