Viable fibroblast matrix patch induces angiogenesis and increases myocardial blood flow in heart failure after myocardial infarction.

TitleViable fibroblast matrix patch induces angiogenesis and increases myocardial blood flow in heart failure after myocardial infarction.
Publication TypeJournal Article
Year of Publication2010
AuthorsLancaster J, Juneman E, Hagerty T, Do R, Hicks M, Meltzer K, Standley P, Gaballa M, Kellar R, Goldman S, Thai H
JournalTissue Eng Part A
Volume16
Issue10
Pagination3065-73
Date Published2010 Oct
ISSN1937-335X
KeywordsAnimals, Biomechanical Phenomena, Coronary Circulation, Cytokines, Echocardiography, Fibroblasts, Heart Failure, Male, Myocardial Infarction, Neovascularization, Physiologic, Rats, Rats, Sprague-Dawley, Tissue Engineering
Abstract

BACKGROUND: This study examines a viable biodegradable three-dimensional fibroblast construct (3DFC) in a model of chronic heart failure. The viable fibroblasts, cultured on a vicryl mesh, secrete growth factors that stimulate angiogenesis.

METHODS: We ligated the left coronary artery of male Sprague-Dawley rats, implanted the 3DFC 3 weeks after myocardial infarction and obtained end point data 3 weeks later, that is, 6 weeks after myocardial infarction.

RESULTS: Implanting the 3DFC increases (p<0.05) myocardial blood flow twofold, microvessel formation (0.02±0.01 vs. 0.07±0.03 vessels/μm2), and ventricular wall thickness (0.53±0.02 to 1.02±0.17mm). The 3DFC shifts the passive pressure volume loop toward the pressure axis but does not alter left ventricular (LV) ejection fraction, systolic displacement, LV end-diastolic pressure/dimension, or LV cavity area. The 3DFC stimulates selected cytokine activation with a decrease in the proinflammatory cascade and increased total protein content stimulated by strained 3DFC in vitro.

CONCLUSION: The 3DFC functions as a cell delivery device providing matrix support for resident cell survival and integration into the heart. The imbedded fibroblasts of the 3DFC release a complex blend of cardioactive cytokines promoting increases in microvessel density and anterior wall blood flow but does not improve ejection fraction or alter LV remodeling.

DOI10.1089/ten.TEA.2009.0589
Alternate JournalTissue Eng Part A
PubMed ID20486785