Journal Article
. 2013 Jan; 18(3):270-9.
doi: 10.1177/1074248412472257.

Intramyocardial injection of heart tissue-derived extracellular matrix improves postinfarction cardiac function in rats

Wangde Dai 1 Paul Gerczuk  Yuanyuan Zhang  Leona Smith  Oleg Kopyov  Gregory L Kay  Aarne J Jyrala  Robert A Kloner  
Affiliations
  • PMID: 23345062
  •     12 citations

Abstract

Aims: We determined whether implantation of heart tissue-derived decellularized matrix, which contains native biochemical and structural matrix composition, could thicken the infarcted left ventricular (LV) wall and improve LV function in a rat myocardial infarction model.

Methods And Results: Myocardial infarction was induced by left coronary ligation in Fischer rats. One week later, saline (75 μL, n = 17) or matrix (75 μL, n = 19) was directly injected into the infarcted area. At 6 weeks after injection, cardiac function was assessed by left ventriculogram, echocardiography, and Millar catheter. The hearts were pressure fixed to measure postmortem LV volume and processed for histology. Left ventriculogram demonstrated that LV ejection fraction (EF) was significantly greater in the matrix-treated (56.7% ± 1.4%) than in the saline-treated group (52.4% ± 1.5%; P = .043), and paradoxical LV systolic bulging was significantly reduced in the matrix-treated group (6.2% ± 1.6% of the LV circumference) compared to the saline-treated group (10.3% ± 1.3%; P = .048). Matrix implantation significantly increased the thickness of infarcted LV wall (0.602 ± 0.029 mm) compared to the saline-treated group (0.484 ± 0.03 mm; P = .0084). Infarct expansion index was significantly lower in the matrix-treated group (1.053 ± 0.051) than in the saline-treated group (1.382 ± 0.096, P = .0058). Blood vessel density and c-kit positive staining cells within the infarct area were comparable between the 2 groups.

Conclusions: Implantation of heart tissue-derived decellularized matrix thickens the LV infarcted wall, prevents paradoxical LV systolic bulging, and improves LV EF after myocardial infarction in rats. This benefit was not dependent on the enhanced angiogenesis or the recruitment of endogenous stem cells to the injury site.

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