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Ann Thorac Surg 2000;70:2113-2118
© 2000 The Society of Thoracic Surgeons
a Angiogenesis Research Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
b Chiron Corporation, Emeryville, California, USA
Address reprint requests to Dr Post, Angiogenesis Research Center, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA 02215
e-mail: mpost{at}caregroup.harvard.edu
Presented at the Poster Session of the Thirty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31Feb 2, 2000.
Background. Therapeutic angiogenesis in ischemic myocardium has been shown to be a feasible and effective strategy to improve regional blood flow and myocardial function. However, the optimal mode of growth factor administration still needs to be established.
Methods. Using a pig model of chronic myocardial ischemia, we evaluated the efficacy of intravenous and intracoronary infusion of FGF-2 at 2 and 6 µg/kg compared with a vehicle control. Improvement in myocardial perfusion and function was assessed by angiography, colored microspheres, and function and perfusion magnetic resonance imaging.
Results. Intracoronary 6-µg/kg FGF-2 increased angiographic collaterals (p = 0.046) and increased regional blood flow to the ischemic area from 0.36 ± 0.07 to 0.59 ± 0.08 mL/min/g at stress (vs control, p = 0.032). Also, after 6 µg/kg intracoronary FGF-2, ejection fraction, regional wall motion, and thickening improved significantly by 9.9% ± 1.9%, 126% ± 39%, and 13.8% ± 3.6%, respectively. Intravenous FGF-2 and intracoronary 2 µg/kg FGF-2 were ineffective.
Conclusions. A single 6-µg/kg intracoronary treatment with FGF-2 resulted in significant improvement in collateralization and regional and global function of chronically ischemic myocardium. Single intravenous infusion of FGF-2 was not effective in this model.
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