Carmen Gacchina Johnson1, Karun V Sharma2, Elliot B Levy1, David L Woods1, Aaron H Morris1, John D Bacher3, Andrew L Lewis4, Bradford J Wood5, Matthew R Dreher6. 1. Center for Interventional Oncology, Radiology and Imaging Sciences, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892. 2. Center for Interventional Oncology, Radiology and Imaging Sciences, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892; Department of Radiology, Children's National Medical Center, Washington, DC. 3. Clinical Center and National Cancer Institute; and Division of Veterinary Resources, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892. 4. Biocompatibles BTG UK, Farnham, United Kingdom. 5. Center for Interventional Oncology, Radiology and Imaging Sciences, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892. Electronic address: bwood@cc.nih.gov. 6. Center for Interventional Oncology, Radiology and Imaging Sciences, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892; Biocompatibles BTG UK, Farnham, United Kingdom.
Abstract
PURPOSE: To quantify changes in tumor microvascular (< 1 mm) perfusion relative to commonly used angiographic endpoints. MATERIALS AND METHODS: Rabbit Vx2 liver tumors were embolized with 100-300-μm LC Bead particles to endpoints of substasis or complete stasis (controls were not embolized). Microvascular perfusion was evaluated by delivering two different fluorophore-conjugated perfusion markers (ie, lectins) through the catheter before embolization and 5 min after reaching the desired angiographic endpoint. Tumor microvasculature was labeled with an anti-CD31 antibody and analyzed with fluorescence microscopy for perfusion marker overlap/mismatch. Data were analyzed by analysis of variance and post hoc test (n = 3-5 per group; 18 total). RESULTS: Mean microvascular density was 70 vessels/mm(2) ± 17 (standard error of the mean), and 81% ± 1 of microvasculature (ie, CD31(+) structures) was functionally perfused within viable Vx2 tumor regions. Embolization to the extent of substasis eliminated perfusion in 37% ± 9 of perfused microvessels (P > .05 vs baseline), whereas embolization to the extent of angiographic stasis eliminated perfusion in 56% ± 8 of perfused microvessels. Persistent microvascular perfusion following embolization was predominantly found in the tumor periphery, adjacent to normal tissue. Newly perfused microvasculature was evident following embolization to substasis but not when embolization was performed to complete angiographic stasis. CONCLUSIONS: Nearly half of tumor microvasculature remained patent despite embolization to complete angiographic stasis. The observed preservation of tumor microvasculature perfusion with angiographic endpoints of substasis and stasis may have implications for tumor response to embolotherapy. Published by Elsevier Inc.
PURPOSE: To quantify changes in tumor microvascular (< 1 mm) perfusion relative to commonly used angiographic endpoints. MATERIALS AND METHODS:Rabbit Vx2 liver tumors were embolized with 100-300-μm LC Bead particles to endpoints of substasis or complete stasis (controls were not embolized). Microvascular perfusion was evaluated by delivering two different fluorophore-conjugated perfusion markers (ie, lectins) through the catheter before embolization and 5 min after reaching the desired angiographic endpoint. Tumor microvasculature was labeled with an anti-CD31 antibody and analyzed with fluorescence microscopy for perfusion marker overlap/mismatch. Data were analyzed by analysis of variance and post hoc test (n = 3-5 per group; 18 total). RESULTS: Mean microvascular density was 70 vessels/mm(2) ± 17 (standard error of the mean), and 81% ± 1 of microvasculature (ie, CD31(+) structures) was functionally perfused within viable Vx2 tumor regions. Embolization to the extent of substasis eliminated perfusion in 37% ± 9 of perfused microvessels (P > .05 vs baseline), whereas embolization to the extent of angiographic stasis eliminated perfusion in 56% ± 8 of perfused microvessels. Persistent microvascular perfusion following embolization was predominantly found in the tumor periphery, adjacent to normal tissue. Newly perfused microvasculature was evident following embolization to substasis but not when embolization was performed to complete angiographic stasis. CONCLUSIONS: Nearly half of tumor microvasculature remained patent despite embolization to complete angiographic stasis. The observed preservation of tumor microvasculature perfusion with angiographic endpoints of substasis and stasis may have implications for tumor response to embolotherapy. Published by Elsevier Inc.
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