This Article Abstract Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sato, K. Articles by Post, M. J. Search for Related Content PubMed PubMed Citation Articles by Sato, K. Articles by Post, M. J.

Efficacy of intracoronary or intravenous VEGF₁₆₅ in a pig model of chronic myocardial ischemia

Kaori Sato, MD^* , Tiangen Wu, MD^*, Roger J. Laham, MD^*, Robert B. Johnson, MD^*, Pamela Douglas, MD, FACC^*, Jianyi Li, MSc, Frank W. Sellke, MD, Stuart Bunting, PhD, Michael Simons, MD, FACC^* and Mark J. Post, MD, PhD^*

^* Angiogenesis Research Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
Division of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
Genentech, Inc., South San Francisco, California, USA

View larger version (36K): [in a new window]   Figure 1 Line plots of collateral index scores (see Methods) at treatment (mid) and three weeks after treatment (final).

View larger version (16K): [in a new window]   Figure 2 Regional blood flow change in the ischemic area between mid-study and final study at rest with individual data and mean and standard deviation. Increase in regional blood flow over time at rest was significant in the intracoronary VEGF group without L-NAME (*p = 0.006).

View larger version (20K): [in a new window]   Figure 3 Change in global ventricular function (fractional shortening) from mid-study to final study with individual data and mean and standard deviation. The asterisk indicates a significant decrease in global LV function at rest (p = 0.002) in the control group. Con = control group, slowIV: intravenous VEGF 0.05 µg/kg/min, fastIV: intravenous VEGF 0.25 µg/kg/min, IC: intracoronary VEGF 0.25 µg/kg/min, IC+LN: intracoronary VEGF 0.25 µg/kg/min plus L-NAME.

View larger version (19K): [in a new window]   Figure 4 Change in regional LV wall thickening from mid-study to final study with individual data and mean and standard deviation. In none of the groups did the indexed regional wall thickening change significantly over time. Con = control group, slowIV: intravenous VEGF 0.05 µg/kg/min, fastIV: intravenous VEGF 0.25 µg/kg/min, IC: intracoronary VEGF 0.25 µg/kg/min, IC+LN: intracoronary VEGF 0.25 µg/kg/min plus L-NAME.

View larger version (23K): [in a new window]   Figure 5 Endothelium dependent elaxation of microvessels. Relaxation was induced by adenosine diphosphate (ADP). Microvessels were taken from the ischemic area (LCX, dotted lines) and the normal area (LAD, uninterrupted lines) from pigs that were treated with intracoronary VEGF, intracoronary VEGF + L-NAME or vehicle. * LCX microvessels from intracoronary VEGF + L-NAME treated animals had a lower response to maximum dose of ADP than the intracoronary VEGF group (p = 0.011).