HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map 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 Saeed, M. Articles by Higgins, C. B. Search for Related Content PubMed PubMed Citation Articles by Saeed, M. Articles by Higgins, C. B.

Adeno-associated Viral Vector–Encoding Vascular Endothelial Growth Factor Gene: Effect on Cardiovascular MR Perfusion and Infarct Resorption Measurements in Swine¹

¹ From the Departments of Radiology (M.S., D.S., A.M., L.D., O.W., A.J., C.B.H.), Pathology (P.C.U.), and Medicine/Cardiology (R.L.), University of California San Francisco, 513 Parnassus Ave, HSW 207 B, San Francisco, CA 94134-0628. Received May 29, 2006; revision requested July 31; revision received September 22; accepted October 26; final version accepted November 15. Supported by a grant from National Institutes of Health (RO1HL07295). A.J. supported by the French Radiological Society, Paris, France. Address correspondence to M.S. (e-mail: Maythem.Saeed{at}radiology.UCSF.edu).

View larger version (71K): [in this window] [in a new window] [Download PPT slide]   Figure 1: First-pass perfusion MR images show AAR (black arrowheads) and delayed MR images show extent of enhanced regions (white arrowheads) in two control animals. Left: Images show 3-day-old infarcts. Right: Images show 8-week-old infarcts. Color sections from histochemistry show true infarcts at postmortem evaluation (white arrows). (TTC stain; one-third of original magnification.)

View larger version (67K): [in this window] [in a new window] [Download PPT slide]   Figure 2: First-pass perfusion MR images show AAR (black arrowheads) and delayed MR images show extent of enhanced regions (white arrowheads) in two AAV-VEGF–treated animals. Left: Images show 3-day-old infarcts. Right: Images show 8-week-old infarcts. Color sections from histochemistry show true infarcts at postmortem evaluation (white arrows). (TTC stain; one-third of original magnification.)

View larger version (23K): [in this window] [in a new window] [Download PPT slide]   Figure 3: Graphs of first-pass perfusion dynamics of LV blood, remote myocardium, and AAR. Left: Control animals (n = 6). Right: AAV-VEGF–treated animals (n = 6). Treated animals showed better perfusion than control animals at 8 weeks, as reflected by magnitude of signal intensity increase and maximum upslope of curves in AAR. a.u. = arbitrary units, Gd-DOTA = gadoterate meglumine.

View larger version (21K): [in this window] [in a new window] [Download PPT slide]   Figure 4: Graphs of comparison of percentage change in signal intensities of normal myocardium and AAR at 3 days and 8 weeks after infarction. Left: Control animals (n = 6). Right: AAV-VEGF–treated animals (n = 6). Bottom: Difference reached significance (P = .001) in treated compared with control animals. Maximum upslopes of curves in AAR were 225 msec ± 19 in control and 166 msec ± 16 in treated animals (P = .038). Gd-DOTA = gadoterate meglumine.

View larger version (14K): [in this window] [in a new window] [Download PPT slide]   Figure 5: Graphs of extents of infarcts, as percentage of LV surface area, in control (n = 6) and treated (n = 6) animals at delayed cardiovascular MR imaging at 3 days and 8 weeks and TTC histochemical staining at 8 weeks. Enhanced regions at 8 weeks (white columns) were significantly smaller in both groups than those at 3 days (black columns). However, the decline in extent of infarcts was significantly greater in treated than in control animals at cardiovascular MR imaging and TTC staining (striped columns). * = P value of .01, = P value of .04.

View larger version (10K): [in this window] [in a new window] [Download PPT slide]   Figure 6: Graphs of changes in LV ejection fraction. Top: Control animals (n = 6). Bottom: AAV-VEGF–treated animals (n = 6). Control animals had progressive deterioration in ejection fraction 8 weeks after infarction. AAV-VEGF prevented decline in ejection fraction in treated animals subjected to same intervention. ** = P less than .01 compared with that at 3 days after infarction (paired t test), = P less than .01 compared with that of control animals (unpaired t test).

View larger version (140K): [in this window] [in a new window] [Download PPT slide]   Figure 7: Micrographs of representative infarcts in, A, C, E, control animals and, B, D, F, AAV-VEGF–treated animals. A, B, At low magnification, infarct in control animal shows no appreciable neovascularization. A, Remodeled thick-walled blood vessels (arrows). B, AAV-VEGF–treated animal contains numerous vessels (arrowheads) in linear array representing injection needle track. C, D, At high magnification, control infarct has a few scattered remodeled thick-walled vessels (arrows), while AAV-VEGF–treated infarct contains numerous thin-walled vessels (arrowheads) filled with blood, suggesting active blood vessels. E, F, Biotinylated isolectin B4 stain localizes all vessels with brown reaction product. Sparse vessels in control infarct (arrows) and numerous vessels in AAV-VEGF–treated infarct (arrowheads) were demonstrated with lectin stain. I = infarct, LV = left ventricular cavity. A, B, Calibration bars = 1000 µm. C, D, E, F, Calibration bars = 200 µm. (A, B, C, D, Masson trichrome stain; E, F, immunoperoxidase methods with biotinylated isolectin B4 stain.)