Background—
The aim of this substudy of the EUROINJECT-ONE double-blind randomized trial was to analyze changes in myocardial perfusion in NOGA-defined regions with intramyocardial injections of plasmid encoding plasmid human (ph)VEGF-A
165
using an elaborated transformation algorithm.
Methods and Results—
After randomization, 80 no-option patients received either active, phVEGF-A
165
(n=40), or placebo plasmid (n=40) percutaneously via NOGA-Myostar injections. The injected area (region of interest, ROI) was delineated as a best polygon by connecting of the injection points marked on NOGA polar maps. The ROI was projected onto the baseline and follow-up rest and stress polar maps of the 99m-Tc-sestamibi/tetrofosmin single-photon emission computed tomography scintigraphy calculating the extent and severity (expressed as the mean normalized tracer uptake) of the ROI automatically. The extents of the ROI were similar in the VEGF and placebo groups (19.4±4.2% versus 21.5±5.4% of entire myocardium). No differences were found between VEGF and placebo groups at baseline with regard to the perfusion defect severity (rest: 69±11.7% versus 68.7±13.3%; stress: 63±13.3% versus 62.6±13.6%; and reversibility: 6.0±7.7% versus 6.7±9.0%). At follow-up, a trend toward improvement in perfusion defect severity at stress was observed in VEGF group as compared with placebo (68.5±11.9% versus 62.5±13.5%,
P
=0.072) without reaching normal values. The reversibility of the ROI decreased significantly at follow-up in VEGF group as compared with the placebo group (1.2±9.0% versus 7.1±9.0%,
P
=0.016). Twenty-one patients in VEGF and 8 patients in placebo group (
P
<0.01) exhibited an improvement in tracer uptake during stress, defined as a ≥5% increase in the normalized tracer uptake of the ROI.
Conclusions—
Projection of the NOGA-guided injection area onto the single-photon emission computed tomography polar maps permits quantitative evaluation of myocardial perfusion in regions treated with angiogenic substances. Injections of phVEGF A
165
plasmid improve, but do not normalize, the stress-induced perfusion abnormalities.
Quantitation of size of relative myocardial perfusion defect by single-photon emission computed tomography.
