Therapeutic angiogenesis with recombinant fibroblast growth factor-2 improves stress and rest myocardial perfusion abnormalities in patients with severe symptomatic chronic coronary artery disease

Article

关键词: VIABLE MYOCARDIUM;    CANINE MODEL;    GENE-THERAPY;    HUMAN HEART;    ISCHEMIA;    TL-201;    SCINTIGRAPHY;    TOMOGRAPHY;    INJECTION;    REDUCTION;   

DOI  :  10.1161/01.CIR.102.14.1605

来源: SCIE

【 摘 要 】

Background-We report the effects of the administration of recombinant fibroblast growth factor-2 (rFGF-2) protein on myocardial perfusion using single photon emission computed tomography imaging in humans with advanced coronary disease. Methods and Results-A total of 59 patients with coronary disease that was not amenable to mechanical revascularization underwent intracoronary (n=45) or intravenous (n=14) administration of rFGF-2 in ascending doses, Changes in perfusion were evaluated at baseline and again at 29, 57, and 180 days after rFGF-2 administration. In this uncontrolled study, perfusion scans were analyzed by 2 observers who were blinded to patient identity and test sequence; scans were displayed in random order, with scans from nonstudy patients randomly interspersed to enhance blinding. Combining all dose groups, a reduction occurred in the per-segment reversibility score (reflecting the magnitude of inducible ischemia) from 1.7+/-0.4 at baseline to 1.1+/-0.6 at day 29 (P<0.001), 1.2+/-0.7 at day 57 (P<0.001), and 1.1+/-0.7 at day 180 (P<0.001). The 37 patients with evidence of resting hypoperfusion had evidence of improved resting perfusion: their per-segment rest perfusion score of 1.5+/-0.5 at baseline decreased to 1.0+/-0.8 at day 29 (P<0.001), 1.0+/-0.8 at day 57 (P=0.003), and 1.1+/-0.9 at day 180 (P=0.11). Conclusions-These preliminary data suggest that the administration of rFGF-2 to patients with advanced coronary disease resulted in an attenuation of stress-induced ischemia and an improvement in resting myocardial perfusion; these findings are consistent with a favorable effect of therapeutic angiogenesis.

【 授权许可】

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