OBJECTIVE: Recent investigation has demonstrated that prostaglandin E(1) (PGE(1)) therapy increased capillary density in explanted hearts. Dynamic (13)N-ammonia positron emission tomography (PET) is reliable for non-invasive measurement of myocardial blood flow and myocardial perfusion reserve (MPR). The aim of this study was to investigate the effects of PGE(1) therapy during 4 weeks on reduction of myocardial perfusion abnormalities and increase of MPR in the patients with ischemic heart disease. METHODS: In this double-blind, placebo-controlled trial, we randomly assigned 11 patients who had symptomatic heart failure and documented myocardial ischemia to 4 weeks intravenous infusion ofPGE(1) (2.5 ng/kg/min; 8 patients, age 60 ± 13 years) or saline (3 patients, age 57 ± 13 years). Dynamic (13)N-ammonia PET scans at rest and during adenosine stress were obtained at baseline and 12 weeks after treatment completion. Quantitative size/severity of perfusion defects and MPR change from baseline to follow-up PET were determined using a 17-segment model. RESULTS: Compared with the control group, baseline MPR in the PGE(1) group was significantly lower (1.96 ± 0.78 vs. 2.71 ± 0.73; P < 0.001). MPR significantly improved 12 weeks after completion of PGE(1) infusion (1.96 ± 0.78 to 2.16 ± 0.77; P < 0.001). In contrast, MPR declined significantly in the placebo group (2.71 ± 0.73 to 2.01 ± 0.58, P < 0.001). CONCLUSION: Four weeks of PGE(1) infusion sustained MPR improvement in patients with ischemic heart disease. This may be an attractive therapeutic approach for no-option patients with severe ischemic cardiomyopathy.
RCT Entities:
OBJECTIVE: Recent investigation has demonstrated that prostaglandin E(1) (PGE(1)) therapy increased capillary density in explanted hearts. Dynamic (13)N-ammonia positron emission tomography (PET) is reliable for non-invasive measurement of myocardial blood flow and myocardial perfusion reserve (MPR). The aim of this study was to investigate the effects of PGE(1) therapy during 4 weeks on reduction of myocardial perfusion abnormalities and increase of MPR in the patients with ischemic heart disease. METHODS: In this double-blind, placebo-controlled trial, we randomly assigned 11 patients who had symptomatic heart failure and documented myocardial ischemia to 4 weeks intravenous infusion of PGE(1) (2.5 ng/kg/min; 8 patients, age 60 ± 13 years) or saline (3 patients, age 57 ± 13 years). Dynamic (13)N-ammonia PET scans at rest and during adenosine stress were obtained at baseline and 12 weeks after treatment completion. Quantitative size/severity of perfusion defects and MPR change from baseline to follow-up PET were determined using a 17-segment model. RESULTS: Compared with the control group, baseline MPR in the PGE(1) group was significantly lower (1.96 ± 0.78 vs. 2.71 ± 0.73; P < 0.001). MPR significantly improved 12 weeks after completion of PGE(1) infusion (1.96 ± 0.78 to 2.16 ± 0.77; P < 0.001). In contrast, MPR declined significantly in the placebo group (2.71 ± 0.73 to 2.01 ± 0.58, P < 0.001). CONCLUSION: Four weeks of PGE(1) infusion sustained MPR improvement in patients with ischemic heart disease. This may be an attractive therapeutic approach for no-option patients with severe ischemic cardiomyopathy.