Background and Objectives; Beta catenin is the distal component of the highly conserved Wnt pathway that governs cell fate and proliferation. Beta catenin promotes proliferation and migration of vascular endothelial cells in our previous studies and also up-regulates VEGF expression in malignancy-associated angiogenesis. We hypothesized that intramyocardial gene delivery of constitutively-active beta catenin could enhance angiogenesis via VEGF overexpression and finally improve myocardial systolic function in rat myocardial infarction model. Material and method; We used 6-8 week old female Sprague-Dawley rats. We ligated the proximal left anterior descending coronary artery over 30 min to induce acute myocardial infarction. After 30 min of ligation, we injected total 2.5 X 109 pfu of adenovirus vector coding constitutively active mutant of beta catenin at four points of peri-infarct zone (n=10). As a control group we used adenovirus vector coding GFP gene (n=10). We performed trans-thoracic echocardiography at D-1(baseline) and 7 days. We examined the infarct size, capillary density at 7,14 days and performed western blot analysis for VEGF at 3,7 days. Results; In the western blot, expression of VEGF in the ischemic myocardium was significantly increased in the beta catenin group. Capillary density also significantly increased from 500+/-80 /mm2 (control) to 850+/-70 /mm2 in the beta catenin group (p< 0.01). The infarct size significantly decreased from 35+/-5 % (control) to 28+/-4 % in the beta catenin delivery group (p<0.05). The myocardial function also significantly improved in the beta catenin group. Conclusion; Beta catenin gene delivery enhanced angiogenesis through induction of VEGF, which resulted in the reduction of infarct size and improvement of myocardial function after AMI. Such gene therapy to modulate angiogenesis and cell proliferation, could be applied to the post-infarction heart failure in the future clinical field.