The VEGF levels and its binding to its receptors are key stages in the regulation of angiogenesis. Acetylsalicylic acid (ASA), widely used in post-myocardial infarction treatment, has been shown to have an anti-angiogenic effect in tumor models. This potentially counterproductive effect requires to be studied in myocardium. The aim of this study is to quantify the effect of ASA and salicylic acid (SA) on the vascularization in chick allantochorionic membrane (CAM) and on the levels of VEGF-A and VEGFR2 in myocardium of chicken embryos. Thirty White Leghorn chicken fetuses were instilled at 10 days of gestation with 60 mL of 0.1 % DMSO (control) or also containing 0.3 mmol of ASA or SA. After 48 hours, CAM histological processing was performed to count blood vessels and heart tissue to quantify VEGF-A and VEGFR2 by immunohistochemistry. Immunoreactivity was quantified by Image J. Both ASA and SA decreased CAM microvascular density. In myocardium, AAS, although not SA, decreased the concentration of VEGFR2. There was no effect on VEGF-A. In our experimental model, chicken fetuses at 10 days of gestation, the inhibitory effect of ASA on angiogenesis in CAM were also observed. The decrease in VEGFR2 in cardiomyocytes suggests that ASA also affects angiogenesis in healthy myocardium, modifying the availability of the receptor to VEGF. These findings allow us to postulate that ASA could interfere with tissue regeneration, when it is required, as post myocardial infarction.