This hypertrophic response increases oxygen demand, stimulates the HIF-1a-VEGF axis and eventually leads to vascular neogenesis in the myocardium, aiming to meet the heightened metabolic demand.35 Izumiya et al.36 demonstrated not only cardiac hypertrophy on cardiomyocyte and organ level, but also an increase in cardiac expression of VEGF-A after thoracic aortic constriction (TAC) in mice, an established model of afterload increase. This evidence concerns the gene VEGFA and persistent truncus arteriosus.