In this context, therapeutic lymphangiogenesis emerges as a novel modality to limit both chronic oedema and inflammation in the heart post-MI to prevent HF development.6–8 Recently, experimental findings on the beneficial impact of lymphatics during cardiac remodelling have been extended to models of non-ischaemic hypertensive heart disease, induced by either salt-loading in rats or chronic angiotensin-II infusion in mice.9,10 Promisingly, lymphangiogenic therapy with Vegfc limited cardiac hypertrophy in these settings. This evidence concerns the gene VEGFC and cardiac hypertrophy.