The lymphatic system plays an important role in regulating interstitial fluid homeostasis, lipid metabolism, and immune functions. After myocardial infarction, enhanced lymphangiogenesis accelerates clearance of infiltrating immune cells, reduces production of proinflammatory cytokines, reduces edema, inflammation, and fibrosis, and promotes recovery of impaired heart functions. Vascular endothelial growth factor-C (VEGF-C) and its receptor, VEGFR-3, are components of the lymphangiogenesis pathway and play a critical role in maintaining the tissue fluid balance and myocardial functions after cardiac injury. Lymphatic vessels are closely related to the immune system. Various immune cell populations stimulate or inhibit lymphatic remodeling. Macrophages are congenital immune cells distributed widely in organs and tissues, play an important role in various physiological and pathological processes such as organ development, host defense, acute and chronic inflammation, and tissue homeostasis and remodeling. More mechanisms of lymphangiogenesis need to be clarified to provide effective targets for clinical stimulation of lymphangiogenesis to treat heart disease. This article reviews basic pathological changes of the heart and lymphatic vessels after myocardial infarction, the regulatory factors of lymphangiogenesis, and the influence of macrophages on lymphangiogenesis.