Hyperglycaemia and insulin resistance also promote a pro‐inflammatory state with increased oxidative stress, mitochondrial dysfunction and increased levels of advanced glycation end‐products (AGEs), reduction in insulin‐like growth factor‐1 (IGF‐1) and activation of RAAS, all mechanisms that ultimately lead to fibrosis and myocardial damage.30, 31. This evidence concerns the gene IGF1 and Insulin resistance.