Additionally, it increases oxidative stress [8] and endothelial dysfunction, accelerates atherosclerosis [10], and disrupts the renin-angiotensin-aldosterone system (RAAS), leading to cardiac fibrosis and hypertrophy, all of which may increase the risk of thromboembolic events such as AMI or stroke and worsening of HF [40]. This evidence concerns the gene REN and endothelial dysfunction.