The choice of valsartan was motivated by the role of the renin—angiotensin—aldosterone system (RAAS) in cardiovascular disease, whose activation results in increased serum level of angiotensin II that perpetuates vasoconstriction, endothelial dysfunction, LV hypertrophy, myocardial fibrosis and remodeling [24–26]. Here, AGT is linked to endothelial dysfunction.