Furthermore, sympathetic overactivity could increase the catecholamine-mediated modulation of heart rate, vasomotor tone [11,28], and platelet aggregability [29] and contribute to the activation of the renin–angiotensin–aldosterone system, subsequently stimulating myocardial contractility, constricting peripheral arteries, and promoting heart failure and atherosclerosis [11,30,31,32]. This evidence concerns the gene REN and heart failure.