If there is a lower availability of endogenous antioxidants, super-oxide-dismutase (SOD), glutathione-peroxidase (GPS) and catalase or coenzyme Q10, it may cause the worsening of cardiac function, resulting in sub-endocardial damage, which may be the second stage of HF [8,9], There may be an uncoupling of the NOS with structural instability, which further increases the generation of ROS, leading to left ventricular (LV) enlargement, dysfunction in the contraction [1], and remodeling of LV [1,4]. The gene discussed is NOS2; the disease is hydrops fetalis.