Since it is known that elevated testosterone levels enhance the activity of hormone-sensitive lipase and promote lipolysis in cardiomyocytes, keeping long long-chain fatty acids free for ATP synthesis and following augmentation of reactive oxygen species (ROS) production also [55], it could be concluded that these mechanisms all together promote oxidative damage induced by hyperandrogenism and consecutive CV damage confirmed by oxidative stress in CVE. This evidence concerns the gene LIPE and hyperandrogenism.