The contribution of Lp(a) in accelerating cardiovascular disease involves several mechanisms, as follows [1, 3]: (1) promoting the formation of reactive oxygen species, which further augments endothelial permeability, produces cytokine, and results in inflammation, apoptosis, and vascular wall remodeling; (2) accelerating the uptake of oxidized low-density lipoprotein cholesterol by macrophages-induced formatting of foam cells and subsequent atherogenesis; and (3) facilitating monocyte adhesion and migration by the interaction of apolipoprotein(a) with β2-integrin Mac1. Here, LPA is linked to cardiovascular disorder.