[Lp(a): What we know, what we don't know and what we hope for]

There is no doubt that lipoprotein(a) [Lp(a)] is a structurally complex molecule with unique biological functions. It plays an important role in the inflammatory process through multiple mechanisms, contributes to endothelial dysfunction, activation of monocytes, macrophages and proliferation of smooth muscle cells, and promotes the development of atherosclerotic cardiovascular disease (ASCVD). It is important to point out the complex bidirectional relationship between Lp(a) and inflammation, influencing one another and even exerting anti-inflammatory effects in certain situations. Likewise, Lp(a) can favor the development of heart valve disease, especially of the aortic valve. Numerous publications emphasize the need to determine Lp(a) levels in the population at least once in life and possible strategies to mitigate the risk of ASCVD generated by high Lp(a) levels. However, doubts or lack of knowledge persist about the need to measure this parameter, either due to the uncertainty of how to manage patients with high levels of Lp(a), due to insufficient knowledge about its physiological function or because its levels persist unchanged, to a large extent, throughout life as the genetic character of this molecule takes precedence. On the other hand, there are still no specific approved therapies that reduce its levels and arouse sufficient interest for its management. However, many societies, such as the European Society of Cardiology (SEC) or the Spanish Society of Atherosclerosis (SEA), raise the need to determine Lp(a) and intensive management of cardiovascular risk factors in patients with high Lp(a) levels along with therapies that mitigate the associated ASCVD risk. Likewise, the identification of high levels of Lp(a) offers the opportunity to screen family members, better control of cardiovascular risk and the possibility of developing clinical trials that profile individual and population risk that allow for more personalized actions.