17 z Will earlier measurement of Lp(a) and effective interventions to lower it help to improve outcomes? z Is it reasonable to recommend universal testing of Lp(a) in all individuals in early adulthood regardless of family history or health status? z How will Lp(a) screening inform clinical decisionmaking for more aggressive management of cardiovascular risk in high Lp(a) patients? z What will be the benefit of medical interventions that target Lp(a) lowering, and how will such therapies change outcomes of people at risk and those currently affected by CVD? z Will Lp(a)-lowering therapy be effective in people with low LDL-C, in light of new promising LDL-C–lowering therapies beyond statins, ezetimibe and PCSK9 inhibitors? z What role will LA continue to play in reduction of LDL and Lp(a) in people with FH? z What part will artificial intelligence and machine learning play in risk assessment that will expedite patient diagnosis and treatment? To answer these and myriad other questions, it’s encouraging that randomized, placebo-controlled, double blind cardiovascular outcomes trials of pelacarsen, olpasiran and lepodisaran that specifically and effectively reduce Lp(a), are ongoing and due to report between 2025 and 2029. In addition, there are several other potential therapies in earlier stages of development. This underscores an urgent need for better standardization of Lp(a) measurement and an improved understanding of Lp(a) metabolism, physiology and the pathologic mechanisms by which Lp(a) and oxidized phospholipids on Lp(a) lead to CVD. Finally, the knowledge gaps for unique populations need to be addressed, including the possible relationship of high Lp(a) with stroke in children and to better define the unmet medical needs for Lp(a) reduction in people of all ancestries. Lp(a): A Toolkit for Health Care Professionals
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