Lipoprotein(a) [Lp(a)] is a significant cardiovascular risk factor, with elevated levels associated with increased risk of cardiovascular disease (CVD) and coronary heart disease (CHD). Recent genetic studies suggest that elevated Lp(a) levels, like elevated LDL cholesterol, are causally linked to premature CVD/CHD. The association is continuous without a threshold and is not dependent on LDL or non-HDL cholesterol levels. Mechanistically, elevated Lp(a) may contribute to atherothrombosis through prothrombotic/anti-fibrinolytic effects due to its structural similarity to plasminogen and plasmin, or through accelerated atherosclerosis due to its cholesterol-rich nature. The European Atherosclerosis Society Consensus Panel recommends screening for elevated Lp(a) in individuals at intermediate or high CVD/CHD risk, particularly those with premature CVD, familial hypercholesterolemia, a family history of premature CVD, or elevated Lp(a). A desirable Lp(a) level is <50 mg/dL. Niacin is recommended as the primary treatment for Lp(a) reduction, with LDL apheresis as an option for extreme cases. The consensus emphasizes the importance of measuring Lp(a) using isoform-insensitive assays and highlights the need for further research to better understand Lp(a) metabolism and develop targeted therapies. The role of Lp(a) in CVD prevention and treatment is increasingly recognized, and integrating Lp(a) into clinical guidelines is essential for effective risk management.Lipoprotein(a) [Lp(a)] is a significant cardiovascular risk factor, with elevated levels associated with increased risk of cardiovascular disease (CVD) and coronary heart disease (CHD). Recent genetic studies suggest that elevated Lp(a) levels, like elevated LDL cholesterol, are causally linked to premature CVD/CHD. The association is continuous without a threshold and is not dependent on LDL or non-HDL cholesterol levels. Mechanistically, elevated Lp(a) may contribute to atherothrombosis through prothrombotic/anti-fibrinolytic effects due to its structural similarity to plasminogen and plasmin, or through accelerated atherosclerosis due to its cholesterol-rich nature. The European Atherosclerosis Society Consensus Panel recommends screening for elevated Lp(a) in individuals at intermediate or high CVD/CHD risk, particularly those with premature CVD, familial hypercholesterolemia, a family history of premature CVD, or elevated Lp(a). A desirable Lp(a) level is <50 mg/dL. Niacin is recommended as the primary treatment for Lp(a) reduction, with LDL apheresis as an option for extreme cases. The consensus emphasizes the importance of measuring Lp(a) using isoform-insensitive assays and highlights the need for further research to better understand Lp(a) metabolism and develop targeted therapies. The role of Lp(a) in CVD prevention and treatment is increasingly recognized, and integrating Lp(a) into clinical guidelines is essential for effective risk management.