Lipoprotein(a) as a cardiovascular risk factor: current status

Lipoprotein(a) as a cardiovascular risk factor: current status

2010 | Børge G. Nordestgaard, M. John Chapman, Kausik Ray, Jan Borén, Felicita Andreotti, Gerald F. Watts, Henry Ginsberg, Pierre Amarenco, Alberico Catapano, Olivier S. Descamps, Edward Fisher, Petri T. Kovanen, Jan Albert Kuivenhoven, Philippe Lesnik, Luis Masana, Zeljko Reiner, Marja-Riitta Taskinen, Lale Tokgözoglu, Anne Tybjærg-Hansen
The article reviews the current status of Lipoprotein(a) (Lp(a)) as a cardiovascular risk factor. Lp(a) is a plasma lipoprotein composed of an LDL-like particle with apolipoprotein B100 and an additional protein, apolipoprotein(a). Elevated Lp(a) levels are associated with an increased risk of cardiovascular disease (CVD) through prothrombotic and anti-fibrinolytic effects, as well as accelerated atherogenesis. The relationship between Lp(a) concentration and CVD risk is continuous without a threshold, and it is not confounded by conventional risk factors such as LDL or non-HDL cholesterol. Genetic studies, including Mendelian randomization, support the causal role of elevated Lp(a) in premature CVD. The article also discusses the metabolism of Lp(a), its pathophysiological mechanisms, measurement methods, and recommendations for screening, desirable levels, and treatment. It emphasizes the need for further research to better understand the role of Lp(a) in atherothrombosis and to develop selective therapies for lowering Lp(a) levels.The article reviews the current status of Lipoprotein(a) (Lp(a)) as a cardiovascular risk factor. Lp(a) is a plasma lipoprotein composed of an LDL-like particle with apolipoprotein B100 and an additional protein, apolipoprotein(a). Elevated Lp(a) levels are associated with an increased risk of cardiovascular disease (CVD) through prothrombotic and anti-fibrinolytic effects, as well as accelerated atherogenesis. The relationship between Lp(a) concentration and CVD risk is continuous without a threshold, and it is not confounded by conventional risk factors such as LDL or non-HDL cholesterol. Genetic studies, including Mendelian randomization, support the causal role of elevated Lp(a) in premature CVD. The article also discusses the metabolism of Lp(a), its pathophysiological mechanisms, measurement methods, and recommendations for screening, desirable levels, and treatment. It emphasizes the need for further research to better understand the role of Lp(a) in atherothrombosis and to develop selective therapies for lowering Lp(a) levels.
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Understanding Lipoprotein(a) as a cardiovascular risk factor%3A current status