Abstract
There is now significant evidence to support an independent causal role for lipoprotein(a) (Lp(a)) as a risk factor for atherosclerotic cardiovascular disease. Plasma Lp(a) concentrations are predominantly determined by genetic factors. However, research into Lp(a) has been hampered by incomplete understanding of its metabolism and proatherogeneic properties and by a lack of suitable animal models. Furthermore, a lack of standardized assays to measure Lp(a) and no universal consensus on optimal plasma levels remain significant obstacles. In addition, there are currently no approved specific therapies that target and lower elevated plasma Lp(a), although there are recent but limited clinical outcome data suggesting benefits of such reduction. Despite this, international guidelines now recognize elevated Lp(a) as a risk enhancing factor for risk reclassification. This review summarises the current literature on Lp(a), including its discovery and recognition as an atherosclerotic cardiovascular disease risk factor, attempts to standardise analytical measurement, interpopulation studies, and emerging therapies for lowering elevated Lp(a) levels.
Highlights
There is significant evidence to support an independent causal role for elevated lipoprotein(a) (Lp(a)) as a risk factor for atherosclerotic cardiovascular disease (ASCVD)
Subsequent cloning of the cDNA encoding the apolipoprotein(a) (apo(a)) portion revealed its homology with the fibrinolytic proenzyme, plasminogen [2], distinct structural differences were later recognized, including the disappearance of the tail domain and the first three kringle domains [3]
Genetic variants of Apolipoprotein e gene (APOE) have been shown to affect plasma Lp(a) levels [19], with the APOE ε2 variant strongly associated with low Lp(a) concentrations, this did not appear to modify any association with myocardial infarction or aortic valve stenosis [20]
Summary
There is significant evidence to support an independent causal role for elevated lipoprotein(a) (Lp(a)) as a risk factor for atherosclerotic cardiovascular disease (ASCVD). A lack of standardized assays to measure Lp(a) and no universal consensus on optimal plasma levels in different patient populations remain significant obstacles. Most international guidelines recognize elevated Lp(a) as a risk-enhancing factor that warrants further investigation. This review summarises the current Lp(a) literature including its discovery and recognition as a risk factor, attempts to standardise analytical methods, consideration of ethnic differences, as well as new treatments to lower elevated Lp(a) levels. The literature search included the search terms “lipoprotein(a)” and “Lp(a)” in combination with diagnosis, treatment, pathogenesis, and guidelines, with additional key references provided by authors of this article
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