Purpose of review: The aim of this review is to put the research of lipoprotein(a) [Lp(a)] into context with the recent advances in genetic studies and risk assessment of coronary heart disease (CHD).
Recent findings: Lp(a) has become an established independent but moderate risk factor for the development of CHD. The blood level of Lp(a) is largely controlled by the LPA gene locus itself, and a number of recent genetic studies of the LPA gene have confirmed this. The impact of the LPA gene on the risk of CHD is less well established The size of these effects is moderate and will make it difficult to obtain added predictability to risk assessment using conventional risk factors.
Summary: Although there is highly suggestive evidence for a causal relationship between Lp(a) levels and CHD, large well prepared 'Mendelian randomization' studies are needed to fully explore that relationship. The moderate effect of Lp(a) on cardiovascular risk as well as the difficulty in lowering Lp(a) blood levels makes it less useful in the practice of medicine and public health.