Purpose of review
The purpose of this review is to summarize recent observations on the role of lipoprotein(a) [Lp(a)] as a risk factor mediating cardiovascular disease.
Recent findings
Lp(a) is a highly prevalent cardiovascular risk factor, with levels >30 mg/dL affecting 20–30% of the global population. Up until now, no specific therapies have been developed to lower Lp(a) levels. Three major levels of evidence support the notion that elevated Lp(a) levels are a causal, independent, genetic risk factor for cardiovascular disease; epidemiologic studies and meta-analyses, genome wide association studies and mendelian randomization studies. Recent studies also have noted that individuals with low levels of Lp(a) are associated with a higher risk of incident type 2 diabetes mellitus, and conversely individuals with high levels have a lower risk, but this association does not appear to be causal. Novel therapies to lower Lp(a) include PCSK9 inhibitors and antisense oligonucleotides directly preventing translation of apolipoprotein(a) mRNA.
Summary
With this robust and expanding clinical database, a re-awakening of interest in Lp(a) as clinical risk factor is taking place. Trials are underway with novel drugs that substantially lower Lp(a) and may reduce its contribution to cardiovascular disease.