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European Atherosclerosis Society recommends screening for Lp(a)
JUNE 23, 2010 | Reed Miller

Hamburg, Germany - Patients at high to moderate risk of cardiovascular disease should be screened for elevated levels of lipoprotein(a) (Lp[a]) and take niacin to bring their Lp(a) level under 50 mg/dL, according to a consensus statement from the European Atherosclerosis Society (EAS) [1].

Congress Center Hamburg, Germany
The EAS consensus panel's new scientific consensus statement on Lp(a) is not yet published, but the key points of the statement were announced during the final session of the EAS 2010 Congress here by Dr Børge Nordestgaard (University of Copenhagen, Denmark), who led some of the key studies supporting the statement.

The statement will recommend that patients with moderate or high risk of cardiovascular disease be screened for plasma lipoprotein levels. Bringing a patient's Lp(a) level under 50 mg/dL should be a treatment priority, after the management of low-density-lipoprotein cholesterol, the statement recommends.

Lp(a) is a plasma lipoprotein consisting of a cholesterol-rich LDL particle with one molecule of apolipoprotein B-100 and a molecule of apolipoprotein A. About 20% of people are thought to have plasma Lp(a) levels over 50 mg/dL; there are no gender differences in Lp(a) concentrations, but racial differences have been observed, with whites and Asians having lower levels while black and Hispanics generally have somewhat higher levels.

Since lifestyle appears to have little impact on an individual's Lp(a) level, the EAS consensus panel recommends that 1 to 3 g of niacin (nicotinic acid) daily is the best treatment for lowering Lp(a) levels. However, the group acknowledges that there have not been randomized, controlled trials selectively targeting plasma levels of Lp(a) and calls for further studies in both primary- and secondary-prevention settings to better define which patients should be targeted for treatment and what the target level of Lp(a) should be.

Lp(a) is "a risk factor that many clinicians and scientists have been aware of for a long time . . . but now it's come of age in terms of the evidence base," consensus panel cochair Dr John Chapman (Hôpital de la Pitié, Paris, France) told heartwire. "For the first time, we are proposing that there be screening of a significant number of different groups who are at intermediate as well as at high risk for atherosclerosis and cardiovascular disease.

"We consider the level of evidence to be sufficient to warrant the identification of Lp(a) as a causal, independent cardiovascular risk," Chapman said. "So that raises the ante on Lp(a) very considerably from its position over the past five or 10 years. [There have been] a series of publications, both epidemiological and genetic, over the past two years that have really clarified the evidence base around Lp(a) and its role as a risk factor."

The major studies underlying the recommendations include the June 2009 study by Dr Pia R Kamstrup (Copenhagen University Hospital, Denmark), reported by heartwire, which analyzed genetic data from three studies to prove that Lp(a) is a causal factor in MI [2]. The statement also cites a study led by Chapman, published in the June 2010 issue of Pharmacology & Therapeutics, which shows that niacin-based therapies improved patients' atherogenic lipid profile (HDL-C, LDL-C, Lp(a), triglycerides, and LDL-particle size/density) and that therefore the most effective available pharmacological approach to raise low HDL-C levels across a wide range of atherogenic lipid phenotypes is extended-release niacin, either alone or in combination with a statin [3].

This is the first statement from the consensus panel, which includes 19 experts from around the world, who began meeting in November 2009 to critically appraise the evidence for Lp(a), triglyceride-rich lipoproteins, and HDL in relation to cardiovascular risk. "One of the great difficulties in this field is evaluating the relative importance of different cardiovascular risk factors in different populations—different ethnicities and different metabolic backgrounds," Chapman said. "The society is blessed with a wide membership that covers both basic science and clinical medicine, so we decided that we would draw on that expertise in the format of the EAS consensus panel."