EAS beveelt Lp(a) screening bij CVD risico patiënten aan
EAS doet aanbeveling screening Lp(a) bij patiënten met verhoogd risico op cardiovasculaire aandoeningen
New recommendations from the European Atherosclerosis Society Consensus Panel resolve controversy about lipoprotein(a) and cardiovascular risk
EAS, Hamburg, Germany, June 23 2010– On the basis of new, extensive epidemiological and genetic evidence (1-3), the European Atherosclerosis Society (EAS) Consensus Panel recommends screening for elevated lipoprotein(a), Lp(a), a plasma lipoprotein, in people at moderate to high risk of cardiovascular disease. Desirable Lp(a) levels < 50 mg/dL should be a treatment priority, after therapeutic management of low-density lipoprotein (LDL) cholesterol. This new guidance was presented today by Professor Børge G. Nordestgaard, University of Copenhagen, Denmark a member of the EAS Consensus Panel at a Late-Breaking Session of the EAS 2010 Congress, Hamburg, Germany.
‘‘The evidence clearly supports Lp(a) as a priority for reducing cardiovascular risk, beyond that associated with LDL cholesterol. Clinicians should consider screening statin-treated patients with recurrent heart disease, in addition to those considered at moderate to high risk of heart disease,’ commented Professor Nordestgaard.
Lp(a) is a plasma lipoprotein consisting of a cholesterol-rich LDL particle with one molecule of apolipoproteinB100 and an additional protein, apolipoprotein(a) (4). Plasma levels of Lp(a) are similar in men and women: one in five or 20% have levels above 50 mg/dL. Levels are lowest in non-Hispanic Caucasians and Asians, and higher in Hispanics and Blacks (5).
Meta-analysis of studies in the general population showed that elevated Lp(a) was associated with increased heart disease and stroke risk (2). Individuals with levels above 50 mg/dL have 2-3 fold risk of myocardial infarction (1). The association between elevated Lp(a) and increased cardiovascular disease risk was continuous without any threshold and did not depend on LDL cholesterol levels.
These data are supported by studies which investigated genetic variation in Lp(a) and risk for heart disease (1,3). Two variants of Lp(a), present in one in six people, together explained about 36% of the variation in plasma Lp(a) levels. Individuals with two or more of these variants had more than 2.5-fold increase in heart disease risk (3).
The EAS Consensus Panel recommends niacin (nicotinic acid, 1-3 g day) as the primary treatment for lowering elevated Lp(a) levels, based on its efficacy in reducing levels by 30-40% and in reducing cardiovascular disease (6).
‘Lifestyle appears to have little impact on Lp(a) levels. Therefore, in the absence of randomised, controlled trials selectively targeting plasma levels of Lp(a) levels, the EAS Consensus Panel supports the clinical use of niacin for lowering Lp(a) levels in individuals at-risk. However, there is a clear need for further studies in both primary and secondary prevention settings to better define who to treat and to what targets,’ said Professor John Chapman, President of the EAS, INSERM UMR-S939, Hopital de la Pitié, Paris, France.
SOURCE: European Atherosclerosis Society