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Published on: October 12, 2017
Lipoprotein(a) as a cardiovascular risk factor: current status
Børge G Nordestgaard1, M John Chapman, Kausik Ray
1Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, University of Copenhagen, DK-2730 Herlev, Denmark. brno@heh.regionh.dk
Elevated lipoprotein(a) [Lp(a)] is a causal risk factor for cardiovascular disease (CVD). Screening is recommended for intermediate to high-risk individuals, with a target Lp(a) level below 50 mg/dL and niacin as a primary treatment.
Area of Science:
- Cardiovascular Medicine and Genetics
- Lipid Metabolism and Atherosclerosis
- Preventive Cardiology
Background:
- Lipoprotein(a) [Lp(a)] is an independent and causal risk factor for cardiovascular disease (CVD), including coronary heart disease (CHD).
- The association between elevated Lp(a) and CVD risk is continuous, without a discernible threshold, and independent of LDL- or non-HDL-cholesterol levels.
- Mechanisms for Lp(a)]'s pathogenicity include prothrombotic/anti-fibrinolytic effects and acceleration of atherosclerosis due to its cholesterol-rich particle.
Framework:
- Evaluation of Lp(a) as a cardiovascular risk factor.
- Recommendations for screening, desirable levels, and therapeutic strategies for elevated Lp(a).
Implementation:
- Screening for Lp(a) is advised once, using an isoform-insensitive assay, in individuals at intermediate or high CVD/CHD risk.
- Specific indications for screening include premature CVD, familial hypercholesterolemia, family history of premature CVD, recurrent CVD despite statin therapy, and defined 10-year CVD/CHD risk percentages.
- A desirable Lp(a) level is recommended below the 80th percentile (approximately <50 mg/dL), prioritized after LDL-cholesterol reduction.
Implications:
- Niacin therapy (1-3 g/day) is recommended for Lp(a) and CVD/CHD risk reduction, supported by meta-analyses of randomized controlled trials.
- LDL-apheresis is an effective treatment for Lp(a) removal in severe cases.
- These strategies aim to mitigate the causal link between elevated Lp(a) and premature cardiovascular events.
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