Lipoprotein (a)
Other names: Lp(a), Lipoprotein a, LIPOPROTEIN-a
Lipoprotein(a) [Lp(a)] is a distinct plasma lipoprotein composed of a cholesterol-rich low-density lipoprotein (LDL) particle covalently bound to apolipoprotein(a), a structurally unique protein with pro-atherogenic and pro-thrombotic properties. Lp(a) is recognized as an independent and causal risk factor for cardiovascular disease, separate from traditional lipid markers such as LDL-C or total cholesterol.
Lp(a) levels are largely genetically determined and remain relatively stable throughout life. Unlike LDL cholesterol, Lp(a) concentrations are not meaningfully reduced through lifestyle modification, including diet, exercise, or weight loss. Because of this, individuals may have a significant inherited cardiovascular risk despite otherwise normal lipid profiles.
Elevated Lp(a) contributes to atherosclerosis by promoting cholesterol deposition within arterial walls, enhancing vascular inflammation, and interfering with normal fibrinolysis (clot breakdown). High Lp(a) levels have been strongly associated with increased risk of:
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Myocardial infarction (heart attack)
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Ischemic stroke
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Peripheral arterial disease
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Aortic valve stenosis
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Recurrent arterial narrowing after revascularization
Because Lp(a) is not included in routine lipid panels, targeted testing is particularly valuable in individuals with premature cardiovascular disease, unexplained atherosclerosis, or a strong family history of heart disease.
Clinical Use
Lp(a) testing may be appropriate for individuals with:
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A family history of premature coronary artery disease
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Known or suspected genetic hypercholesterolemia
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Established atherosclerosis despite a normal standard lipid panel
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Hyperlipidemia that is resistant to conventional treatment
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Recurrent arterial stenosis or early cardiovascular events
What does it mean if your Lipoprotein (a) result is too high?
Elevated Lp(a) levels are associated with a significantly increased risk of cardiovascular disease, including heart attack, stroke, and progressive narrowing of arteries supplying vital organs.
Large population studies, including the Copenhagen Heart Study, have demonstrated that genetically elevated Lp(a) levels are causally linked to increased risk of myocardial infarction, independent of LDL cholesterol and other traditional risk factors. Because Lp(a) promotes both atherosclerosis and thrombosis, individuals with high levels may be at risk even when LDL-C is well controlled.
Elevated Lp(a) is best viewed as a lifelong, inherited risk marker, highlighting the need for aggressive management of all other modifiable cardiovascular risk factors.
Potential Treatment Considerations
For educational purposes only. Treatment decisions should be made by a qualified healthcare professional.
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Assess family history of cardiovascular disease
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Evaluate inflammatory and plaque-instability markers such as Lp-PLA₂ and MPO
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Abnormal findings may indicate vulnerable plaque and elevated thrombotic risk
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Consider vascular imaging:
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Carotid intima-media thickness (CIMT)
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Coronary artery calcium (CAC) scoring
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Optimize control of all modifiable risk factors (LDL-C, blood pressure, glucose, inflammation)
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Antiplatelet therapy (e.g., aspirin or clopidogrel) may be considered in select high-risk individuals if not contraindicated
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Niacin therapy has historically been used to lower Lp(a), though its role should be carefully evaluated on an individual basis
Emerging therapies specifically targeting Lp(a) are currently under active clinical investigation.
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What does it mean if your Lipoprotein (a) result is too low?
Low Lp(a) levels—typically defined as <5 mg/dL (approximately the lowest 20% of the population)—are generally associated with a reduced risk of myocardial infarction, ischemic stroke, and aortic stenosis.
However, multiple prospective studies have observed an inverse relationship between Lp(a) concentration and type 2 diabetes risk. Very low Lp(a) levels (often <7 mg/dL) have been associated with a modestly increased prevalence of type 2 diabetes, though the mechanisms underlying this association are not fully understood.
Importantly, low Lp(a) is not considered pathological and does not require intervention. Interpretation should always be made in the context of overall metabolic and cardiovascular risk.
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