What you carry at this position in your DNA and what research says about it.
Heart Disease Risk: 10/10 evidence, 76 publications.
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Sample genotype (not yours): A/A
Typical Heart Disease Risk
Two copies of the common allele are associated with baseline levels of lipoprotein(a) and typical cardiovascular health.
What this genotype means: Typical lipoprotein(a) levels; Standard baseline cardiovascular risk; Normal response to statin therapy.
Sample genotype (not yours): A/G
~1.5x Higher Heart Disease Risk
Carrying one copy of the risk allele is linked to elevated lipoprotein(a) levels and an increased risk of cardiovascular events.
What this genotype means: Elevated circulating lipoprotein(a); Increased risk of coronary artery narrowing; Potentially reduced response to standard statins.
Sample genotype (not yours): G/G
~2.6x Higher Heart Disease Risk
Carrying two copies of the risk allele is associated with highly elevated lipoprotein(a) levels and a significantly higher risk of heart disease.
What this genotype means: Significantly elevated lipoprotein(a) levels; Substantially increased risk of heart valve calcification; Poorer response to standard statin medications.
Gene function and biological role
Gene Function: The LPA gene provides instructions for making apolipoprotein(a), a crucial component of a specialized cholesterol particle called lipoprotein(a) or Lp(a). This protein binds to low-density lipoprotein particles to form a highly sticky, dense complex that circulates in the bloodstream. Elevated levels of this complex promote plaque buildup in the arteries and trigger inflammatory processes in blood vessels. Unlike standard cholesterol markers, circulating levels of this lipoprotein are largely determined by genetics rather than diet or lifestyle. Consequently, variations in this gene are among the strongest known genetic risk factors for premature cardiovascular conditions.
Variant Impact: This variant, located within an intron of the LPA gene, acts as a powerful genetic regulator of lipoprotein(a) levels. The presence of the G allele significantly increases the expression of the gene, leading to elevated concentrations of circulating lipoprotein(a) particles [1]. These elevated levels directly contribute to the calcification of heart valves and the narrowing of arterial walls [2]. Because this change is structural and regulatory, its impact on cardiovascular risk remains highly consistent across different populations.
Key Insight: The risk allele not only increases the likelihood of developing heart disease but also predicts a poorer response to standard cholesterol-lowering statin therapies.
Location: LPA. Chromosome 6 · 6q25.3 · 160.6 Mb
Estimated prevalence by population
Global 91.8%; European 86.6%; African 97.6%; East Asian 99.8%; South Asian 98.0%; Americas 92.5%; Ashkenazi 94.1%; Finnish 93.0%; Middle Eastern 98.6%; Amish 95.2%.
Estimated AA genotype frequency.
Global 8.0%; European 12.9%; African 2.4%; East Asian 0.2%; South Asian 2.0%; Americas 7.4%; Ashkenazi 5.8%; Finnish 6.8%; Middle Eastern 1.4%; Amish 4.7%.
Estimated AG genotype frequency.
Global 0.2%; European 0.5%; African < 0.1%; East Asian < 0.1%; South Asian < 0.1%; Americas 0.1%; Ashkenazi 0.1%; Finnish 0.1%; Middle Eastern < 0.1%; Amish 0.1%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Cardiovascular & Metabolic
Heart Disease
Coronary Artery Disease. Evidence: 10/10. Source: PMID 36474045. Typical Risk.
Aortic Valve Stenosis. Evidence: 10/10. Source: PMID 32141789. Typical Risk.
Lipids & Cholesterol
Lipoprotein(a) Levels. Evidence: 10/10. Source: PMID 21900290. Typical Levels.
Pharmacogenomics
Lipid-Lowering Drug Response
Statin Response. Evidence: 8/10. Source: PMID 25350695. Typical Response.
Showing effects for A/G genotype
Coronary Artery Disease. Evidence: 10/10. Source: PMID 36474045. ~1.5x Increased Risk.
Aortic Valve Stenosis. Evidence: 10/10. Source: PMID 32141789. Increased Risk.
Lipoprotein(a) Levels. Evidence: 10/10. Source: PMID 21900290. Elevated Levels.
Statin Response. Evidence: 8/10. Source: PMID 25350695. Reduced Response.
Showing effects for G/G genotype
Coronary Artery Disease. Evidence: 10/10. Source: PMID 36474045. ~2.6x Increased Risk.
Aortic Valve Stenosis. Evidence: 10/10. Source: PMID 32141789. Highly Increased Risk.
Lipoprotein(a) Levels. Evidence: 10/10. Source: PMID 21900290. Highly Elevated.
Statin Response. Evidence: 8/10. Source: PMID 25350695. Poorer Response.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
This genotype represents the most common genetic profile globally, carrying two copies of the standard maternal and paternal alleles. Circulating levels of lipoprotein(a) are typically low or within the normal range for individuals with this profile [1]. Consequently, there is no genetically elevated risk for early-onset coronary artery disease or heart valve calcification from this specific marker [2]. Standard cardiovascular prevention guidelines and routine lipid screenings remain the most appropriate path. Furthermore, conventional lipid-lowering medications like statins generally perform with expected efficacy if prescribed [3].
Typical lipoprotein(a) levels; Standard baseline cardiovascular risk; Normal response to statin therapy.
Sample genotype: AG (Heterozygous)
Inheriting one copy of the risk allele leads to a moderate elevation in circulating lipoprotein(a) particles in the bloodstream [1]. This elevation is associated with an approximate 1.5-fold increase in the risk of developing coronary artery disease and heart attacks [2]. Additionally, the sticky nature of these particles increases the likelihood of mineral deposits forming on the aortic heart valve, which can restrict blood flow over time [3]. Individuals with this genotype may also experience a slightly less robust reduction in LDL cholesterol when taking standard statin medications [4]. Managing other cardiovascular risk factors, such as blood pressure and lifestyle habits, becomes particularly important to offset this genetic predisposition.
Elevated circulating lipoprotein(a); Increased risk of coronary artery narrowing; Potentially reduced response to standard statins.
Sample genotype: GG (Homozygous)
Having two copies of the risk allele is a strong genetic driver of highly elevated lipoprotein(a) concentrations [1]. This profile is linked to an approximate 2.6-fold increase in the risk of premature coronary artery disease and myocardial infarction [2]. The high concentration of these sticky particles accelerates plaque accumulation and promotes calcification of the aortic valve [3]. Furthermore, clinical studies indicate that individuals with this genetic profile show a poorer response to standard statin therapies, often leaving them with higher residual cardiovascular risk [4]. Early screening of lipoprotein(a) levels and comprehensive cardiovascular risk management are highly relevant for individuals with this genetic signature.
Significantly elevated lipoprotein(a) levels; Substantially increased risk of heart valve calcification; Poorer response to standard statin medications.
Variants with shared genetic architecture
rs140570886 · LPA Gene · Chr 6 · Heart Disease Risk
rs55730499 · LPA Gene · Chr 6 · Heart Disease Risk
rs73596816 · LPA Gene · Chr 6 · Lipoprotein a Levels
Genetic associations with valvular calcification and aortic stenosis.
LPA Variants Are Associated With Residual Cardiovascular Risk in Patients Receiving Statins.
Content updated August 2026.
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