U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Lipoprotein A

; ; .

Author Information and Affiliations

Last Update: February 27, 2024.


Lipoprotein(a), or Lp(a), is an established and genetically determined risk factor for atherosclerosis, coronary artery disease, stroke, thrombosis, and aortic stenosis.[1] Structurally, it is a variant of low-density lipoprotein and features apolipoprotein(a), or apo(a), which is bound to apolipoprotein B-100, or apoB100. These 2 structures are assembled in the hepatocyte cell membranes and are bound by 1 disulfide bridge.[2] The electrophoretic mobility of Lp(a) is typically pre-β but can vary between that of low-density lipoprotein (β) and albumin (pre-α).[3]

Plasma concentrations of Lp(a) and the apo(a) isoform are inversely related.[4] The variation in isoforms is induced by the number of kringle IV repeats in the LP(a) gene. The variation in kringle units leads to the variable levels of Lp(a) observed in the general population. In general, individuals with fewer kringle repeats tend to have smaller Lp(a) particles but higher serum levels. In addition, larger isoforms of apo(a) lead to an increased accumulation of its precursor intracellularly within the endoplasmic reticulum.[5] 

Lp(a) levels >50 mg/dL are associated with an increased risk of cardiovascular diseases.[2] Internationally, there is a general disagreement on screening guidelines. Screening patients for elevated Lp(a) levels could help identify those who need more aggressive lipid therapy and cardiovascular disease risk management. The suggestion has been made that, for younger patients, coronary artery disease could be explained by Lp(a), with or without other risk factors.[6]

No specific therapy exists for treating elevated Lp(a). Most generalized screening aims to identify elevated Lp(a) as an existing risk factor, followed by subsequent optimization of overall cardiac health as the primary treatment. While certain medications such as proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors and niacin directly lower Lp(a) levels, there is no Food and Drug Administration (FDA)-approved medication for the treatment of elevated Lp(a). Further research will contribute to the improvement of both screening guidelines and treatment modalities.[7]

Etiology and Epidemiology

Elevated Lp(a) levels are associated with an increased risk of cardiovascular disease and stroke.[6] The increased risk has generally been attributed to the atherosclerotic and thrombotic properties of this lipoprotein.

Lp(a) levels are also considered to be determined genetically. Lp(a) gene polymorphisms generally lead to highly variable Lp(a) levels within the population, ranging from <1 mg/dL to >1000 mg/dL. On average, individuals of African descent tend to have higher Lp(a) levels compared to those of White and Asian racial backgrounds.[8][2] Patients with Lp(a) levels >50 mg/dL are considered to have an increased risk of heart disease.[9] To date, there is no convincing evidence that mild-to-moderate elevations (<50 mg/dL) lead to an increased risk of heart disease or stroke. 


Lp(a) is a distinct lipoprotein structurally related to low-density lipoprotein, containing an apoB100 per particle and sharing a similar lipid composition. Lp(a) also includes a carbohydrate-rich protein called apo(a), which is covalently bound to apo B 100 through a disulfide linkage.[2] Apo(a) exhibits significant sequence homology with plasminogen; however, unlike plasminogen, it is not an active protease.[10] Apo(a) contains a high degree of variation in its polypeptide chain length because of a variable number of kringle domains.[8] Plasminogen contains 5 kringle domains, whereas apo(a) contains only kringle types 4 and 5. There are 10 distinct classes of kringle IV-like domains in apo(a) that differ in amino acid sequences. Kringle IV type 1 and kringle IV types 3 to 10 are present as a single copy, whereas kringle IV type 2 exists in varying numbers of repeats (1 to >40). Thus, there are different-sized isoforms of apo(a) classically described as either large, high molecular weight or small, low molecular weight forms.[11]

Paradoxically, due to the ease of hepatic production and secretion of the low molecular weight isoforms compared to high molecular weight isoforms, there can be a significant discordance between Lp(a) mass and Lp(a) particle (Lp(a)-P) concentrations. At the same Lp(a) mass, those with low molecular weight isoforms will have a higher Lp(a)-P concentration compared to those with high molecular weight isoforms.[12] Low molecular weight isoforms are believed to be a significant cause of cardiovascular disease compared to high molecular weight isoforms. However, this may be primarily related to their higher Lp(a)-P concentration rather than anything inherent in the particle. Adding to the complexity is the codominant type of inheritance that occurs with Lp(a), with patients frequently having 2 different types of apo(a)-size isoforms expressed differently.[13]

According to genetic and epidemiological studies, Lp(a) is considered pro-atherosclerotic, pro-inflammatory, pro-thrombotic, and anti-fibrinolytic.[6] Lp(a) increases the expression of vascular cell adhesion molecule-1 (VCAM-1) and E-selectin, thereby promoting the adhesion of monocytes to the endothelium and initiating atherosclerotic plaque formation.[14] Lp(a) exhibits a higher affinity for the vascular wall, proteoglycans, and fibronectin on the endothelial cell surface compared to low-density lipoprotein cholesterol and other apo B-containing lipoproteins. This leads to the accumulation of Lp(a) in the arterial intima, contributing to the development of atherosclerotic lesions. Macrophages can take up Lp(a), leading to the formation of foam cells, which is a hallmark of early atherosclerosis.[15]

Because of its structure, Lp(a) leads to reduced fibrinolysis. Specifically, apo(a) carries a structure similar to tissue plasminogen activator and plasminogen. This similarity allows it to compete with plasminogen for its specific binding site, thereby interfering with its function and leading to reduced fibrinolysis.[16] Thrombogenesis is also stimulated by Lp(a) as it leads to increased plasminogen activator inhibitor-1. The potential benefits of Lp(a) for the human body remain uncertain.[17] A theory suggests that Lp(a) has a role in the healing of wounds. However, individuals with significantly lower Lp(a) levels do not appear to have long-term health risks.[18]

Specimen Requirements and Procedure

Serum or plasma is generally acceptable for measuring Lp(a) levels. The serum or plasma should be separated from cells as soon as possible, within 2 hours. Fasting is not required for Lp(a) measurement, and despite being genetically determined, inflammation may influence Lp(a) levels.[19] The specific specimen requirements provided by the laboratory performing the test should be followed to ensure accurate and reliable results. Specimens that are grossly hemolyzed, lipemic, or icteric may be rejected.[20]

Diagnostic Tests

Lp(a) is screened through a serum blood test. The general purpose of screening for Lp(a) is to identify individuals at higher risk for cardiovascular disease. Today, there is variability in expert opinion on when to screen for elevated Lp(a). The National Lipid Association (NLA) recommends considering Lp(a) testing in cases with a significant family history of premature atherosclerotic cardiovascular disease among first-degree relatives, personal history of premature atherosclerotic cardiovascular disease, and severe primary hyperlipidemia. The NLA also recommends considering Lp(a) testing to aid in the process of shared decision-making regarding statin therapy for individuals in the borderline atherosclerotic cardiovascular disease risk category.[21] The American College of Cardiology and the American Heart Association do not have official Lp(a) screening guidelines. Canadian guidelines recommend universal screening for Lp(a).[22]

The European Atherosclerosis Society (EAS) has established guidelines outlining situations where screening for Lp(a) is typically advised. These criteria include patients with a personal history of premature cardiovascular disease, those experiencing recurrent cardiovascular disease events while on statin therapy, and individuals with a ≥10% 10-year risk of cardiovascular disease. A family history of premature cardiovascular disease, elevated Lp(a), and familial hypercholesterolemia are also indications for Lp(a) screening. The European Society of Cardiology (ESC) recommends screening for Lp(a) at least once during an individual's lifetime.[23]

No recommendations or guidelines exist for testing Lp(a) in pediatric patient populations, mainly due to insufficient data on Lp(a) within this age group. Further research is required in this patient population to help develop better screening guidelines. 

Testing Procedures

Several commercially available immunoassays, such as enzyme-linked immunosorbent assay (ELISA), immunoturbidometric, and immunonephelometric assays, are used to quantify Lp(a). Most of these assays, except for ELISA, use polyclonal antibodies from various animal species. Commercially available, direct-binding, sandwich-type ELISAs typically combine monoclonal and polyclonal antibodies.[24]

The precise measurement of Lp(a) in human plasma is significantly impacted by the structural variability of Lp(a) that results from apo(a) size heterogeneity. Different Lp(a) particles contain varying quantities of repeating antigenic determinants, and the responsiveness of the antibodies against these repeated epitopes can change depending on the size of the apo(a) particle. As a consequence, immunoassays using polyclonal or monoclonal antibodies specifically targeting kringle IV type 2 epitopes will tend to underestimate apo(a) concentration in samples with apo(a) of smaller size compared to the apo(a) present in the assay calibrator, and overestimate the apo(a) concentration in samples with apo(a) of larger size.[2] To address these challenges, researchers have developed isoform-independent assays that aim to accurately measure Lp(a) without the impact of apo(a) size polymorphism. For example, a monoclonal antibody (a-40) targeting a unique epitope located in KIV 9 of apo(a) has been used in the development of an ELISA that accurately measures Lp(a) without the impact of apo(a) size polymorphism.[25]

In summary, the varying immunoreactivity of antibodies to different apo(a) size isoforms can lead to inaccurate measurements of Lp(a) levels, leading to overestimating or underestimating the true values. This highlights the importance of using standardized assays and considering the impact of apo(a) size heterogeneity when interpreting Lp(a) measurements.[24]

Interfering Factors

Ethanol consumption, niacin supplements, aspirin, and oral estrogen supplementation may affect the results' accuracy. The duration for which an individual should stop taking medications or supplements that can interfere with Lp(a) analysis results may vary.[26] The specific instructions provided by the laboratory performing the test should be followed.[27] 

Results, Reporting, and Critical Findings

Lp(a) is traditionally measured in mg/dL, whereas ideally, it should be measured in nmol/L due to large interindividual size heterogeneity resulting from kringle IV type 2.[28] The desirable and optimal Lp(a) test result range is <14 mg/dL. The highest risk range is >50 mg/dL. Patients with an Lp(a) of 14 to 30 mg/dL are considered to be at borderline risk, whereas those within the range of 31 to 50 mg/dL are at high risk.[29]

Lp(a) levels directly contribute to serum low-density lipoprotein levels because Lp(a) particles contain low-density lipoprotein particles. Laboratory testing for Lp(a) often also includes lipoprotein-X (LpX) levels reported as a separate result. These compounds consist of cholesterol and phospholipids, and high levels are associated with cholestasis and hyperviscosity syndromes.[30]

Since Lp(a) is genetically transmitted, screening is considered for young individuals whose parents have high Lp(a) levels; conversely, reverse cascade screening is recommended when a child is found to have an elevated level of Lp(a).[31]

Clinical Significance

The primary reason for screening patients for Lp(a) is to help further identify those at high risk for heart disease, especially in the absence of other major risk factors. In addition, it also helps identify those patients who may require more intensive lipid therapy.[32] Patients with significantly elevated Lp(a) levels should generally be treated to achieve a target of <50 mg/dL. A treatment option is daily niacin, which may lower Lp(a) levels by 20% to 30%. However, niacin has not been associated with improved cardiac outcomes despite its known beneficial effect on all lipid markers and Lp(a).[33]

Statins have shown mixed results and, in some cases, have been shown to increase Lp(a).[34] Nonetheless, statins are a primary treatment option for patients with hyperlipidemia. High Lp(a) levels may indicate the need for more intensive statin therapy to optimize a patient's low-density lipoprotein level and reduce their risk for coronary artery disease. PCSK9 inhibitors are also an option for lowering Lp(a). A meta-analysis showed PCSK9 inhibitors lowered Lp(a) by 26%, in addition to improved cardiac outcomes.[35] Cumulatively, it is not yet evident if elevated Lp(a) remains to be an independent significant risk factor even after successful treatment. 

Less commonly used options include lipid apheresis and an investigational therapy called antisense therapy. Generally, lipid apheresis may be reserved for the most severe refractory cases and has a very limited role in treating elevated Lp(a). Apheresis will also cause transient declines in Lp(a) levels and serum levels can generally begin to climb back up.[6]

Hormonal drugs may improve Lp(a) levels but are not necessarily associated with improved cardiovascular outcomes. Estrogen can improve Lp(a) levels and has been discussed in the context of improving potential cardiac risk profiles, but it is not currently used as a therapy to improve lipid markers. Estrogen also carries other potential risks for certain patient populations and is unlikely to be established as a treatment modality.[36] 

Testosterone replacement therapy has been shown to lower Lp(a) levels. Further research on testosterone replacement therapy is necessary to draw a conclusion regarding its role in preventative cardiology, as the cumulative evidence is currently unclear. Of note, testosterone replacement therapy can lead to lower HDL levels, thereby increasing the risk of atherosclerosis.[37] L-carnitine may also lower Lp(a) levels, but it has been associated with increased levels of trimethylamine N-oxide (TMAO), potentially leading to atherosclerosis.[38] More therapies continue to arise, and a key factor will be whether or not cardiac outcomes are improved.[39] Further research is needed to help identify medications that directly decrease Lp(a) levels. 

Lp(a) levels are primarily determined by genetics, but some lifestyle changes can help reduce the risk of cardiovascular disease associated with high Lp(a) levels.[40] Consuming more vegetables, fruits, nuts, and flaxseed may help decrease Lp(a) levels. In a 2-week study involving 10 individuals, a diet rich in these foods led to a reduction of Lp(a) levels by 24%.[41] In a 6-week study involving 38 individuals with high Lp(a) levels, ground flaxseed was found to reduce Lp(a) levels by ~7%. Similarly, in another 10-week study involving 62 individuals, Lp(a) decreased by 14%.[42]

The relationship between exercise and Lp(a) levels is still not fully understood. Some studies suggest that moderate exercise has little effect on serum Lp(a) concentration. However, other studies suggest that intense load-bearing exercise training, such as distance running or weight lifting, may increase serum Lp(a) levels over several months to years.[43]

Quality Control and Lab Safety

The clinical laboratory is involved in many aspects of the analytical phase to ensure high-quality testing.[44] Overseeing quality management procedures in the clinical laboratory includes the initial step of controlling a procedure, quality control (QC), and quality assurance, a broader component providing proficiency testing, personnel competency testing, inventory monitoring, and equipment calibration and maintenance.[45] Internal QC ensures that measurement procedures meet specifications when patient testing occurs. QC samples are measured at intervals along with patient samples. Recovery of the expected target values for the QC samples allows the laboratory to verify that a measurement procedure is working correctly and the results for patient samples can be reported.[46]

For non-waived tests, laboratory regulations require analysis of at least 2 levels of QCl materials once every 24 hours as a minimum requirement. If necessary, laboratories can assay QC samples more frequently to ensure accurate results. QC samples should be assayed after calibration or maintenance of an analyzer to verify the correct method performance.[47]

Considerations in the design of a QC plan include the analytical performance capability of a measurement procedure and the risk of harm to a patient that might occur from erroneous laboratory test results used for clinical care decisions. An erroneous laboratory test result is a hazardous condition that may or may not cause harm to a patient depending on how the laboratory test is used for patient monitoring and treatment, the magnitude of the error, and subsequent action or inaction taken by a clinical care provider.[48]

The laboratory must participate in the external QC or proficiency testing program.[49] This is a regulatory requirement published by the Centers for Medicare and Medicaid Services (CMS) in the Clinical Laboratory Improvement Amendments (CLIA) regulations. External QC, also called external quality assessment or proficiency testing, is an assessment process in which samples are received from an independent external organization, and the laboratory does not know the expected values. The results for the external quality assessment or proficiency testing samples are compared with target values assigned to the samples to verify that a laboratory’smeasurement procedures meet the expected performance.[50] In addition to internal and external QC, the results obtained from testing patient samples (for example, medians of patient results) can be used to assess and monitor the performance of measurement procedures.[51]

Laboratory personnel should wear appropriate personal protective equipment such as lab coats, gloves, safety goggles, and masks to protect against chemical splashes, biological hazards, and other potential risks in the laboratory.[52] Material safety data sheets should be followed to ensure proper handling, storage, and disposal of chemicals. Other QC procedures include regular inspection and maintenance of laboratory equipment to ensure they are in proper working condition, adhering to regulations and guidelines for disposing of hazardous waste materials, using designated waste disposal containers for different types of waste, washing hands thoroughly before and after working in the laboratory, and refraining from eating, drinking, and applying cosmetics in the lab area.[53] All personnel working in the clinical laboratory should actively maintain a safe working environment and adhere to established safety protocols to ensure the well-being of all individuals involved.[54]

Enhancing Healthcare Team Outcomes

Lp(a) is a genetically determined independent risk factor for the development of atherosclerosis. Today, it is unclear if direct interventions and treatments of Lp(a) help change patient outcomes from a cardiac standpoint. However, given that it is a known risk factor for heart disease, a team-based effort is required to minimize the patient's other cardiac risks to improve cardiac outcomes.

Lipid therapy often requires an interprofessional healthcare team approach to achieve maximum success for the patient. The clinician oversees the prescription of lipid therapy medications, installs appropriate lifestyle modifications, and makes appropriate referrals. Treatment of more advanced lipid disorders benefits from having a pharmacist and dietitian involved to ensure appropriate medication protocols are in place and optimized dietary interventions are instituted. This team-based effort is vital in preventative cardiology for the patient population.

Lp(a) testing is an essential tool in cardiovascular risk assessment, requiring the collective efforts of a multidisciplinary healthcare team. By fostering communication, standardizing protocols, and emphasizing patient education, healthcare teams can enhance their ability to provide comprehensive care, ultimately leading to improved patient outcomes in cardiovascular health.

Review Questions


Scipione CA, Koschinsky ML, Boffa MB. Lipoprotein(a) in clinical practice: New perspectives from basic and translational science. Crit Rev Clin Lab Sci. 2018 Jan;55(1):33-54. [PubMed: 29262744]
Maranhão RC, Carvalho PO, Strunz CC, Pileggi F. Lipoprotein (a): structure, pathophysiology and clinical implications. Arq Bras Cardiol. 2014 Jul;103(1):76-84. [PMC free article: PMC4126764] [PubMed: 25120086]
Yamauchi K. [Electrophoretic Analysis of Serum Lipoproteins: Its Usefulness and Problems]. Rinsho Byori. 2014 Nov;62(11):1079-87. [PubMed: 27509725]
Rader DJ, Cain W, Ikewaki K, Talley G, Zech LA, Usher D, Brewer HB. The inverse association of plasma lipoprotein(a) concentrations with apolipoprotein(a) isoform size is not due to differences in Lp(a) catabolism but to differences in production rate. J Clin Invest. 1994 Jun;93(6):2758-63. [PMC free article: PMC294537] [PubMed: 8201014]
Enas EA, Varkey B, Dharmarajan TS, Pare G, Bahl VK. Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction. Indian Heart J. 2019 Mar-Apr;71(2):99-112. [PMC free article: PMC6620428] [PubMed: 31280836]
Nordestgaard BG, Chapman MJ, Ray K, Borén J, Andreotti F, Watts GF, Ginsberg H, Amarenco P, Catapano A, Descamps OS, Fisher E, Kovanen PT, Kuivenhoven JA, Lesnik P, Masana L, Reiner Z, Taskinen MR, Tokgözoglu L, Tybjærg-Hansen A., European Atherosclerosis Society Consensus Panel. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010 Dec;31(23):2844-53. [PMC free article: PMC3295201] [PubMed: 20965889]
Kotani K, Banach M. Lipoprotein(a) and inhibitors of proprotein convertase subtilisin/kexin type 9. J Thorac Dis. 2017 Jan;9(1):E78-E82. [PMC free article: PMC5303088] [PubMed: 28203441]
Boerwinkle E, Leffert CC, Lin J, Lackner C, Chiesa G, Hobbs HH. Apolipoprotein(a) gene accounts for greater than 90% of the variation in plasma lipoprotein(a) concentrations. J Clin Invest. 1992 Jul;90(1):52-60. [PMC free article: PMC443062] [PubMed: 1386087]
Klausen IC, Sjøl A, Hansen PS, Gerdes LU, Møller L, Lemming L, Schroll M, Faergeman O. Apolipoprotein(a) isoforms and coronary heart disease in men: a nested case-control study. Atherosclerosis. 1997 Jul 11;132(1):77-84. [PubMed: 9247362]
Romagnuolo R, Marcovina SM, Boffa MB, Koschinsky ML. Inhibition of plasminogen activation by apo(a): role of carboxyl-terminal lysines and identification of inhibitory domains in apo(a). J Lipid Res. 2014 Apr;55(4):625-34. [PMC free article: PMC3966697] [PubMed: 24478033]
Sandmark J, Tigerström A, Akerud T, Althage M, Antonsson T, Blaho S, Bodin C, Boström J, Chen Y, Dahlén A, Eriksson PO, Evertsson E, Fex T, Fjellström O, Gustafsson D, Herslöf M, Hicks R, Jarkvist E, Johansson C, Kalies I, Karlsson Svalstedt B, Kartberg F, Legnehed A, Martinsson S, Moberg A, Ridderström M, Rosengren B, Sabirsh A, Thelin A, Vinblad J, Wellner AU, Xu B, Östlund-Lindqvist AM, Knecht W. Identification and analyses of inhibitors targeting apolipoprotein(a) kringle domains KIV-7, KIV-10, and KV provide insight into kringle domain function. J Biol Chem. 2020 Apr 10;295(15):5136-5151. [PMC free article: PMC7152747] [PubMed: 32132173]
Chan DC, Watts GF, Coll B, Wasserman SM, Marcovina SM, Barrett PHR. Lipoprotein(a) Particle Production as a Determinant of Plasma Lipoprotein(a) Concentration Across Varying Apolipoprotein(a) Isoform Sizes and Background Cholesterol-Lowering Therapy. J Am Heart Assoc. 2019 Apr 02;8(7):e011781. [PMC free article: PMC6509712] [PubMed: 30897995]
Reyes-Soffer G, Ginsberg HN, Berglund L, Duell PB, Heffron SP, Kamstrup PR, Lloyd-Jones DM, Marcovina SM, Yeang C, Koschinsky ML., American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Radiology and Intervention; and Council on Peripheral Vascular Disease. Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association. Arterioscler Thromb Vasc Biol. 2022 Jan;42(1):e48-e60. [PMC free article: PMC9989949] [PubMed: 34647487]
Cook-Mills JM, Marchese ME, Abdala-Valencia H. Vascular cell adhesion molecule-1 expression and signaling during disease: regulation by reactive oxygen species and antioxidants. Antioxid Redox Signal. 2011 Sep 15;15(6):1607-38. [PMC free article: PMC3151426] [PubMed: 21050132]
Lu Y, Cui X, Zhang L, Wang X, Xu Y, Qin Z, Liu G, Wang Q, Tian K, Lim KS, Charles CJ, Zhang J, Tang J. The Functional Role of Lipoproteins in Atherosclerosis: Novel Directions for Diagnosis and Targeting Therapy. Aging Dis. 2022 Apr;13(2):491-520. [PMC free article: PMC8947823] [PubMed: 35371605]
Anglés-Cano E, de la Peña Díaz A, Loyau S. Inhibition of fibrinolysis by lipoprotein(a). Ann N Y Acad Sci. 2001;936:261-75. [PubMed: 11460483]
Ugovšek S, Šebeštjen M. Lipoprotein(a)-The Crossroads of Atherosclerosis, Atherothrombosis and Inflammation. Biomolecules. 2021 Dec 24;12(1) [PMC free article: PMC8773759] [PubMed: 35053174]
Orsó E, Schmitz G. Lipoprotein(a) and its role in inflammation, atherosclerosis and malignancies. Clin Res Cardiol Suppl. 2017 Mar;12(Suppl 1):31-37. [PMC free article: PMC5352764] [PubMed: 28188431]
Nordestgaard BG, Langsted A, Mora S, Kolovou G, Baum H, Bruckert E, Watts GF, Sypniewska G, Wiklund O, Borén J, Chapman MJ, Cobbaert C, Descamps OS, von Eckardstein A, Kamstrup PR, Pulkki K, Kronenberg F, Remaley AT, Rifai N, Ros E, Langlois M., European Atherosclerosis Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) joint consensus initiative. Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points-a joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. Eur Heart J. 2016 Jul 01;37(25):1944-58. [PMC free article: PMC4929379] [PubMed: 27122601]
Nikolac N. Lipemia: causes, interference mechanisms, detection and management. Biochem Med (Zagreb). 2014;24(1):57-67. [PMC free article: PMC3936974] [PubMed: 24627715]
Wilson DP, Jacobson TA, Jones PH, Koschinsky ML, McNeal CJ, Nordestgaard BG, Orringer CE. Use of Lipoprotein(a) in clinical practice: A biomarker whose time has come. A scientific statement from the National Lipid Association. J Clin Lipidol. 2019 May-Jun;13(3):374-392. [PubMed: 31147269]
Grundy SM, Stone NJ, Bailey AL, Beam C, Birtcher KK, Blumenthal RS, Braun LT, de Ferranti S, Faiella-Tommasino J, Forman DE, Goldberg R, Heidenreich PA, Hlatky MA, Jones DW, Lloyd-Jones D, Lopez-Pajares N, Ndumele CE, Orringer CE, Peralta CA, Saseen JJ, Smith SC, Sperling L, Virani SS, Yeboah J. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Jun 18;139(25):e1046-e1081. [PubMed: 30565953]
Mach F, Baigent C, Catapano AL, Koskinas KC, Casula M, Badimon L, Chapman MJ, De Backer GG, Delgado V, Ference BA, Graham IM, Halliday A, Landmesser U, Mihaylova B, Pedersen TR, Riccardi G, Richter DJ, Sabatine MS, Taskinen MR, Tokgozoglu L, Wiklund O., ESC Scientific Document Group. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020 Jan 01;41(1):111-188. [PubMed: 31504418]
Marcovina SM, Albers JJ. Lipoprotein (a) measurements for clinical application. J Lipid Res. 2016 Apr;57(4):526-37. [PMC free article: PMC4808779] [PubMed: 26637278]
Marcovina SM, Navabi N, Allen S, Gonen A, Witztum JL, Tsimikas S. Development and validation of an isoform-independent monoclonal antibody-based ELISA for measurement of lipoprotein(a). J Lipid Res. 2022 Aug;63(8):100239. [PMC free article: PMC9352967] [PubMed: 35688187]
Kostner KM, März W, Kostner GM. When should we measure lipoprotein (a)? Eur Heart J. 2013 Nov;34(42):3268-76. [PubMed: 23735860]
Herzum I, Giehl C, Soufi M, Junclas H, Wahl HG. Interference in a homogeneous assay for low-density lipoprotein cholesterol by lipoprotein X. Clin Chem Lab Med. 2007;45(5):667-71. [PubMed: 17484632]
Cegla J, France M, Marcovina SM, Neely RDG. Lp(a): When and how to measure it. Ann Clin Biochem. 2021 Jan;58(1):16-21. [PMC free article: PMC7791270] [PubMed: 33040574]
Nissen SE, Wolski K, Cho L, Nicholls SJ, Kastelein J, Leitersdorf E, Landmesser U, Blaha M, Lincoff AM, Morishita R, Tsimikas S, Liu J, Manning B, Kozlovski P, Lesogor A, Thuren T, Shibasaki T, Matei F, Silveira FS, Meunch A, Bada A, Vijan V, Bruun NE, Nordestgaard BG., Lp(a)HERITAGE Investigators. Lipoprotein(a) levels in a global population with established atherosclerotic cardiovascular disease. Open Heart. 2022 Oct;9(2) [PMC free article: PMC9577925] [PubMed: 36252994]
Ćwiklińska A, Mickiewicz A, Kowalski R, Kortas-Stempak B, Kuchta A, Mucha K, Makowiecki M, Gliwińska A, Lewandowski K, Pączek L, Fijałkowski M, Gruchała M, Jankowski M. Detection of Lipoprotein X (LpX): A challenge in patients with severe hypercholesterolaemia. J Med Biochem. 2020 Sep 02;39(3):283-289. [PMC free article: PMC7682847] [PubMed: 33269016]
Chakraborty A, Chan DC, Ellis KL, Pang J, Barnett W, Woodward AM, Vorster M, Norman R, Moses EK, Watts GF. Cascade testing for elevated lipoprotein(a) in relatives of probands with high lipoprotein(a). Am J Prev Cardiol. 2022 Jun;10:100343. [PMC free article: PMC9062205] [PubMed: 35517871]
Saeedi R, Frohlich J. Lipoprotein (a), an independent cardiovascular risk marker. Clin Diabetes Endocrinol. 2016;2:7. [PMC free article: PMC5471681] [PubMed: 28702242]
Boden WE, Sidhu MS, Toth PP. The therapeutic role of niacin in dyslipidemia management. J Cardiovasc Pharmacol Ther. 2014 Mar;19(2):141-58. [PubMed: 24363242]
Tsimikas S, Gordts PLSM, Nora C, Yeang C, Witztum JL. Statin therapy increases lipoprotein(a) levels. Eur Heart J. 2020 Jun 21;41(24):2275-2284. [PubMed: 31111151]
Navarese EP, Kolodziejczak M, Schulze V, Gurbel PA, Tantry U, Lin Y, Brockmeyer M, Kandzari DE, Kubica JM, D'Agostino RB, Kubica J, Volpe M, Agewall S, Kereiakes DJ, Kelm M. Effects of Proprotein Convertase Subtilisin/Kexin Type 9 Antibodies in Adults With Hypercholesterolemia: A Systematic Review and Meta-analysis. Ann Intern Med. 2015 Jul 07;163(1):40-51. [PubMed: 25915661]
Harman SM, Vittinghoff E, Brinton EA, Budoff MJ, Cedars MI, Lobo RA, Merriam GR, Miller VM, Naftolin F, Pal L, Santoro N, Taylor HS, Black DM. Timing and duration of menopausal hormone treatment may affect cardiovascular outcomes. Am J Med. 2011 Mar;124(3):199-205. [PMC free article: PMC3107840] [PubMed: 21396500]
Zmunda JM, Thompson PD, Dickenson R, Bausserman LL. Testosterone decreases lipoprotein(a) in men. Am J Cardiol. 1996 Jun 01;77(14):1244-7. [PubMed: 8651107]
Samulak JJ, Sawicka AK, Hartmane D, Grinberga S, Pugovics O, Lysiak-Szydlowska W, Olek RA. L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women. Ann Nutr Metab. 2019;74(1):11-17. [PubMed: 30485835]
Serban MC, Sahebkar A, Mikhailidis DP, Toth PP, Jones SR, Muntner P, Blaha MJ, Andrica F, Martin SS, Borza C, Lip GY, Ray KK, Rysz J, Hazen SL, Banach M. Impact of L-carnitine on plasma lipoprotein(a) concentrations: A systematic review and meta-analysis of randomized controlled trials. Sci Rep. 2016 Jan 12;6:19188. [PMC free article: PMC4709689] [PubMed: 26754058]
Nurmohamed NS, Kraaijenhof JM, Stroes ESG. Lp(a): a New Pathway to Target? Curr Atheroscler Rep. 2022 Nov;24(11):831-838. [PMC free article: PMC9534805] [PubMed: 36066785]
Enkhmaa B, Petersen KS, Kris-Etherton PM, Berglund L. Diet and Lp(a): Does Dietary Change Modify Residual Cardiovascular Risk Conferred by Lp(a)? Nutrients. 2020 Jul 07;12(7) [PMC free article: PMC7400957] [PubMed: 32646066]
Sahebkar A, Katsiki N, Ward N, Reiner Ž. Flaxseed Supplementation Reduces Plasma Lipoprotein(a) Levels: A Meta-Analysis. Altern Ther Health Med. 2021 May;27(3):50-53. [PubMed: 31634874]
Mackinnon LT, Hubinger LM. Effects of exercise on lipoprotein(a). Sports Med. 1999 Jul;28(1):11-24. [PubMed: 10461709]
Plebani M. Errors in clinical laboratories or errors in laboratory medicine? Clin Chem Lab Med. 2006;44(6):750-9. [PubMed: 16729864]
Allen LC. Role of a quality management system in improving patient safety - laboratory aspects. Clin Biochem. 2013 Sep;46(13-14):1187-93. [PubMed: 23648455]
Ricós C, Fernandez-Calle P, Perich C, Westgard JO. Internal quality control - past, present and future trends. Adv Lab Med. 2022 Oct;3(3):243-262. [PMC free article: PMC10197334] [PubMed: 37362142]
Ezzelle J, Rodriguez-Chavez IR, Darden JM, Stirewalt M, Kunwar N, Hitchcock R, Walter T, D'Souza MP. Guidelines on good clinical laboratory practice: bridging operations between research and clinical research laboratories. J Pharm Biomed Anal. 2008 Jan 07;46(1):18-29. [PMC free article: PMC2213906] [PubMed: 18037599]
Nichols JH. Laboratory quality control based on risk management. Ann Saudi Med. 2011 May-Jun;31(3):223-8. [PMC free article: PMC3119960] [PubMed: 21623049]
Carter JY. External quality assessment in resource-limited countries. Biochem Med (Zagreb). 2017 Feb 15;27(1):97-109. [PMC free article: PMC5382860] [PubMed: 28392732]
James D, Ames D, Lopez B, Still R, Simpson W, Twomey P. External quality assessment: best practice. J Clin Pathol. 2014 Aug;67(8):651-5. [PubMed: 24621574]
Lock RJ. My approach to internal quality control in a clinical immunology laboratory. J Clin Pathol. 2006 Jul;59(7):681-4. [PMC free article: PMC1860423] [PubMed: 16803947]
Meisenhelder J, Bursik S, Lunn G, Strober W. Laboratory safety. Curr Protoc Hum Genet. 2008 Apr;Appendix 2:Appendix 2A. [PubMed: 18428418]
Lo J. Biological safety in the medical laboratory. Hong Kong Med J. 2015 Jun;21(3):200. [PubMed: 26045068]
Drury P. Health and safety in the medical laboratory. Can J Med Technol. 1988 Aug;50(3):177-81. [PubMed: 10289978]

Disclosure: Khashayar Farzam declares no relevant financial relationships with ineligible companies.

Disclosure: Muhammad Zubair declares no relevant financial relationships with ineligible companies.

Disclosure: S Senthilkumaran declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK570621PMID: 34033383


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...