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Identifying
elevated
Lp(a)* can inform
a lifetime of
cardiovascular care
Lp(a) test results can assist in shared
decision-making with your patients
*Elevated Lp(a) levels defined as ≥50 mg/dL or ≥125 nmol/L.
An elevated Lp(a) result can help inform an assessment of overall cardiovascular risk1-4
An elevated Lp(a) result provides an opportunity to monitor, identify, and initiate or intensify management of other cardiovascular risk factors1-4
For people with elevated Lp(a), monitoring and/or management of a patient's other cardiovascular risk factors such as hypertension, HbA1c, hyperglycemia, coronary calcium, high LDL, or low HDL are especially important.5-11
An elevated Lp(a) result can help drive conversations with your patients about treatment initiation, adherence, and lifestyle behaviors1,6,12
A discussion guide is available to help in conversations with your patients who would like to know more about Lp(a)
You can refer to it for help with language around what Lp(a) is, what it means for people who have elevated Lp(a), and what steps they can take to reduce their overall cardiovascular risk.
An elevated Lp(a) result can reinforce conversations in the primary care setting1,6,12
Your patients can help take control of their overall cardiovascular risk
Simple and sustainable choices for a heart-healthy lifestyle include weight management, physical activity, healthy sleep habits, avoiding smoking, and more.1,6,12
Once elevated Lp(a) is identified in a patient, testing family members can identify those who are also at risk for premature cardiovascular and valvular disease13
Lp(a) inheritance and incidence of coronary artery disease in 3 families with elevated Lp(a)13
Study Description: Relatives from adult probands with an Lp(a) concentration ≥100 mg/dL were tested for elevated Lp(a) (≥50 mg/dL) via a cascade testing program in a tertiary hospital setting. The prevalence and yield of detecting new cases of elevated Lp(a) among the relatives were assessed. A total of 182 relatives, including children and adolescents were tested for elevated Lp(a) and clinical details such as cardiovascular risk factors were recorded. The figure shows pedigrees of 3 selected families with high yield of detection of elevated Lp(a). Arrows indicate probands. Men are indicated by a square, women by a circle. An asterisk (*) indicates coronary artery disease.
Adapted with permission from Chakraborty et al. (13).
Measurement of Lp(a) in youth helps identify those at higher risk for atherosclerotic cardiovascular outcomes14
If an elevated level of Lp(a) is detected in a youth, it is important to emphasize lifelong adoption of a heart-healthy lifestyle.14
A 2020 consensus statement from the ACE/AACE recommends all individuals with a family history of increased Lp(a) be tested. For additional recommendations from this statement, please visit the "Screening" page on this site.15
Adding an Lp(a) test can improve the accuracy of overall cardiovascular risk assessments and inform treatment responses16-19
Reclassification of individuals predicted to be at intermediate 15-year risk of cardiovascular disease (CVD) by additional assessment of Lp(a). Predicted risk groups were defined as lower risk (<15%); intermediate-risk (15 to <30%); and higher risk (≥30%).19
Study description: Lp(a) levels were measured in 826 men and women in the general community who were followed for 15 years to observe incidence of CVD. A review of medical records was performed to determine if a cardiovascular event occurred. The study evaluated whether Lp(a) measurement helps identify risk of CVD by calculating categorical net reclassification improvement for participants who experienced a cardiovascular event (n=148) and those who remained free of CVD (n=502).
Reprinted with permission from Willeit et al. (19).
Patients with no other apparent cardiovascular risk factors can still be at risk from elevated Lp(a)2,4,19-22
Because elevated Lp(a) is an independent cardiovascular risk factor, an Lp(a) test may lead to a reclassification of patients otherwise considered at lower risk for cardiovascular disease.19
Because a standard lipid panel does not distinguish Lp(a) from LDL-C, adding an Lp(a) test can also help explain less-than expected responses to LDL-C–lowering therapies.16-18,21
Programs and communities are available to support people living with elevated Lp(a)
AACE=American Association of Clinical Endocrinology; ACE=American College of Endocrinology; HDL=high-density lipoprotein; LDL=low-density lipoprotein; PCOS=polycystic ovary syndrome; TIA=transient ischemic attack.
References: 1. Thanassoulis G. Screening for high lipoprotein(a). Circulation. 2019;139(12):1493-1496. 2. Kronenberg F, Mora S, Stroes ESG, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur Heart J. 2022 Oct 14;43(39):3925-3946. 3. Farzam K, Senthilkumaran S. Lipoprotein A. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022. Updated September 2, 2022. Accessed August 22, 2023. https://www.statpearls.com/ArticleLibrary/viewarticle/130795 4. Virani SS, Koschinsky ML, Maher L, et al. Global think tank on the clinical considerations and management of lipoprotein(a): The top questions and answers regarding what clinicians need to know. Prog Cardiovasc Dis. 2022;73:32-40. 5. Nelson RH. Hyperlipidemia as a risk factor for cardiovascular disease. Prim Care. 2013;40(1):195-211. 6. Perrot N, Verbeek R, Sandhu M, et al. Ideal cardiovascular health influences cardiovascular disease risk associated with high lipoprotein(a) levels and genotype: The EPIC-Norfolk prospective population study. Atherosclerosis. 2017;256:47-52. 7. Pistrosch F, Natali A, Hanefeld M. Is hyperglycemia a cardiovascular risk factor?. Diabetes Care. 2011;34(suppl 2):S128-S131. 8. Ruan Y, Guo Y, Zheng Y, et al. Cardiovascular disease (CVD) and associated risk factors among older adults in six low-and middle-income countries: results from SAGE Wave 1. BMC Public Health. 2018;18(1):778. 9. Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41(1):111-188. 10. Mehta A, Vasquez N, Ayers CR, et al. Independent association of lipoprotein(a) and coronary artery calcification with atherosclerotic cardiovascular risk. J Am Coll Cardiol. 2022;79(8):757-768. 11. Goto A, Noda M, Matsushita Y, et al; JPHC Study Group. Hemoglobin a1c levels and the risk of cardiovascular disease in people without known diabetes: a population-based cohort study in Japan. Medicine (Baltimore). 2015;94(17):e785. 12. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol: A report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines. Circulation. 2019;139(25):e1082-e1143. 13. Chakraborty A, Pang J, Chan DC, et al. Cascade testing for elevated lipoprotein(a) in relatives of probands with familial hypercholesterolaemia and elevated lipoprotein(a). Atherosclerosis. 2022;349:219-226. 14. Raitakari O, Kartiosuo N, Pahkala K, et al. Lipoprotein(a) in youth and prediction of major cardiovascular outcomes in adulthood. Circulation. 2023;147(1):23-31. 15. Handelsman Y, Jellinger PS, Guerin CK, et al. Consensus statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the management of dyslipidemia and prevention of cardiovascular disease algorithm - 2020 Executive Summary. Endocr Pract. 2020;26(10):1196-1224. 16. Yeang C, Witztum JL, Tsimikas S. 'LDL-C' = LDL-C + Lp(a)-C: implications of achieved ultra-low LDL-C levels in the proprotein convertase subtilisin/kexin type 9 era of potent LDL-C lowering. Curr Opin Lipidol. 2015;26(3):169-178. 17. Tsimikas S, Gordts PLSM, Nora C, Yeang C, Witztum JL. Statin therapy increases lipoprotein(a) levels. Eur Heart J. 2020;41(24):2275-2284. 18. Willeit P, Yeang C, Moriarty PM, et al. Low-density lipoprotein cholesterol corrected for lipoprotein(a) cholesterol, risk thresholds, and cardiovascular events. J Am Heart Assoc. 2020;9(23):e016318. doi: 10.1161/JAHA.119.016318 19. Willeit P, Kiechl S, Kronenberg F, et al. Discrimination and net reclassification of cardiovascular risk with lipoprotein(a): prospective 15-year outcomes in the Bruneck Study. J Am Coll Cardiol. 2014;64(9):851-860. 20. 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;71(2):99-112. 21. Reyes-Soffer G, Ginsberg HN, Berglund L, et al; 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;42(1):e48-e60. 22. Tsimikas S. A test in context: Lipoprotein(a): Diagnosis, prognosis, controversies, and emerging therapies. J Am Coll Cardiol. 2017;69(6):692-711.