What Is Lp(a), and When Should We Check It?
As we all know, atherosclerotic cardiovascular disease is a chronic, progressive condition characterized by the accumulation of lipids, inflammatory cells, and other cells in arteries that results in the formation of atherosclerotic plaques. As these plaques build up and rupture, they cause partial or complete obstruction of blood flow, tragically leading to clinical events such as myocardial infarctions or ischemic strokes.
I'm sure all of us in primary care can sadly recall individuals who have suffered heart attacks or strokes who appeared to be very healthy, with no obvious cardiovascular risk factors. We all know that elevated LDL cholesterol levels (or bad cholesterol) are a proven and direct cause of atherosclerotic cardiovascular disease, and it has been estimated that for each 1 mmol/L reduction in LDL cholesterol, there's a relative risk reduction of 23% for major cardiovascular events.
Well, Lp(a) is an LDL-like particle that is an independent, genetically determined risk factor for major cardiovascular events and cardiovascular mortality. But unlike LDL cholesterol, Lp(a) levels are not significantly affected by lifestyle choices or statins. Lp(a) is found in atherosclerotic plaques and has proinflammatory, prothrombotic, and proatherogenic effects driving that progression of atherosclerosis. Epidemiological and genetic studies strongly support a causal and continuous association between Lp(a) levels and cardiovascular outcomes. In fact, Lp(a) is a risk factor even at very low levels of LDL cholesterol. Lp(a) is also an independent risk factor for calcific aortic stenosis.
So, how common are elevated Lp(a) levels? Well, around 1 in 5 people globally are at high risk of developing atherosclerotic cardiovascular disease due to elevated Lp(a) levels. However, there are differences with regard to Lp(a) levels across different ethnicities. Black individuals are more likely to have elevated Lp(a) than White, Hispanic, or Asian individuals.
Importantly, Lp(a) levels are inherited in a predominantly autosomal dominant manner, which means a child of an affected parent with high Lp(a) levels has a 50% chance of being affected him- or herself.
So, what levels of Lp(a) drive an increased risk of atherosclerotic cardiovascular disease? Levels of 32-90 nmol/L confer a minor risk. Levels between 90 and 200 nmol/L confer a moderate risk. Levels of 200-400 nmol/L confer a high risk, and levels greater than 400 nmol/L confer a very high risk. Lp(a) levels need to only be measured once in a lifetime, unless a specific treatment is being undertaken to lower levels, which I will discuss shortly.
Heart UK, the UK cholesterol charity, published a consensus statement and call to action on Lp(a) during 2019 that included some useful, pragmatic recommendations for all of us working in primary care. Notably, this consensus gave a number of recommendations on when we should consider checking Lp(a) levels.
We should consider checking Lp(a) levels in those with a personal or family history of premature atherosclerotic cardiovascular disease, particularly under the age of 60 years. We should consider checking levels in those with a first-degree relative with high Lp(a) levels over 200 nmol/L. We should consider checking levels in those with a history of familial hypercholesterolemia or another genetic dyslipidemia. We should consider checking levels in those with a background of calcific aortic valve stenosis. And we should also consider checking levels in those with a borderline increased 10-year cardiovascular risk of around about 10% to 15%. This is to aid reclassification of these individuals at intermediate risk of atherosclerotic cardiovascular disease and hopefully encourage acceptance of LDL cholesterol-lowering therapies such as statins.
So, how do we manage elevated Lp(a) levels? Currently, there are no approved therapies to treat elevated Lp(a) levels. The most effective therapy for high Lp(a) levels is apheresis, which is a blood filtering process like dialysis. This procedure is reserved for the highest risk individuals, as it is very expensive, requires weekly visits to the apheresis center, and is not without harm. However, newer therapies targeting Lp(a) directly are in development, which will transform the management of high-risk individuals.
So, what can we do meanwhile in primary care for those with high Lp(a) levels? We need to mitigate overall cardiovascular risk with aggressive lipid management and targeting of all other cardiovascular risk factors. For those with Lp(a) levels greater than 90 nmol/L (moderate risk and above), we should initiate a high-intensity statin and aim for a greater than 50% reduction in non-HDL cholesterol and an LDL cholesterol of less than 1.8 mmol/L liter or non-HDL cholesterol level of less than 2.5 mmol/L.
We should also consider referral to a specialist lipid clinic for those with high-risk Lp(a) levels (greater than 200 nmol/L) but manage all cardiovascular risk factors while waiting for them to be seen. Cascade screening and family should also be offered to individuals with a familial or personal history of high Lp(a) levels or an early history of atherosclerotic cardiovascular disease in the family under the age of 60 years.
So, a call to action for us all in primary care: Lp(a) is an independent, genetically determined risk factor for atherosclerotic cardiovascular disease that is not significantly affected by lifestyle choices or statins. We should consider checking Lp(a) levels in those with a personal or family history of premature atherosclerotic cardiovascular disease under the age of 60 years, in those with calcific aortic valve stenosis, or in those where an atherosclerotic event has occurred with no obvious underlying risk factors. Finally, I produced a Medscape UK primary care hack or clinical aide-mémoire on lipid management for the primary and secondary prevention of cardiovascular disease for healthcare professionals. I hope you find this resource helpful.
Medscape Family Medicine © 2025 WebMD, LLC
Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.
Cite this: What Is Lp(a), and When Should We Check It? - Medscape - Jul 10, 2025.
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Tell all your healthcare providers that you are taking Wegovy® before you are scheduled to have surgery or other procedures The most common side effects of Wegovy® may include: nausea, diarrhea, vomiting, constipation, stomach (abdomen) pain, headache, tiredness (fatigue), upset stomach, dizziness, feeling bloated, belching, low blood sugar in people with type 2 diabetes, gas, stomach flu, heartburn, and runny nose or sore throat. Please click HERE for Wegovy® Prescribing Information and Medication Guide. About Novo Nordisk Novo Nordisk is a leading global healthcare company that's been making innovative medicines to help people with diabetes lead longer, healthier lives for more than 100 years. This heritage has given us experience and capabilities that also enable us to drive change to help people defeat other serious chronic diseases such as obesity, rare blood, and endocrine disorders. We remain steadfast in our conviction that the formula for lasting success is to stay focused, think long-term, and do business in a financially, socially, and environmentally responsible way. With a US presence spanning 40 years, Novo Nordisk US is headquartered in New Jersey and employs over 10,000 people throughout the country across 12 manufacturing, R&D and corporate locations in eight states plus Washington DC. For more information, visit Facebook, Instagram, and X. Novo Nordisk is committed to the responsible use of our semaglutide-containing medicines which represent distinct products with different indications, dosages, prescribing information, titration schedules, and delivery forms. These products are not interchangeable and should not be used outside of their approved indications. Learn more at References Wegovy® (semaglutide) injection [package insert]. Plainsboro, NJ: Novo Nordisk Inc. Sanyal AJ, Newsome PN, Kliers I, et al. Phase 3 Trial of Semaglutide in Metabolic Dysfunction-Associated Steatohepatitis. N Engl J Med. 2025;392(21):2089-2099. doi:10.1056/NEJMoa2 413258 Younossi ZM, Mangla KK, Chandramouli AS, et al. Estimating the economic impact of comorbidities in patients with MASH and defining high-cost burden in patients with noncirrhotic MASH. Hepatol Commun. 2024;8(8):e0488. doi:10.1097/HC9.00000 00000000488 Allen AM, Charlton M, Cusi K, et al. Guideline-based management of metabolic dysfunction-associated steatotic liver disease in the primary care setting. Postgrad Med. 2024;136(3):229-245. doi:10.1080/00325481.2024.2325332 Kugelmas M, Noureddin M, Gunn N, et al. The use of current knowledge and non-invasive testing modalities for predicting at-risk non-alcoholic steatohepatitis and assessing fibrosis. Liver Int. 2023;43(5):964-974. doi:10.1111/liv.15555 Quek J, Chan KE, Wong ZY, et al. Global prevalence of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in the overweight and obese population: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2023;8(1):20-30. doi:10.1016/S2468-1253(22)00317-X Newsome PN, Sanyal AJ, Engebretsen KA, et al. Semaglutide 2.4 mg in participants with metabolic dysfunction-associated steatohepatitis: baseline characteristics and design of the phase 3 ESSENCE trial. Aliment Pharmacol Ther. 2024;60(11-12):1525-1533. doi:10.1111/apt.18331 National Institute of Diabetes and Digestive and Kidney Diseases. Definition & facts of NAFLD & NASH. Accessed June 13, 2025. Sheka AC, Adeyi O, Thompson J, et al. Nonalcoholic steatohepatitis: a review. JAMA. 2020;323(16):1619. doi:10.1001/jama.2020.5249 Younossi ZM, Koenig AB, Abdelatif D, et al. Global epidemiology of nonalcoholic fatty liver disease-Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2016;64(1):73-84. doi:10.1002/hep.28431 Wegovy® is a registered trademark of Novo Nordisk A/S. Novo Nordisk is a registered trademark of Novo Nordisk A/S. All other trademarks, registered or unregistered, are the property of their respective owners. © 2025 Novo Nordisk All rights reserved. US25SN00042 August 2025 View original content to download multimedia: SOURCE NOVO NORDISK INC. Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
