{"id":7954,"date":"2025-07-17T12:53:40","date_gmt":"2025-07-17T09:53:40","guid":{"rendered":"https:\/\/jordan-cardiac.org\/?p=7954"},"modified":"2025-07-17T12:53:40","modified_gmt":"2025-07-17T09:53:40","slug":"7954","status":"publish","type":"post","link":"https:\/\/jordan-cardiac.org\/en\/7954\/","title":{"rendered":""},"content":{"rendered":"
What Is Lp(a), and When Should We Check It?\u00a0<\/strong><\/div>\n
<\/div>\n
Published : July 10, 2025 on Medscape\u2013 Scientific Summary:<\/div>\n
<\/div>\n
1. What is Lp(a)?<\/span><\/div>\n
\u2013 Lipoprotein(a) [Lp(a)] is an LDL-like lipoprotein particle with an added apolipoprotein(a) tail, making it more atherogenic,<\/div>\n
proinflammatory, and prothrombotic.<\/div>\n
\u2013 (Measuring LDL, ApoB, lipoprotein(a), and triglycerides provides a comprehensive assessment of a patient\u2019s atherogenic lipid profile and is usually sufficient to evaluate cardiovascular risk related to dyslipidaemia. While LDL is the primary driver of atherosclerosis,ApoB, on the other hand represents the total number of atherogenic particles; LDL, VLDL, IDL, and Lp(a). Each of these particles contains one molecule of ApoB, making ApoB a reliable indicator of the total atherogenic particle burden.\u00a0 Triglycerides reflect the burden of triglyceride-rich lipoproteins such as VLDL and remnants, which are particularly relevant in metabolic syndrome and diabetes. Together, this panel offers a practical and advanced lipid evaluation to guide cardiovascular prevention)<\/div>\n
<\/div>\n
\u2013 Lipoprotein(a) is a genetically determined, independent risk factor for both:<\/div>\n
* Atherosclerotic cardiovascular disease (ASCVD)<\/div>\n
* Calcific aortic valve stenosis<\/div>\n
2. Why is Lp(a) important?<\/span><\/div>\n
\u2013 Lp(a) levels are not significantly modified by diet, exercise, or statin therapy.<\/div>\n
\u2013 It contributes to plaque progression and rupture even when LDL-C is low.<\/div>\n
\u2013 It is found in atherosclerotic plaques and accelerates cardiovascular events like MI and stroke.<\/div>\n
3. How common is elevated Lp(a)?<\/span><\/div>\n
\u2013 Roughly 1 in 5 people worldwide have high Lp(a) levels that raise ASCVD risk.<\/div>\n
4. Inheritance pattern:<\/span><\/div>\n
\u2013 Lp(a) is inherited in an autosomal dominant manner.<\/div>\n
\u2013 A child of a parent with elevated Lp(a) has a 50% chance of having elevated levels as well.<\/div>\n
5. Risk thresholds for Lp(a) (nmol\/L):<\/span><\/div>\n
\u2022 32\u201390: Mild risk<\/span><\/div>\n
\u2022 90\u2013200: Moderate risk<\/span><\/div>\n
\u2022 200\u2013400: High risk<\/span><\/div>\n
\u2022 >400: Very high risk<\/span><\/div>\n
\u27a4 In most cases, One-time lifetime measurement to assess inherited risk.<\/div>\n
6. Who should be tested? (Targeted screening recommended):<\/span><\/div>\n
\u2013 Individuals with personal or family history of premature ASCVD (<60 years)<\/div>\n
\u2013 Those with familial hypercholesterolemia (FH) or other inherited dyslipidaemias<\/div>\n
\u2013 First-degree relatives of someone with Lp(a) > 200 nmol\/L<\/div>\n
\u2013 Patients with calcific aortic valve stenosis<\/div>\n
\u2013 Individuals with borderline 10-year CV risk (10\u201315%), to help reclassify risk and guide statin initiation<\/div>\n
\u2013 Anyone with an unexplained atherosclerotic event despite low traditional risk factors<\/div>\n
7. What is the clinical utility?<\/span><\/div>\n
\u2013 Identifying elevated Lp(a) can:<\/div>\n
* Explain \u201ccryptogenic\u201d cardiac events<\/div>\n
* Justify earlier or more aggressive statin use<\/div>\n
* Trigger family (cascade) screening<\/div>\n
8. Current management for elevated Lp(a):<\/span><\/div>\n
\u2013 No currently approved Lp(a)-lowering medications<\/div>\n
\u2013 Apheresis (LDL filtration) is available but costly and invasive\u2014reserved for very high-risk cases<\/div>\n
\u2013 Novel therapies (e.g. antisense oligonucleotides) are in late-stage development<\/div>\n
\u2013 Meanwhile, treat all modifiable risk factors intensively:<\/div>\n
* High-intensity statin for Lp(a) > 90 nmol\/L<\/div>\n
* Target: LDL-C < 70 mg\/dL (\u2248 1.8 mmol\/L)<\/div>\n
or non-HDL-C < 100 mg\/dL (\u2248 2.5 mmol\/L)<\/div>\n
* Address BP, smoking, glucose, weight, and lifestyle<\/div>\n
9. Specialist referral :<\/span><\/div>\n
\u2013 Refer patients with Lp(a) > 200 nmol\/L to lipid clinics<\/div>\n
\u2013 Offer cascade screening to first-degree relatives of those with elevated Lp(a) or early CVD<\/div>\n
10. Clinical call to action:<\/span><\/div>\n
\u2013 Lp(a) screening is underutilised, despite being a powerful predictor of CV risk.<\/div>\n
\u2013 GPs should be proactive in identifying at-risk individuals using Lp(a) testing.<\/div>\n
\u2013 Even a single test can significantly alter prevention strategies and help reduce future events.<\/div>\n
<\/div>\n
<\/div>\n
https:\/\/click.mail.medscape.com\/?qs=17d5d5fe9d25d5b82dc29600a90a08f170694ffa3546d344a33b5f15f2b1cfe87aff479adbc3d0179018478dca21d2f8b83a7437416784566e979ddda327f326<\/a><\/div>\n","protected":false},"excerpt":{"rendered":"

What Is Lp(a), and When Should We Check It?\u00a0 Published : July 10, 2025 on Medscape\u2013 Scientific Summary: 1. What is Lp(a)? \u2013 Lipoprotein(a) [Lp(a)] is an LDL-like lipoprotein particle with an added apolipoprotein(a) tail, making it more atherogenic, proinflammatory, and prothrombotic. \u2013 (Measuring LDL, ApoB, lipoprotein(a), and triglycerides provides a comprehensive assessment of a […]<\/p>\n","protected":false},"author":145,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[1],"tags":[],"class_list":["post-7954","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"_links":{"self":[{"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/posts\/7954","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/users\/145"}],"replies":[{"embeddable":true,"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/comments?post=7954"}],"version-history":[{"count":1,"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/posts\/7954\/revisions"}],"predecessor-version":[{"id":7955,"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/posts\/7954\/revisions\/7955"}],"wp:attachment":[{"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/media?parent=7954"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/categories?post=7954"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/jordan-cardiac.org\/en\/wp-json\/wp\/v2\/tags?post=7954"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}