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LP little a, a specific type of low-density lipoprotein (LDL), is found in about 20-25% of the global population. Genetically elevated levels of LP little a are linked to a higher risk of atherosclerosis and aortic valve dysfunction. Understanding the pathology and measurement of LP little a is crucial as elevated levels can indicate increased cardiovascular risk.
LP little a is produced in the liver, where it binds to LDL particles containing ApoB. LP little a consists of unique peptide structures, known as 'Kringles,' which play a role in promoting wound healing but can also contribute to inflammatory responses and clot formation in the arterial wall. The genetic variability in LP little a production can lead to differing molecular weights of LP little a particles.
Measuring LP little a particle numbers is essential for assessing cardiovascular risk, regardless of the individual's ApoB levels. High LP little a levels are associated with an increased risk of atherosclerosis and aortic valve dysfunction, making it important to evaluate particle counts to gauge risk accurately.
Elevated LP little a levels are considered particularly high risk when they surpass certain thresholds, such as 100-125 nanomoles per liter. Understanding individual particle counts and genetic factors can help predict susceptibility to atherosclerotic and valve-related issues, warranting close monitoring and potential intervention.
Having an elevated level of lipoprotein little a (LPa) is associated with increased cardiovascular risk, contributing to various pathological conditions like atherosclerosis. LPa is characterized by prothrombotic, procoagulant, proinflammatory properties, making it a significant risk factor for atherosclerosis and aortic valve dysfunction.
LPa levels can be measured in different units, including mass or particle concentration. High levels of LPa, above 50 milligrams per deciliter or 100-125 nanomoles per liter, indicate moderate to high cardiovascular risk. Periodic monitoring of LPa, along with optimization of APOB, is recommended based on an individual's baseline risk of cardiovascular disease.
Significant ethnic variations impact risk thresholds for LPa across populations, with varied ranges and implications for different ethnic groups. Ongoing pharmaceutical developments and clinical trials focus on potential therapies targeting LPa reduction, offering promising future treatments like Pelikarsin, CRISPR techniques, and other novel therapeutic approaches.
LPa's influence extends to aortic valve disease, affecting valve function and increasing the risk of aortic stenosis. Future considerations involve potential CRISPR therapies targeting the apo little a gene for long-term reduction. The potential for LPa-targeted therapies, like Pelikarsin and CRISPR techniques, signifies a paradigm shift in managing cardiovascular risk associated with elevated LPa levels.
Episode #320. Are you part of the 20% of people with this dangerous gene? There’s a cheap, simple test you can do just once in your life to find out. Join me as I sit down with renowned lipidologist Dr Thomas Dayspring to help you understand Lipoprotein(a) and the test that might change your life.
In this episode, you’ll learn what Lp(a) is and how it can affect your cardiovascular disease risk through two key pathways. Dr Dayspring unpacks why it’s so important to test, how to ask for this test, and what to do with your results.
Specifically, we discuss:
Connect with Dr Thomas Dayspring on Twitter/X. Listen to our previous lipid series and download the cheat sheet here.
This episode is brought to you by:
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Simon Hill, MSc, BSc (Hons)
Creator of theproof.com and host of The Proof with Simon Hill
Author of The Proof is in the Plants
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