Lipoprotein(a) is a unique lipoprotein that has emerged as an independent risk factor for developing vascular disease.
→ Lp(a) levels are genetically determined1 and not affected by changes in lifestyle.
→ Lp(a) is a plasma lipoprotein consisting of a cholesterolrich LDL particle attached to an additional apolipoprotein called apo(a).
→ Lipoproteins are made of protein and fat. They carry cholesterol through your blood. Lp(a) is a type of low-density lipoprotein (LDL).
→ LDL is known as “bad” cholesterol. High levels of Lp(a) can create plaque in your blood vessels. This is a buildup of cholesterol that lessens blood flow through your arteries.
Clinical Use:
The Lp(a) test may be performed on individuals with a family history of premature coronary heart disease, a genetic predisposition for hypercholesterolemia, established atherosclerosis but with a normal routine lipid profile, hyperlipidemia refractory to treatment, or a history of recurrent arterial stenosis.
References:
– Routi T et al. Correlation of toddlers’ serum lipoprotein(a) concentrations with parental values and grandparents’ coronary heart disease: The STRIP baby study. Acta Paediatr. 1996; 85: 407-412.
– Mackinnon LT et al. Effects of physical activity and diet on lipoprotein(a). Med Sci Sports Exerc. 1997; 29: 1429-1436.
– Anuurad E et al. Lipoprotein(a): A unique risk factor for cardiovascular disease. Clin Lab Med. 2006; 26: 751-772.
– Berglund L et al. Lipoprotein(a): An elusive cardiovascular risk factor. Arterioscler Thromb Vasc Biol. 2004; 24: 2219-2226.
– Boffa MB et al. Lipoprotein(a) as a risk factor for atherosclerosis and thrombosis: Mechanistic insights from animal models. Clin Biochem. 2004; 37: 333-343.
– Bostom AG et al. Elevated plasma lipoprotein(a) and coronary heart disease in men age 55 years and younger. A prospective study. JAMA. 1996; 276: 544-548.
– Kamstrup PR et al. Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA. 2009; 301: 2331-2339.
– Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease. Stroke. 1995; 26: 1841-1848.
– Kolodgie FD et al. Lipoprotein-associated phospholipase A2 protein expression in the natural progression of human coronary atherosclerosis. Arterioscler Thromb Vase Biol. 2006; 26: 2523- 2529.
– Paige, E., Masconi, K.L., Tsimikas, S. et al. Lipoprotein(a) and incident type-2 diabetes: results from the prospective Bruneck study and a meta-analysis of published literature. Cardiovasc Diabetol 16, 38 (2017). https://doi.org/10.1186/s12933-017-0520-z
– McCormick SP. Lipoprotein(a): biology and clinical importance. Clin Biochem Rev. 2004 Feb;25(1):69-80. PMID: 18516206; PMCID: PMC1853362.
– Jacobson TA. Lipoprotein(a), cardiovascular disease, and contemporary management. Mayo Clin Proc. 2013 Nov;88(11):1294-311. doi: 10.1016/j.mayocp.2013.09.003. PMID: 24182706.
– Banach M. Lipoprotein (a)-We Know So Much Yet Still Have Much to Learn …. J Am Heart Assoc. 2016 Apr 23;5(4):e003597. doi: 10.1161/JAHA.116.003597. PMID: 27108250; PMCID: PMC4859302.
– Kamstrup PR, Tybjaerg-Hansen A, Steffensen R, Nordestgaard BG. Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA. 2009 Jun 10;301(22):2331-9. doi: 10.1001/jama.2009.801. PMID: 19509380.
– Najjar RS, Moore CE, Montgomery BD. Consumption of a defined, plant-based diet reduces lipoprotein(a), inflammation, and other atherogenic lipoproteins and particles within 4 weeks. Clin Cardiol. 2018 Aug;41(8):1062-1068. doi: 10.1002/clc.23027. Epub 2018 Aug 17. PMID: 30014498; PMCID: PMC6489854.
Other links:
https://www.rush.edu/news/meet-bad-cholesterols-trouble-making-sidekick
https://www.uptodate.com/contents/lipoprotein-a
https://www.uptodate.com/contents/lipoprotein-a-and-cardiovascular-disease
https://ufhealth.org/lipoprotein
https://www.nhlbi.nih.gov/health/blood-cholesterol
https://labtestsonline.org/understanding/analytes/lp-a/tab/faq
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Increased levels are associated with an increased risk of heart attack, stroke, or narrowed arteries supplying blood to vital organs. In the Copenhagen Heart study, Kamstrup et al found that genetic elevations of Lp(a) were associated with an increased risk of myocardial infarction. [L]
Potential treatment considerations:
These treatment considerations are for educational purposes only. Specific treatment plans should be provided and reviewed by the treating practitioner:
A study published on June 8th 2018 has found that consumption of a defined plant-based diet can reduce Lp(a) and other atherogenic lipoproteins and particles in four weeks. [L]
→ Assess family history of heart disease.
→ Assess Lp-PLA2 and MPO levels. If abnormal, treat individual biomarkers and retest in 3-6 months.
NOTE: Lp-PLA2 and MPO may help to identify the presence of vulnerable plaque and increased risk of thrombosis in patients with early onset heart disease.
→ Assess the presence of CAD with imaging techniques such as CIMT or coronary artery calcium scoring.
Consider aspirin therapy if not contraindicated.
Consider clopidogrel if history of CAD (i.e., myocardial infarction or revascularization) and/or a history of cerebrovascular disease (i.e., TIA or stroke).
→ If abnormal, consider niacin therapy
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The low levels of Lp(a) defined as <5 mg/dl (lower 20% of population) are associated with decreased risk of MI, aortic stenosis, and ischemic stroke, but have been shown to have a higher prevalence of diabetes.
The current available evidence from prospective studies suggests that there is an inverse association between Lp(a) concentration and risk of type-2 diabetes, with a higher risk of type-2 diabetes at low Lp(a) concentrations (approximately <7 mg/dL).
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