Lp(a): For the Accurate Detection of CVD Risk
Lp(a) is an independent risk factor for cardiovascular disease (CVD), even when classical risk factors such as hypertension, elevated cholesterol, and diabetes have been taken into consideration. High levels of Lp(a) is a heredity condition, associated with complex mechanisms involving the proatherogenic and prothrombotic pathways (1).
Traditional CVD testing panel
According to the World Health Organisation (WHO), CVD is the leading cause of death globally, accounting for 31 percent of deaths, totalling 17.7 million deaths per year. 80 percent of all CVD deaths are attributed to heart attacks and strokes, equivalent to 1 in 4. Identifying those who are at a high risk of developing CVD and ensuring that they are receiving the appropriate treatment can prevent premature deaths (2).
The lipid profile is frequently used to assess an individual’s risk of CVD developing later in life. Routine tests to assess CVD risk include: triglycerides, high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C). LDL-C has been found to strongly correlate with CVD risk (3). NICE recommend measuring total cholesterol, HDL cholesterol, non-HDL cholesterol and triglycerides as the full lipid profile and then review other risk factors, including: age, diet, smoking, QRISK, co-morbidities to view risk and the management of risk (4). However, the current lipid panel needs to be adjusted to ensure that its utilisation is effective in meeting clinician and patient needs.
Lipoprotein (a) or Lp(a) consists of two protein molecules, apolipoprotein (a) or apo(a) is covalently linked by a disulphide bond to the apolipoprotein B-100 or apoB-100 of a cholesterol-rich low-density lipoprotein or LDL like particle. Lp(a) is synthesised in the liver and is detectable in the bloodstream (5).
The structure of Lp(a) resembles that of the proteins involved in the breakdown of blood clots, plasminogen and tissue plasminogen activator (TPA). As a result, the biggest concern with Lp(a) is that it prohibits the ability of these proteins to break down blood clots by competing for the ‘binding to fibrin’, boosting the blood’s clotting ability within arteries, thus heightening the risk of heart attacks and strokes. Consequently, high levels of Lp(a) is characterised by atherosclerosis including coronary heart disease, peripheral vascular disease, aortic stenosis, thrombosis and stroke (6).
The Journal of the American Medical Association reviewed 36 studies in 2009 which assessed ‘the role of Lp(a) and vascular disease’ in 126,634 individuals. The study found that a 3.5-fold increase in Lp(a) levels was accompanied with a 13 percent higher risk of coronary heart events and a 10 percent higher risk of stroke (7).
Later, an Italian population study carried out on 826 individuals in 2014 found that elevated levels of Lp(a) is due to two different variations of the apo(a) gene which is determined by the kringle sequence differences at the apo(a) locus. The study found that individuals with one variation had a 50 percent greater risk of CVD, while individuals with both variations had 2.5 times greater risk (7).
According to the Lipoprotein Foundation (2015), based on genetic factors, from birth, one in five or 20% of individuals have high Lp(a) levels greater than 50mg/dL, with most blissfully unaware they have it. Overtime, high levels of Lp(a) gradually narrow the arteries, limiting blood supply to the brain, heart, kidneys and legs, increasing the risk of heart attacks and strokes (5).
Testing for high Lp(a) levels
The Lipoprotein (a) Foundation (2015) recommends that Lp(a) levels should be tested if:
- There is a family history of cardiovascular disease including stroke, heart attack, circulation problems in the legs and/or narrowing of the aorta, at a young age
- Stroke or heart attack if classical risk factors including high LDL-cholesterol, obesity, diabetes and smoking have been eliminated
- High levels of LDL-cholesterol following treatment with statins or other LDL lowering medications(5)
When selecting a Lp(a) assay, the Internal Federation of Clinical Chemistry (IFCC) (2004) Working Group on Lp(a) recommends that laboratories use assays that do not suffer from apo(a) size-related bias to minimise the potential risk of misclassification of patients for coronary heart disease (8).
The Lp(a) Foundation reference Marcovina and Albers (2016) in their recommendations for the best Lp(a) test. The study came to the following conclusions:
- Robust assays based on the Denka method, reportable in nanomoles per litre (nmol/L) are traceable to WHO/IFCC reference material
- Five-point calibrators with accuracy-based assigned target values will minimise the sensitivity of to the size of apo(a)
- Upon request, manufacturers should provide the certificate of evaluation of the calibrator and reagent lots with the relative expiration dates (9)
Benefits of the Randox Lp(a) assay
The Randox Lp(a) assay is one of the only methodologies on the market that detects the non-variable part of the Lp(a) molecule and so suffers minimal size related bias providing more accurate and consistent results. This methodology allows for the detection of Lp(a) in serum and plasma. The Randox Lp(a) kit is standardized to the WHO/IFCC reference material, SRM 2B, and is the closest in terms of agreement to the ELISA reference method.
A five-point calibrator is provided with accuracy-based assigned target values which accurately reflects the heterogeneity of isoforms present in the general population.
Liquid ready-to-use reagents are more convenient as the reagent does not need to be reconstituted, reducing the risk of errors.
Applications are available for a wide range of biochemistry analysers which details instrument-specific settings for the convenient use of the Randox Lp(a) assay on a variety of systems. Measuring units in nmol/L are available upon request.
- Li, Yonghong, et al. Genetic Variants in the Apolipoprotein(a) Gene and Coronary Heart Disease. Circulation: Genomic and Precision Medicine. [Online] October 2011. [Cited: April 24, 2018.] http://circgenetics.ahajournals.org/content/4/5/565.
- World Health Organisation. Cardiovascular Disease. [Online] 2017. [Cited: April 30, 2018.] http://www.who.int/cardiovascular_diseases/en/.
- Doc’s Opinion. Lipoprotein (a). [Online] 2013. [Cited: April 30, 2018.] https://www.docsopinion.com/health-and-nutrition/lipids/lipoprotein-a/.
- National Institutional for Health and Care Excellence. Cardiovascular disease: risk assessment and reduction, including lipid modification. [Online] July 2014. [Cited: April 30, 2018.] https://www.nice.org.uk/guidance/cg181/chapter/1-recommendations#lipid-modification-therapy-for-the-primary-and-secondary-prevention-of-cvd-2.
- Lipoprotein(a) Foundation. Understand Inherited Lipoprotein(a). [Online] 2015. [Cited: April 24, 2018.] http://www.lipoproteinafoundation.org/?page=UnderstandLpa.
- Heart UK. Lipoprotein (a). [Online] June 23, 2014. [Cited: April 24, 2018.] https://heartuk.org.uk/files/uploads/huk_fs_mfss_lipoprotein_02.pdf.
- Ashley, Robert. High lipoprotein(a) levels may indicate heart disease in some. The Brunswick News. [Online] March 05, 2018. [Cited: April 24, 2018.] https://thebrunswicknews.com/opinion/advice_columns/high-lipoprotein-a-levels-may-indicate-heart-disease-in-some/article_16ab1049-7a6f-5da0-8966-59e94ae31b6d.html.
- Dati, F; Tate, J R; Marcovina, S M; Steinmetz, A; International Federation of Clinical Chemistry and Laboratory Medicine; IFCC Working Group for Lipoprotein(a) Assay Standardization. First WHO/IFCC International Reference Reagent for Lipoprotein(a) for Immunoassay–Lp(a) SRM 2B. NCBI. [Online] 2004. [Cited: April 30, 2018.] https://www.ncbi.nlm.nih.gov/pubmed/15259385.
- Tsimikas, Sotirios. A Test in Context: Lipoprotein(a) – Diagnosis, Prognosis, Controversies, and Emergining Therapies. 6, s.l. : Elsevier, 2017, Vol. 69. 0735-1097.
“CVDs are the number 1 cause of death globally: more people die annually from CVDs than from any other cause”. In 2015, roughly 17.7 million people died from CVD, representing 31% of all global deaths: 7.4 million were due to coronary heart disease and 6.7 million were due to stroke. (WHO, 2017)
Cardiac health and regular cardiovascular screening is important to enable risk factors to be detected in their earliest stages. There are a few factors which contribute to CVD. These include: smoking, unhealthy diet, excessive alcohol consumption, low physical activity levels. Whilst there are only a few factors contributing to CVD, these can be maintained by the patient through living a healthy lifestyle including: quitting smoking, consuming no more than the recommended allowance of alcohol, cutting out junk food, and exercising for 30 minutes a day, 3 – 5 days a week. In a perfect world, this would be easy and CVD would not be a global problem. However, due to busy lifestyles, cravings, reduced willpower, and convenience, not all individuals in today’s world will be able to avoid CVDs. Therefore, it is vitally important that individuals are tested for CVDs to detect them in the earliest stages to reduce damage, prevent further damage, or even death. Furthermore, many individuals suffer from inherited cardiac risk factors, which stresses the need for accurate testing of both traditional and novel cardiac risk biomarkers.
Randox offer the complete solution to cardiac risk assessment including: RX analysers, traditional and novel reagents, internal quality control (Acusera), and external quality control (RIQAS).
Randox has developed the RX series range of clinical chemistry analysers for high-quality semi-automated and fully automated testing. Choose between the RX misano, RX monaco, RX daytona+, RX imola, and the RX modena depending on the throughput of your laboratory. The RX series offers a suitable analyser for your laboratory’s needs. For more information on the Randox RX series, please click here or email email@example.com
As previously mentioned, early assessment of cardiac risk is vital. Randox offer a range of novel risk biomarkers for both very early and the genetic assessment of cardiac risk.
The niche Adiponectin assay allows for the early assessment of CVD. Adiponectin levels are inversely correlated with abdominal visceral fat which has proven to be a strong predictor of T2DM. Body-Mass Index (BMI) is a common method for determining which patients are classified as underweight, healthy, overweight or obese, however, BMI does not take into account gender, ethnicity or activity levels. For example, measuring the BMI of athletes who have a high BMI due to muscle weighing heavier than fat would classify them as obese which is inaccurate. Measuring adiponectin levels is therefore a much more reliable indicator of at-risk patients compared to BMI.
LDL cholesterol is often referred to as the ‘bad cholesterol’. High concentrations of LDL-cholesterol is considered to be the most important clinical predictor, of all single parameters, with respect to coronary atherosclerosis. However, sLDL is a smaller, more dense subfraction of LDL-cholesterol. sLDL particles more readily permeate the inner arterial wall and are more susceptible to oxidation. Individuals with a predominance of sLDL have a 3-fold increased risk of myocardial infarction. Measurement of sLDL allows the clinician to get a more comprehensive picture of lipid risk factors and tailor treatment accordingly.
Elevated levels of Lp(a) are considered to be both a casual risk factor and independent genetic marker of atherosclerotic disorders. The major challenge associated with Lp(a) measurement is the size variation of apo(a) within Lp(a). Dependent upon the size of apo(a) in the assay calibrator, many assays under or overestimate apo(a) size in the patient sample. Numerous commercially available products suffer apo(a) size related bias, resulting in an over estimation of Lp(a) in samples with large apo(a)molecules and an under estimation in samples with small apo(a) molecules. The antibody used in the Randox method detects the complete Lp(a) molecule providing accurate and consistent results. This was proven by the IFCC who developed a gold standard ELISA reference assay and compared 22 commercially available tests. The Randox Lp(a) method displayed the least (minimal) amount of apo(a) size related bias, proving it be a superior offering.
HDL3 Cholesterol is a smaller and more dense subfraction of the HDL particle. HDL is the scavenger of cholesterol within arterial walls and the levels of HDL3 is too low, the ability to remove this cholesterol is reduced. Therefore, it is widely accepted that there is an inverse correlation between HDL3 and CVD risk.
Instrument Specific Applications (ISA’s) are available for a wide range of biochemistry analysers. Contact us to enquire about your specific analyser.
Acusera – Internal Quality Control
The Acusera cardiac controls have been designed to cover a wide range of cardiac markers at clinical decision levels, eliminating the extra expense of an additional low level control. The controls are available in a both liquid ready-to-use and lyophilized formats making them ideal for all situations and manufactured from 100% human serum a matrix similar to that of the patient is guaranteed. For more information on the Randox Acusera internal quality control, please click here or email firstname.lastname@example.org
RIQAS – External Quality Control
The RIQAS Liquid Cardiac EQA programme is designed to monitor the performance of up to 9clinically significant cardiac markers including: CK-MB mass, D-dimer, Digoxin, homocysteine, hsCRP, myoglobin, NT proBNP, troponin I, and troponin T. RIQAS is ISO/IEC 17043 accredited and allows the registration of up to five instruments at no extra cost. All samples are 100% human serum and provided in a liquid ready-to-use format for enhanced convenience. Submit your results bi-weekly and view reports online via RIQAS.Net. For more information on RIQAS, the world’s largest international EQA scheme, please click here or email email@example.com
For further information, please contact the Randox PR team via email: firstname.lastname@example.org or phone 028 9442 2413
The Lipoprotein(a) Foundation have commended health and fitness expert Bob Harper for speaking out after recently suffering a heart attack. The celebrity personal trainer and host of the US television series ‘The Biggest Loser’, has revealed that high levels of Lp(a) were responsible for the heart attack he suffered at the age of 51 at the beginning of this year.1
Harper had been completing a normal workout at his gym when he suffered full cardiac arrest. Luckily, two doctors were in the vicinity who saved his life by performing CPR and using an Automated External Defibrillator (AED). In an interview following his heart attack, Harper has said,
“I’ve learned a lot about the fact genetics does play a part in this, it is so important to know your health… I’m a guy that lives a very healthy lifestyle, very regimented, I work out all the time, but there were things going on inside of my body that I needed to be more aware of and I strongly encourage anyone that’s listening right now to go to their doctor, get their cholesterol checked, see what’s going on on the inside”.
Scroll down to watch the interview in full.
What is Lp(a)?
Lp(a) is a particle which is produced in the liver and found in the blood which carries cholesterol, fats and proteins. Levels of Lp(a) in individuals are genetically determined, and are not affected by diet, exercise or lifestyle changes.2
So how does a seemingly fit and healthy person have a heart attack at the age of 51?
Lp(a) is currently the strongest inherited risk factor for heart attack and stroke, with one in five people globally inheriting high Lp(a).1 Levels of Lp(a) are not routinely tested in standard cardiovascular assessments, and despite the particle itself being an altered form of LDL cholesterol, standard cholesterol tests do not reveal inherited Lp(a) levels as it is independent from total cholesterol and LDL levels.3
High Lp(a) can also be unrelated to other common risks factors of cardiovascular diseases for example, smoking, diet, diabetes, high blood pressure and lack of exercise. This is why seemingly healthy individuals can have high Lp(a) in their genes and still be at high risk of cardiovascular diseases.
Why is Lp(a) not routinely measured if high levels pose such a risk?
The widespread use of Lp(a) as an independent risk factor for cardiovascular disease risk has, until recently, been hindered by the lack of internationally accepted standardisation and the fact that many commercial Lp(a) methods suffer from apo(a) size related bias, potentially leading to patient misclassification.
The size of the apo(a) protein is genetically determined and varies widely hence, levels of Lp(a) can vary up to 1000-fold between individuals.4 To find out more about the clinical significance of Lp(a), please refer to the section below entitled ‘For Health Professionals’.
What can you do if you have high Lp(a)?
Research has shown that lowering Lp(a) could significantly reduce the impact of cardiovascular diseases. A recent study published in the American Heart Association journal, Arteriosclerosis, Thrombosis and Vascular Biology, found that reducing high Lp(a) could potentially prevent up to 1 in 14 cases of myocardial infarction (heart attack) and 1 in 7 cases of aortic valve stenosis.5 Of those studied, nearly one third of heart attacks and half of all cases of aortic stenosis were attributed to high Lp(a).6 This study demonstrates the clinical significance of measuring Lp(a), making it a major independent genetic risk factor for cardiovascular diseases.
Why test Lp(a)?
Lp(a) will be tested as part of a lipid profile if: there is a strong family history of CVD, a patient has existing heart or vascular diseases, a patient has an inherited predisposition for high cholesterol or if a person has had a stroke or heart attack but has normal lipid levels.7
Dr Christie Ballantyne, Chief of Cardiology at Baylor College of Medicine, has said “the most important part of knowing your Lp(a) level is understanding your overall risk and finding the right lifestyle modifications or medications to target all the other traditional risk factors. Those risk factors become even more important to monitor when your Lp(a) levels are high”.8
If you are concerned that you may be at risk of having elevated levels of Lp(a) due to your family history, ask your doctor or medical provider to test lipoprotein (a), along with other lipid tests, to clinically evaluate your risk of developing cardiovascular diseases.
For health professionals
Click below for information regarding the challenges associated with the measurement of Lp(a) and the clinical significance it holds.
The widespread use of Lp(a) as an independent risk factor for cardiovascular disease risk has, until recently, been impeded by the lack of internationally accepted standardisation and the fact that many commercial Lp(a) methods suffer from apo(a) size related bias, potentially leading to patient misclassification. The size of the apo(a) protein is genetically determined and varies widely hence, levels of Lp(a) can vary up to 1000-fold between individuals.4
As a result, international criteria has been set to overcome these challenges. The International Federation of Clinical Chemistry (IFCC) Working Group on Lp(a) recommends that laboratories use assays which do not suffer from apo(a) size-related bias, in order to minimise the potential risk of misclassification of patients for coronary heart disease. The Lipoprotein(a) Foundation has referenced Marcovina and Albers (2016) as their recommendation for the best Lp(a) test.9 This recommendation is a result of the following conclusions:
- Robust assays based on the Denka method are available, which are reported in nanomoles per litre (nmol/L) and are traceable to WHO/IFCC reference material
- Five point calibrators with accuracy assigned target values will minimise the sensitivity to apo(a) size
A number of guidelines are in place for the testing of Lp(a) in patients.
-The European Guidelines for Management of Dyslipidaemia state that Lp(a) should be measured in individuals considered at high risk of CVD or with a strong family history of premature CVD.
-The European Atherosclerotic Society suggest that Lp(a) should be measured once in all subjects at intermediate or high risk of CVD/CHD who present with10 :
1. Premature CVD
2. Family hypercholesterolaemia
3. A family history of premature CVD and/or elevated Lp(a)
4. Recurrent CVD despite statin treatment
5. ≥3% 10-year risk of fatal CVD according to the European guidelines
6. ≥10% 10-year risk of fatal and/or non-fatal CHD according to the US guidelines
-EAS Consensus Panel states the evidence clearly supports Lp(a) as a priority for reducing cardiovascular risk, beyond that associated with LDL cholesterol. Clinicians should consider screening statin-treated patients with recurrent heart disease, in addition to those considered at moderate to high risk of heart disease.
- The Randox Lp(a) assay is one of the only methodologies on the market that detects the non-variable part of the Lp(a) molecule and therefore suffers minimal size related bias – providing more accurate and consistent results. The Randox Lp(a) kit is standardised to the WHO/ IFCC reference material SRM 2B and is closest in terms of agreement to the ELISA reference method.
- Five calibrators with accuracy-based assigned target values are provided – which accurately reflect the heterogeneity of isoforms present in the general population
- Measuring units available in nmol/L upon request
- Highly sensitive and specific – method for Lp(a) detection in serum and plasma
- Applications are available for a wide range of biochemistry analysers – which detail instrument-specific settings for the convenient use of Randox Lp(a) on a variety of systems
- Liquid ready-to-use reagents – for convenience and ease-of-use
Watch the interview with Bob Harper here:
1. Lipoprotein(a) Foundation, Lipoprotein(a) Foundation Thanks Bob Harper for Revealing High Lp(a) Levels Led to His Recent Heart Attack on The Dr Oz Show, 2017 Available from: http://www.businesswire.com/news/home/20170425006724/en/ [Accessed: 16 March 2017]
2. Lipoprotein Foundation, Understand Inherited Lipoprotein (a), Available from: https://goo.gl/bH5A8R [Accessed: 16 March 2017]
3. Kumar, V., Abbas, A. K. and Aster, J. C., Robbins and Cotran Pathologic Basic of Disease, (Philadelphia: Elsevier Saunders, 2015), p. 494 in Google books, https://goo.gl/VEnVX9 [Accessed 27th April 2017]
4. Kamstrup P.R., Tybjaerg-Hansen A., Steffensen R., Nordestgaard B.G. Genetically elevated lipoprotein (a) and increased risk of myocardial infarction. JAMA. Vol. 301, p. 2331-2339 (2009).
5. Afshar, M. Kamstrup, P.R., Williams, K., Snidermann, A. D., Nordestgaard, B.G., Thanassoulis, G., Estimating the Population Impact of Lp(a) Lowering on the Incidence of Myocardial Infarction and Aortic Stenosis – Brief Report., Ateriosclerosis, Thrombosis, and Vascular Biology, 2016;36:2421-2423, Available from: http://doi.org/10.1161/ATVBAHA.116.308271
6. The Lipoprotein(a) Foundation, Lipoprotein(a) Foundation Supports National Heart Valve Disease Month, Highlights Genetic Link between Lp(a) and Aortic Valve Disease, Business Wire. (2017), Available from: https://goo.gl/LhQFGj [Accessed: 16 March 2017]
7. Lab Tests Online, Lp(a), 2014, Available from: https://goo.gl/W2PWSN [Accessed: 16 March 2017]
8.Gutierrez, G., The heart attack risk factor you haven’t heard of, Baylor College of Medicine, 2017, Available from: https://goo.gl/9X4Xko [Accessed: 16 March 2017]
9. Marcovina, S.M. and Albers, J.J. Lipoprotein (a) measurements for clinical application. Lipid Res. Vol. 57, p. 526-37 (2016).
10. Nordestgaard, B. G., Chapman, M. J., Ray, K., Bore´n, J., Andreotti, F., Watts, G. F., Ginsberg, H., Amarenco, P., Catapano, A., Descamps, O. S., Fisher, E., Kovanen, P. T., Kuivenhoven, J. A., Lesnik, P., Masana, L., Reiner, Z., Taskinen, M. R., Tokgozoglu, L., and Tybjærg-Hansen, A., for the European Atherosclerosis Society Consensus Panel. Lipoprotein(a) as a cardiovascular risk factor: current status. European Heart Journal. Vol. 23, p. 2844-2853 (2010).
Cholesterol is a fatty substance also known as a lipid. It is made by the liver but can also be found in some foods. It is essential to let the body function normally. You will be sad to hear that high levels can increase your risk of serious health conditions. There are two main types; high-density lipoproteins (HDL) and low-density lipoproteins (LDL). HDL is known as good cholesterol. It carries cholesterol back to the liver, where it is broken down. LDL on the other hand carries cholesterol to the cells however if there is a surplus it can build up in the artery walls increasing the chances of a heart attack or stroke occurring.
Here are some scary facts about cholesterol…
- You can’t live without it – Cholesterol has been in your body since the day you were born. It is a building block for all cells. Not only that but all of our cells and hormones need it to function properly…unfortunately you are very unlikely to find good cholesterol in your typical trick-or-treat offerings.
- Not all patients on cholesterol-lowering medication respond optimally to it – In the recent past, aspirin (a drug used to reduce levels) was prescribed for people who had a perceived risk of a heart attack. However aspirin does not always work; up to 30% of patients could have a below optimum response to the drug and therefore be at a considerably increased risk of a recurrent cardiovascular event. This is may also be referred to as “aspirin resistance”.
- One third of adults have high cholesterol – Testing is advised every 5 years to monitor your levels to see any changes. To get the most accurate results tests should be carried out one week apart, however most testing facilities won’t follow this.
- High levels could be down to genetics – Diet you can change, genes you can’t! If your family has a history of high cholesterol then you are likely to have it as well. It has been suggested that 75% of cholesterol is due to genetics and the remaining 25% is down to diet and lifestyle choices.
- Women’s levels will fluctuate over their lifespan – Did you know that ladies? During the average woman’s lifespan, cholesterol levels will rise and fall due to pregnancy and menopause. During pregnancy levels will rise in order to help the baby develop. After birth the mother’s levels should return to normal however after menopause a woman’s LDL levels will rise to that higher of a man’s.
However it is not all doom and gloom this Halloween! Randox are here to treat you to a vast range of specialised blood tests to allow the most accurate diagnosis of cholesterol levels, allowing you to gauge how many sweets you can sneak in this Halloween! We offer a large array of routine and niche tests. The most popular and widely tested are HDL, LDL, total cholesterol and triglycerides. Some further risk assessment cholesterol tests which are not routinely run include sLDL, HDL3, Lp(a). These cholesterol biomarkers are also affected by the usual risk factors such as age, weight, smoking, etc.; however they can also be a result of one’s genes. As mentioned before aspirin resistance is a big problem affecting up to 30% of all patients on aspirin therapy. However Randox offer the TxBCardio™ test which is a unique test to diagnose and assess the effectiveness of aspirin therapy.
From all of us here at Randox we wish you a safe and happy Halloween!
For health professionals
Randox Laboratories manufacture a wide range of routine and niche biochemistry reagents suitable for both research and clinical use. These include a wide variety of automated routine and niche cardiac tests and our new HDL3-C assay. Please contact email@example.com for further information.
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