Tina-quant® Lipoprotein (a) reagent

nmol/L standardisation: It is more than a matter of units

Tina-quant® Lipoprotein (a)

Lipoprotein (a), also known as Lp(a), can serve as a clinically useful risk factor for atherosclerotic cardiovascular disease (ASCVD).


Cardiovascular disease (CVD) is a major health concern that continues to grow. CVD is already responsible for more deaths, globally, than any other disease and the huge burden it places on healthcare systems and society is predicted to become even greater.1

30 % of mortality associated with cardiovascular disease occurs in individuals without elevated conventional risk factors.2 Therefore, there is a clinical need to expand the number of available diagnostic tools for evaluating an individual’s risk to develop CVD.

Testing for elevated Lp(a) is recommended in all patients with premature ASCVD and those considered to be at intermediate-to-high risk of ASCVD.10

Numerous, extensive studies have demonstrated that the concentration of lipoprotein (a) (Lp (a)), but not the mass of Lp (a), can serve as a clinically useful risk factor for CVD.3–10

Tina-quant Lipoprotein (a)

Standardising against an apo (a) size independent method


The major problem of Lp (a) values is related to the inaccuracy of the methods that are affected by apo (a) size heterogeneity, which significantly affects the assessment of individual risk status for coronary artery disease. 11 Levels of Lp (a) can vary up to 1,000-fold among individuals and ethnic groups as the level is predominantly determined by the apo (a) gene. In order to obtain the right values and foremost provide apo (a) size independent results, measuring the concentration of particles (nmol/L), rather than total weight (mg/dL), is ideally recommended by the Australian Atherosclerosis Society (AAS).10

Tina-quant Lipoprotein (a) graph
Mass assays tend to underestimate the apo (a) concentration in subjects with apo (a) of a size smaller than the apo (a) size present in the assay calibrator, and conversely overestimate the concentration of larger apo (a) particles.11


Lp (a) values reported in nmol/L are not influenced by isoform size and thus provide a more specific assessment of CVD risk


Tina-quant® Lipoprotein (a) reagent Gen. 2 is the first method in the world to accurately and reliably measure Lp (a) on a fully consolidated platform.12

The nmol/L standardisation – which is recommended by the Australian Atherosclerosis Society – enables laboratories to measure the right value, which leads to a more accurate assessment of CVD risk.10 The Tina-quant® Lipoprotein (a) reagent Gen. 2 assay determines the concentration of Lp (a), rather than the mass of Lp (a). The measurement of the concentration provides a clear estimate of the number of Lp (a) particles independent of the molecular weight of the particle, which can vary from 187,000 to over 662,000 Daltons.

Tina-quant® Lipoprotein (a) reagent Gen. 2 detects molarity not mass

Before: False high/low value

In terms of mass, the patient on the right may have less risk than the person on the left due to decreased mg/dL

  • Standardised in terms of mass per unit volume (mg/dL)
  • Size heterogeneity of Lp(a) particles between individuals ignored
  • This can result in patient misclassification
Tina-quant Lipoprotein (a) graph

Now: True value

It is the molarity of Lp(a) particles rather than their combined mass which is correlated CVD risk

  • Concentration (nmol/L) of Lp(a) can serve as an excellent and clinically useful risk factor
  • First method in the world to accurately and reliably measure Lp(a) on a fully consolidated platform
  • Roche is only major manufacturer to standardise to nmol/L




Risk underestimation by using a mass assay (mg/dL)11

Tina-quant Lipoprotein (a) graph


  1. World Health Organization. Fact sheet No. 317. Cardiovascular diseases (CVDs). Available at: www.who.int/mediacentre/factsheets/fs317/en/index.html [Accessed June 20, 2017].
  2. Beaglehole, R., Reddy, S., Leeder, S.R. (2007). Poverty and human development: the global implications of cardiovascular disease. Circulation 116, 1871–1873.
  3. Cantin, B., Gagnon, F., Moorjani, S. et al. (1998). Is lipoprotein(a) an independent risk factor for ischemic heart disease in men? The Quebec Cardiovascular Study. J Am Coll Cardiol 31, 519–525.
  4. Luc, G., Bard, J.M., Arveiler, D. et al. (2002). Lipoprotein (a) as a predictor of coronary heart disease: the PRIME Study. Atherosclerosis 163, 377–384.
  5. Suk Danik, J., Rifai, N., Buring, J.E., Ridker, P.M. (2006). Lipoprotein(a), measured with an assay independent of apolipoprotein(a) isoform size, and risk of future cardiovascular events among initially healthy women. JAMA 296, 1363–1370.
  6. Danesh, J., Collins, R., Peto, R. (2000). Lipoprotein(a) and coronary heart disease. Meta-analysis of prospective studies. Circulation 102, 1082–1085.
  7. Bennet, A., Di Angelantonio, E., Erqou, S. et al. (2008). Lipoprotein(a) levels and risk of future coronary heart disease: large-scale prospective data. Arch Intern Med 168, 598–608.
  8. Kamstrup, P.R., Tybjaerg-Hansen, A., Steffensen, R., Nordestgaard, B.G. (2009). Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA 301, 2331–2339.
  9. Clarke, R., Peden, J.F., Hopewell, J.C. et al. (2009). Genetic variants associated with Lp(a) lipoprotein level and coronary disease. N Engl J Med 361, 2518–2528.
  10. Natalie C. Ward et al. (2022): Heart, Lung, and Circulation: 1443-9506, "Australian Atherosclerosis Society Position Statement on Lipoprotein(a) Clinical and Implementation Recommendations"
  11. Marcovina, S.M., Koschinsky, M.L., Albers, J.J., Skarlatos, S. (2003). Report of the National Heart, Lung, and Blood Institute Workshop on Lipoprotein(a) and Cardiovascular Disease: recent advances and future directions. Clin Chem 49, 1785–1796.
  12. Data on file. (2019) Roche Diagnostics International Ltd.

Source: Package inserts available at Roche from the individual web pages (reviewed May 2019) www.abbottdiagnostics.com, www.beckmancoulter.com, www.medical.siemens.com

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