What is lipoprotein(a)?

Lipoprotein(a) is a molecule made from joining a protein the body makes (called apolipoprotein(a)) and LDL, which is a form of cholesterol. The importance of the Measurement and lowering of Lipoprotein(a) is an area of active research. It is one of a group of molecules called ‘lipoproteins’, so called because they have this common form of construction – a protein attached to a cholesterol molecule. Having elevated levels of lipoprotein(a) in their blood has been strongly implicated in research as a risk factor for cardiovascular disease – such as coronary heart disease (CHD) or stroke.


Why measure lipoprotein(a)?

Because higher lipoprotein(a) levels seems to increase risk with or without other factors, it is called an independent risk factor. Furthermore, compounding risk factors – such as a decreased good cholesterol (called HDL) – may further increase the risk of cardiovascular disease. Lipoprotein(a) also has other important effects on the body, such as antifibrinolytic activity (stops blood from clotting). It also stimulates smooth muscle cells in the walls of blood vessels to grow and multiply. Recently, lipoprotein(a) has been shown to interact with inflammatory cells, recruiting them to become part of clots. This article aims to help you understand some of the reasons you or your doctor might be interested in the Measurement and lowering of Lipoprotein(a) in your blood.


What studies have been done on lipoprotein(a)?

There have been numerous studies that have investigated the effects of lipoprotein(a) on the risk of cardiovascular disease. Not all of these studies have had agreed results and there is still much debate regarding the effect of lipoprotein(a), and its risks with regards to cardiovascular disease. There is also a large genetic component which determines an individual’s lipoprotein(a) levels. At present there is still controversy about the importance of the measurement and lowering of Lipoprotein(a).


Who should have their lipoprotein(a) levels checked?

Lipoprotein(a) levels are generally measured in patients with established vascular disease, in particular those with premature cardiovascular disease or stroke – where other risk factors fail to provide reason why the person has the disease. Lipoprotein(a) levels may be measured in other individuals with strong risk factors for cardiovascular disease (such as a strong family history). This is because if the lipoprotein a level is elevated above 30m/dl, the treatment of other cholesterol levels such as LDL may need more aggressive attention. Again this is because it is believed that a combination of factors is much more risky than one risk factor.


What can be done if lipoprotein(a) levels are high?

In terms of treating elevated lipoprotein(a) levels there are limited options. Fish oils may be effective in reducing these levels – however more investigation is needed in order to confirm this. At present there are two reliable, commonly used methods of reducing lipoprotein a levels in the blood:

  1. Nicotinic acid. This is effective in reducing lipoprotein a levels. However, potential side effects such as flushing, ototoxicity (ear damage) and hepatotoxicity (liver damage) must be considered and the benefits versus risks must be deliberated.
  2. Apheresis. This is the most effective way of reducing lipoprotein a levels. Apheresis involves separating the blood externally to the body, so that the lipoprotein(a) may be effectively ‘filtered out’, and the blood is then returned back to the patient. This treatment is very expensive and generally only available to very high risk patients.


Conclusion

An elevated lipoprotein a level may be highly indicative of an increased risk of cardiovascular disease. Measurement of lipoprotein a levels provides usedul additional information about risks in patients with premature cardiovascular disease, and those with other, intermediate risk factors. In patients with an increased lipoprotein(a) level, aggressive treatment of LDL levels is recommended, as treatment options for elevated lipoprotein(a) are limited.

References

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  2. Kostner KM, Kostner GM. Lipoprotein (a): Still an enigma? Curr Opin Lipidol 2002; 13(4): 391-6.
  3. Danesh J, Collins R, Peto R. Lipoprotein(a) and coronary artery disease: meta-analysis of prospective studies. Circulation 2000;102:1082-5.
  4. Tsimikas S, Brilakis ES, Miller ER, McConnell JP, Lennon RJ et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease. N Engl J Med 2005; 353(1): 46-57.
  5. Ridker PM, Hennekens CA, Stampfer MJ. A prospective study of Lp(a) and the risk of myocardial infarction. JAMA 1993; 270:2195-9.
  6. S. Marcovina, M.L. Koschinsky, J. Albers and S. Skarlatos, Report of the National Heart Lung and Blood Institute workshop on lipoprotein(a) and cardiovascular disease. Recent advances and future directions, Clin Chem 2003; 49: 1788-96.
  7. Schlueter W, Keilani T, Batlle DC. Metabolic effects of ACE inhibitors: focus on the reduction of cholesterol and lipoprotein (a) by fosinopril. Am J Cardiol 1993; 72 (20): 37-44.
  8. Effects of Combined Low-Density Lipoprotein Apheresis and Aggressive Statin Therapy on Coronary Calcified Plaque as Measured by Computed Tomography. U. Hoffmann, K. Derfler, M. Haas, A. Stadler, T.J. Brady, K. Kostner. American Journal of Cardiology 2003; 91: 461-4.

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