Our body’s lipids such as triglycerides and cholesterol are insoluble in circulating plasma (the fluid component of our blood.) In order to carry around these lipids, we must package them with proteins to make them dissolve in plasma. These proteins are called apolipoproteins.
Apolipoproteins + lipids together make up what is called a lipoprotein. Some well known lipoproteins are LDL and HDL. These apolipoproteins serve a variety of functions such as directing the lipoprotein to certain cells in the body or regulating enzymes to manage the packaged lipids. These proteins can also interact with other systems of the body that have nothing to do with lipid handling.
Lipoprotein(a) or Lp(a) is a specialized form of LDL. Not surprisingly it is made of LDL and an apolipoprotein designated (a). The exact benefit of Lp(a) is not clear but its potential bad effects have been studied. Lp(a) is similar in structure to a protein called plasminogen. Plasminogen is important in helping the body dissolve blood clots. Believe or not, our bodies are constantly making and dissolving microscopic blood clots in a delicate balance of two blood clotting systems. If Lp(a) competes for binding spots for this blood clot dissolver, the blood system balance may favor forming blood clots. Most heart attacks are caused by a blood clot in a heart artery at a site of atherosclerosis. Lp(a) may also stimulate our immune cells to deposit cholesterol into heart artery walls thereby promoting the development of atherosclerosis.
Higher levels of Lp(a) have been shown to increase the risk of cardiovascular disease. If you have a heart attack, higher Lp(a) levels are associated with a lower chance of survival. Furthermore, high Lp(a) levels seem to more significantly increase the risk of heart disease if you already have high LDL, low HDL, and/or high blood pressure. The main determinant of high Lp(a) levels is your genes and therefore there are some racial differences. African-Americans tend to have higher levels than Caucasians or East Asians. Lp(a) can be measured in the blood but it is not part of a routine lipid panel. A Lp(a) level less than 30mg/dl is considered normal.
Although there is some controversy as to who should get a routine Lp(a) level, most agree that it is reasonable to check the level in the following situations:
-established heart disease and normal lipids (LDL, HDL, triglycerides)
-strong family history of heart disease with normal lipids
-persistently high levels of LDL despite aggressive treatment.
Despite knowing that Lp(a) can increase the risk of heart disease, little data is available today that demonstrates lowering Lp(a) levels directly translate into reduced heart disease risk. Niacin can lower Lp(a) levels substantially but again it’s not clear if this results in overall better heart health. One more aggressive method to remove Lp(a) is called LDL apheresis, a process similar to hemodialysis where blood is filtered through a machine that can remove LDL particles. Unfortunately, this is an invasive and expensive treatment with only limited availability. Therefore, if elevated levels of Lp(a) are detected, then the main goal of treatment is to more aggressively manage other heart disease risk factors. This may mean, for example, aiming for an even lower LDL level. Hopefully, more information will be forthcoming as to how we can better treat this risk factor for heart disease. For now, it remains a marker of risk for which we have little recourse.