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Lipoprotein(a) (lp(a)) is a low-density lipoprotein linked to apolipoprotein(a), formed in the liver, which has been associated with an increased risk of heart disease, stroke, atherosclerosis, and blood clots. Its role in the body is unknown, but it inhibits the activity of plasminogen, resulting in the development of more blood clots than normal. Lp(a) levels are mainly determined by heredity, but exercise, diet, and cholesterol-lowering medications can help modulate elevated levels. Fish oil supplements may also be helpful in lowering lp(a).
When fatty substances, such as cholesterol and triglycerides, travel in the bloodstream, they pair up with a protein called apolipoprotein, which allows them to dissolve in the fluid portion of the blood. Examples of these fat and protein combinations, called lipoproteins, are low-density lipoprotein (LDL) and high-density lipoprotein (HDL) which are commonly measured in cholesterol screening tests. Lipoprotein(a), or simply lp(a), is a low-density lipoprotein linked to apolipoprotein(a), formed in the liver. Increased levels of lp(a) have been associated with an increased risk of heart disease, stroke, atherosclerosis and blood clots. Lipoprotein(a) has also been linked to a decreased chance of survival with these conditions.
Scientists have not been able to discover the role of lp(a) in the body. Its structure is similar to a chemical responsible for breaking down blood clots called plasminogen. If there is a high level of circulating lp(a), lp(a) binds to the same plasminogen receptors. This inhibits the activity of plasminogen, resulting in the development of more blood clots than normal. Blood clots contribute to both heart attacks and strokes.
Lp(a) stimulates the deposition of cholesterol in the cells lining the inner hole of the arteries. This process narrows the arterial diameter and causes the formation of cholesterol plaques at sites with increased blood flow and turbulence. As plaque begins to invade the column of blood flowing through the artery, the tissue supplied by the artery becomes starved of oxygen. Poor blood flow is another risk factor for heart attack and stroke.
The blood level of lipoprotein(a) is not normally evaluated in blood tests. There is no standardized scale to measure this lipid in the blood. Furthermore, there are no clinical studies that clearly demonstrate the relationship between Lp(a) and heart disease, and no studies that show that lowering Lp(a) reduces the overall risk of heart attack or stroke. Also, high lipoprotein(a) levels are more dangerous when low-density cholesterol levels are also high, making it difficult to analyze which blood lipid is causing the problem.
Lipoprotein(a) levels are mainly determined by heredity. African populations tend to have higher lp(a) levels than Caucasians. Exercise, diet, and cholesterol-lowering medications make a big difference in modulating elevated lp(a) levels. Some studies promote the use of low-dose aspirin or niacin to control lipoprotein(a) levels. In a study in Tanzania, fish eaters had lower levels of lp(a) than other segments of the population, giving rise to the possibility that fish oil supplements may be helpful in lowering lipoprotein(a).
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