The measures of lipoprotein particles involved in atherosclerosis, the main cause of coronary heart disease or stroke (termed as cardiovascular disease (CVD)), have been discovered to be very useful assessing risk. Such measurements are LDL particle number (LDL-P), apolipoprotein B and lipoprotein(a).
Although lipoprotein(a), Lp(a), is a strong risk factor for CVD, the lack of clinical trial data have resulted in Lp(a) being largely ignored by clinical guidelines to assess the prevention of CVD.
In 2010, the European Atherosclerosis Society (EAS) consensus panel suggested screening for elevated Lp(a), in patients at moderate to high risk of cardiovascular disease. Desirable Lp(a) levels < 50 mg/dL were considered a treatment priority, after therapeutic management of LDL-C.
Lipoproteins are composed of cholesterol, phospholipids, proteins (apolipoproteins) and triglycerides and are the particles conveying cholesterol and triglycerides in the blood stream. The lipoproteins vary in the major lipoprotein present, and the relative contents of the different lipid components.
Lp(a) is a lipoprotein rich in cholesterol, unlike LDL as it containing an additional protein, apolipoprotein (a) (載脂蛋白 (a)). Similar to LDL, an Lp(a) particle also contains one molecule of apolipoprotein B.
Normal Blood Levels of Lp(a)
Lp(a) is produced by liver cells. But the pathways for the clearance of this substance are not clearly understood. Plasma levels of Lp(a) rise shortly after birth and the levels appear to become consistent within a few months.
For adults, plasma levels of Lp(a) vary widely, ranging from 0.2 – 250 mg/dL. The levels are similar in men and women.
Studies indicate that about one in five individuals have plasma levels above 50 mg/dL (80th percentile), and about one in four individuals have plasma levels above 32 mg/dL (75th percentile). Lp(a) levels less than 30 mg/dL are considered normal.
The EAS Consensus panel recommends that Lp(a) should be measured in high risk patients with premature CVD, familial hypercholesterolemia, family history of premature CVD and/or elevated Lp(a), and individuals with recurrent CVD despite statin therapy.
Lp(a) and Risk for Heart Disease
A number of epidemiological evidence 流行病學證據 indicates that Lp(a) is associated with the risk of CVD. A series of meta-analyses has provided evidence of a link between Lp(a) and CVD. Studies on patients with familial hypercholesterolemia 高膽固醇血症 have provided additional evidence.
Studies have indicated the association between Lp(a) and CVD without a threshold. It does not depend on high levels of LDL or non-HDL cholesterol, or the presence of other cardiovascular risk factors. But some authors have suggested that the risk of elevated Lp(a) is small, if LDL-cholesterol is not elevated.
Involvement of Lp(a) in Atherosclerosis and Heart Disease
Lp(a) and LDL penetrate the inner layer of the arterial wall and accumulate together at sites for atherosclerotic plaque formation.
Evidence suggests that Lp(a) may be more strongly retained in the arterial wall than LDL. Furthermore, Lp(a) transports oxidized phospholipids 磷脂 whose plasma levels are strongly correlated with the severity of coronary artery disease. Interestingly, these Lp(a) associated oxidized phospholipids possess pro-inflammatory activity. This might be one of the links between lipids and inflammation in atherosclerosis.
There is also some experimental data suggesting that Lp(a) may promote clot formation in arteries burdened by atherosclerotic plaque. This may be one of the mechanisms behind the involvement of Lp(a) in heart attack and stroke.
How to Regulate Lp(a)?
Lp(a) is mainly genetically determined and therefore refractory to lifestyle intervention. Change on diet, exercise and weight loss have no effect lowering Lp(a).
Some documents mentioned;
1) Niacin (nicotinic acid) Vitamin B3 lowers Lp(a) by approximately 30 percent
2) Taking DHEA may reduce 10%. However DHEA is a supplement which should be taken under Doctor’s advice.