Official statements are clear: the risk of atherosclerotic vascular disease is directly related to plasma cholesterol levels. Accordingly, all of the national and transnational screening and therapeutic guidelines are based on total or LDL cholesterol.
On the contrary, the risk appears to be rather related to the number of circulating plaque forming particles than to the measured concentration of cholesterol.The concentration of apo B provides a direct measure of the number of these circulating particles.
According to a study published in 2006 in the prestigious Journal of Internal Medicine evidence indicates that apo B is superior to any of the cholesterol indices to recognise those at increased risk of vascular disease and to judge the adequacy of lipid-lowering therapy. The evidence also indicates that the apo B/apo A-I ratio is superior to any of the conventional cholesterol ratios in patients without symptomatic vascular disease or diabetes to evaluate the lipoprotein-related risk of vascular disease.
Lipoproteins are the particles that transport cholesterol and triglycerides in the blood stream. Lp(a) is a lipoprotein rich in cholesterol. It differs from LDL as it contains an additional protein, apolipoprotein (a). Similar to LDL, an Lp(a) particle also contains one molecule of apolipoprotein B.
Recently measures of lipoprotein particles involved in atherosclerosis, which is the main underlying cause of CVD, have been found to be very useful to assess risk. Examples of such measurements are LDL particle number (LDL-P), apolipoprotein B and lipoprotein(a).
The Copenhagen City Heart Study found that individuals with plasma Lp(a) levels above 50 mg/L had 2 to 3 – fold increase risk for heart attack (myocardial infarction).
In 2010, the European Atherosclerosis Society (EAS) consensus panel recommended screening for elevated Lp(a), in people 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.
Desirable: < 14 mg/dL (< 35 nmol/l)
Borderline risk: 14 – 30 mg/dL (35 – 75 nmol/l)
High risk: 31 – 50 mg/dL (75 – 125 nmol/l)
Very high risk: > 50 mg/dL (> 125 nmol/l)
The EAS Consensus panel recommends that Lp(a) should be measured in high risk individuals such as those with premature CVD, familial hypercholesterolemia, family history of premature CVD and/or elevated Lp(a), and individuals with recurrent CVD despite statin therapy.
How Is Lp(a) Involved 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 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 Can Lp(a) Be Modulated?
Lp(a) is mainly genetically determined and therefore refractory to lifestyle intervention.
Dietary changes, exercise and weight loss have not been shown to lower Lp (a).
Fat consumption has not been shown to raise Lp(a). One study documented a lowering of plasma Lp(a) levels in individuals placed on diets rich in saturated fat (a palm oil enriched diet). In keeping with this, other investigators have reported an increase in Lp(a) levels in individuals after they reduced their saturated fat intake. Monounsaturated fats also seem to reduce Lp(a) levels, as shown by a study that reported a significant decrease in Lp(a) levels in individuals whose diets were supplemented with almonds.
Niacin lowers Lp(a) by approximately 30 percent. Therefore, the EAS Consensus Panel has recommended niacin as the primary treatment for lowering elevated Lp(a) levels. However, these recommendations may have to be reevaluated in light of the results from the recentAIM-HIGH and HPS2-THRIVE trials. These trials did not show any clinical benefits of adding niacin to statin therapy.
Source: http://www.docsopinion.com/health-and-nutrition/lipids/lipoprotein-a/
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