Atherosclerosis may be described as a chronic inflammation in the arterial wall. It is caused by a complex interplay between lipoproteins, white blood cells (macrophages), the immune system and the normal elements of the arterial wall.
This process leads to formations of atherosclerotic lesions or plaques that may protrude into the lumen of the artery causing arterial narrowing, which may ultimately limit blood flow.
Rupture of an atherosclerotic plaque may lead to thrombosis (blood clotting) causing an acute occlusion (blockage) of the artery. If this happens in a coronary artery it may cause an acute myocardial infarction (acute heart attack).
There are many factors that contribute to atherosclerosis, one of which is elevated blood levels of cholesterol.
Cholesterol and Lipoproteins
Although cholesterol is an essential substance, elevated plasma levels appear to play an important role in the initiation and progression of atherosclerosis. In animal models, atherosclerosis will not occur in the absence of greatly elevated levels of plasma cholesterol.
High levels of plasma cholesterol also appear to be an important contributor to atherosclerosis in humans, although the threshold level of plasma cholesterol that must be exceeded to produce clinically relevant disease appears to be much lower than that in animal models, possibly because lesion formation occurs over many decades.
Atherosclerotic clinical events, such as myocardial infarction are uncommon among individuals with lifelong very low plasma cholesterol levels.
Because fats are insoluble in water, cholesterol can not be transported in blood on its own.
The body’s solution to this problem is to bind cholesterol to certain proteins that function as transport vehicles carrying different types of fats such as cholesterol, triglycerides (TG) and phospholipids. These combinations of fats and protein are termed lipoproteins.
It is important to emphasize, that it is lipoprotein that interact with the arterial wall and initiate the cascade of events that leads to atherosclerosis.
Cholesterol is only one of many components of lipoproteins. Therefore, measurements of total cholesterol provide little information about the lipoproteins that transport the bulk of cholesterol.
Although LDL’s seem to be the most atherogenic particles, it has to remembered that VLDL and other apoB – containing lipoproteins may also contribute to atherosclerosis.
Apolipoprotein B (apoB)
Lipoproteins are the particles that transport cholesterol and triglycerides in the blood stream.
Lipoproteins are comprised of proteins (apolipoproteins), phospholipids, triglycerides and cholesterol. The lipoproteins vary in the major lipoprotein present, and the relative contents of the different lipid components. ApoB is an important component of many of the most atherogenic lipoprotein particles.
ApoB occurs in 2 main forms, apoB 48 and apoB 100. ApoB 48 is synthesized mainly by the small intestine. ApoB 100 is the apolipoprotein found in lipoproteins synthesized by the liver. Therefore, from the viewpoint of atherosclerosis and cardiovascular risk, apoB100 is the important one. ApoB 48 is primarily found in chylomicrons.
ApoB 100 is found in chylomicrons, VLDL, IDL, LDL and LP(a) particles. All these particles are atherogenic. Each of these particles contains a single apoB molecule. Therefore, measurements of apoB represent the total burden of the main lipoprotein particles involved in the atherosclerotic process.
Usually, 85-90 percent of apoB represent LDL particles. Thus, apoB reflects particle concentration, similar to LDL-P. Although measurements of apoB are not widely available, the assay has been standardized and does not require a fasting sample.
Several studies have shown that apoB may be a better predictor of cardiovascular disease risk than LDL-C. Furthermore, it has been shown that apoB may be elevated despite normal or low concentrations of LDL-C. ApoB also appears to predict on-treatment risk, when LDL-C has been lowered by statin therapy. The INTERHEART study found that the apoB/apoA1 ratio is more effective at predicting heart attack risk, than either the apoB or apoA1 measure alone.
Apo B containing lipoproteins are the ones that are most likely to enter the wall of the arteries. They are capable of trafficking cholesterol into the artery wall, and if present in increased numbers they may be the main initiating factor in atherosclerosis. Retention of ApoB containing lipoprotein particles within the arterial wall is an essential part of the process.
Normal Range For ApoB
The normal range for apoB is 40-125 mg/dL.
Usually less than 100 mg/dL is considered desirable in low or intermediate risk individuals.
Less than 80 mg/dL is desirable in high risk individuals, such as those with cardiovascular disease or diabetes.
How to Lower ApoB
Many doctors will recommend the same general measures to lower apoB as they do for lowering LDL-C. Thus, reducing the amount of saturated fats and cholesterol is often recommended together with increased consumption of vegetables, fiber and mono-and polyunsaturated (omega-3) fatty acids.
Some studies have indicated that carbohydrate restriction may lower apoB, independent of whether the intake of saturated fat is low or high. LDL-C was not lowered by carbohydrate restriction in these studies, suggesting that diet may affect apoB and LDL-C differently.
Physical exercise has also been shown to lower apoB and positively affect the apoB/apoA1 ratio, but the effect on LDL-C appears to be much smaller.
ApoB levels can be reduced by cholesterol lowering drugs (statins).