Thursday, November 18, 2010

Preventing Cardiovascular Disease - Part 3

The higher your serum cholesterol, the more likely you are to have heart disease or other CVD's. Unfortunately, lowering your cholesterol does not guarantee prevention of heart disease. The issues are much more complex. In fact studies have shown that 80 percent of people who have heart attacks have the same total cholesterol level as individuals who don't have an attack. In other words the majority of individuals who have heart attacks have what can be considered as normal cholesterol levels. Total cholesterol levels are important but may not be as important as cholesterol differentiation. Analysis must go far beyond the traditional measurement of LDL/HDL ratios.

LDL's (Low Density Lipoproteins). - bad guys come in different shapes and sizes
There are more than seven subclasses of LDL particles. Each particle varies in its ability to adhere to and penetrate arterial walls to form arthroscerotic plaque. This differentiation is one of the keys to determining how damaging a patient's LDL's are. A bad distribution of these LDL in the cells can cause a 300% greater chance of having heart disease than someone with the same LDL level and a good distribution.

LDL-B is an especially damaging particle. Since they are mixed with triglycerides and are smaller in size than the larger, less harmful LDL-A particles. These small particles are more damaging than larger particles because they can move easily into endothelial cells. The LDL-B particles are picked up by macrophages (scavenger cells) which eventually become foam cells. These foam cells eventual rupture and spill their toxic, oxidized contents onto the arterial wall. These oxidized substances start the formation of atherosclerotic plaque. Because this atherosclerotic lesion contains an oxidized LDL-B particle it grows at 30 times the rate of a LDL-A particle.

Obviously, it is important to know the ratio and types of LDL's in a patients cholesterol readings. Especially since medications such as Lovastatin lower the number of large particles, but leave the smaller more damaging cholesterol particles intact. These medications also do nothing to reduce the oxidation properties of the triglycerides that are interwoven into the small LDL-B particles.

It is theorized that HDL's acts as a scavenger, removing cholesterol from the circulation. In this process free cholesterol comes into contact with the surface of the HDL, where it is esterified by a substance called lecithin- cholesterol acyltransferase (LCAT). This cholesterol is then stored in the centre of the HDL particle.

It is also theorized the HDL acts as a powerful antioxidant. The enzyme associated with HDL,lecithin-cholesterol acyltransferase , blocks the oxidization of LDL cholesterol. LDL levels should be no higher than 3.0 mmol/L (115 mg/dL). An optimal level of HDL should be 45mg/dL or higher .

Another factor that must be considered in conjunction with cholesterol levels is the level of Lipoprotein(a). This genetic factor has a large influence on clot formation in the arteries. Your body has a remarkable mechanism for dissolving clot formation called fibrinolysis. Lipoprotein(a) stops the process of fibrinolysis and greatly increases clot formation. This marker is so significant that many scientists consider this to be a better marker than cholesterol. When you have your cholesterol checked have your blood checked forLipoprotein (a).

In part four of Preventing Cardiovascular Disease we will cover Lifestyle and dietary recommendations to address cholesterol issues

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