Cholesterol and atherosclerosis are always closely linked. To find out more information on cholesterol click here. Now the time has come to look at atherosclerosis.
Atherosclerosis is where a person’s arteries become blocked or partially blocked. This reduces the diameter of the artery in turn reducing blood flow. This can then have one of two effects in
- Either reducing the transportation of oxygen around the body or
- Increasing a person’s blood pressure.
Damage to arteries is a perfectly natural action within the body. Whether our body has a healthy or unhealthy response to this is what determines whether we develop atherosclerosis or not. It has been discovered that atherosclerosis is as a result of inflammation.
Damage has occurred to the arteries and white blood cells are called into action by a series of chemical signals transported in the blood. White blood cells work with various proteins in order to isolate the area of damaged tissue. Once isolated the invader can be destroyed and repair can occur.
This repair happens through a process of collagen, local cells, cholesterol and other repair materials working together to form a granulation tissue. Once this repair tissue has completed its repair then a new blood vessel forms through this repair tissue. This is the final stage of healing and once this vessel forms the healing process is complete.
However this normal process has been disrupted by our western style of living. This disruption has led to a disease called atherosclerosis.
Contrary to popular and unfounded believes atherosclerosis plaques are not lumps of cholesterol and fat stuck to the lining of the arteries. It is in fact a mixture of debris consisting of 68% fibrous tissue, 8% calcium, 7% inflammatory cells, 1% foam cells and 16% lipid-rich necrotic core. The vast majority of this 16% lipid-rich necrotic core is made up of unsaturated fatty acids.
To help understand the process of atherosclerosis let’s take a look at the three stages of atherosclerosis as they occur.
This is where a harmful and unnatural body in the blood attacks the endothelium lining of the blood vessel. White blood cells are immediately called to the scene where they attack the invading body and kill it.
This leads to the arrival of another cell known as the macrophages. These cells are solely responsible for cleaning up the demolition job caused by the white blood cells. They swallow debris from damaged tissue, microbes, toxins and chemically damaged fats. They then swell in size and transform into foam cells.
White blood cells multiply and new ones keep on arriving at the scene and inflammation is now in full motion.
This is where the repair work begins.
The war between your defenses and the invading party is still on-going.
The repair happens by so-called smooth muscle cells passing through the plaque tissue. Their job is to help the artery lining repair the damage. Arteries are formed by these smooth muscle cells.
As these cells pass through the plaque and into the artery lining the plaque becomes better established and permanent. This plaque then stimulates the growth of collagen fibers to help the repair. The collagen also helps to form a fibrous crust on the plaque sealing it off like a scab over a wound.
However when this process goes wrong this is where we develop atherosclerosis. The inflammation never ceases to the repair process and the plaque keeps on growing in size.
The rate at which this growth takes place is dependent on which process is dominant over the other. If it is the repair process then it will be slow and if it is the inflammation process then it will be rapid.
This leads to partially blocked arteries. This process of atherosclerosis will only be stopped once the inflammation has stopped. However if the inflammation process is continuous or kicked back into action for any reason we enter stage 3.
This is where there is persistent inflammation.
The plaque develops a fatty, crumbly core which consists of dead white blood vessels, debris of tissue, toxins and oxidised and chemically altered fats and cholesterol.
This is similar to puss in a flesh wound, where the puss damages the surrounding tissues.
Likewise in atherosclerosis where inflammation is persistent it stimulates the production of an enzyme known as collagenases. This enzyme then starts to dissolve the collagen, which we will remember is a major component of the fibrous cap over the plaque. If this fibrous cap becomes thin and weak as a result of this process then the plaque is likely to burst. Within seconds this leads to the blood coagulating and the development of a thrombosis, blocking the artery. This is where we develop heart attacks and strokes.
E. Falk 2006
The plaque rupture and following thrombosis are the most devastating consequences of atherosclerosis. They cause approximately 76% of all fatal heart attacks.