The typical arterial wall is made up of three basic layers. There are also two forms of fat within the body which can be classified into low density protein and high density protein. The first one is considered a fat molecule, which can penetrate the arterial wall and venture deep into the arterial layers.
There are multiple functions that happen within our body which we are not aware of and atherosclerosis is one such function. It begins with the buildup of fat which is accumulated within the arterial wall which is dependent on the general condition of the arterial wall as well as concentration of the increased quantity of fat levels present in the body. This fat penetrates through the arterial wall and undergoes a mechanism called oxidation which converts the fat molecules into substance which is dangerous to the body and triggers the inflammation process. At this stage, white blood cells called monocytes move from the bloodstream into the arterial wall and start the inflammatory response. This result in cells referred to as macrophages which swallow the oxidized fat molecules, and once this is done, these cells turn into what is referred to as foam cells.
The problem is that often, these foam cells can burst releasing the contents of the cell onto the arterial wall. When this happens regularly, the foam cell will form fibrous material which helps increase the frequency of arteries plaque growth which results from the protein in the arterial wall and can impact the membranes as well.
In the initial phase, this growth allows the walls of the artery to hold only a certain amount blood thereby maintaining a noteworthy but reduced blood flow. This being the case, the tests will reveal only those artery plaques which bulge into the center of the arterial lumen and are not just building up. This happens as the plaque is located deep within the layers. Therefore the results of medical tests cannot be considered as conclusive while determining the growth of plaque and the advent of atherosclerosis in the body.
When the plaque continues to grow, the arterial wall ends up being unable to cope with the growth and forces the atherosclerosis deposit to push into the center of the vessel. Normally, this is found when the plaque growth reaches around 40%. However, the concern at this point would be bursting or dislodging of plaque which could result from swelling of plaque.
It is normally found that unstable plaques burst, particularly those that contain a large amount of lipids covered by weak fibrous layers. Often, these plaques cannot be identified as they are located within the arterial walls and have not pushed into the arterial lumen.
If the plaque bursts, the lipid content is brought into contact with blood, which can result in the growth of blood clots. If the vessel is completely blocked for at least two hours, this can cause a serious condition called myocardial infarction, more commonly known as a heart attack.