Atherosclerosis - Topic Overview
Why does atherosclerosis happen? continued...
Injury may stimulate cells to grow and divide as part of the inflammatory process. This normal, healing response to chronic injury may actually result in the growth of atherosclerotic plaque.
This injury could be caused by any number of things, including:
- Physical stress on the artery lining, such as stress caused by high blood pressure.
- A response to an infection within the artery wall.
- Oxidative damage to the artery lining. Oxidative damage refers to injury caused by unstable molecules called free radicals. Free radicals are formed during reactions between oxygen and LDL ("bad" or low-density lipoprotein) cholesterol.
- Oxidized LDL cholesterol may cause injury to the blood vessel wall and promote an inflammatory reaction that clogs the artery lining with debris. But exactly why high cholesterol levels promote plaque formation is not clear. Cholesterol is found normally in all cell membranes, but it may alter the physical properties of the blood vessel wall, making it more likely to get damaged.
How smoking leads to atherosclerosis
Smoking plays a large role in the development of atherosclerosis. The carbon monoxide and nicotine contained in tobacco smoke affect blood flow through your arteries by:
- Making it easier for cholesterol-carrying lipoproteins to enter the walls of your arteries.
- Promoting the formation of fibrous plaque.
- Promoting the formation of blood clots that can completely block your arteries.
How does atherosclerosis cause an aortic aneurysm?
Atherosclerosis is one of the major causes of abdominal aortic aneurysm.
The wall of the aorta (and all blood vessels) is a dynamic tissue made up of living cells that need nutrients and oxygen. Many of these nutrients seep from the inside of the blood vessel through the walls to nourish the rest of the blood vessel. When the inner lining of the vessel is covered with an atherosclerotic plaque, nutrients can no longer seep through sufficiently. The cells receive no oxygen, and some of them die. As the atherosclerosis progresses and cells continue to die, the walls become weaker and weaker.
At some point, a critical relationship is reached between the pressure experienced in the center of the blood vessel, the wall tension, and the strength of the wall itself. When this point is reached, the wall begins to dilate (grow larger) in the area of the plaque. As the diameter of the vessel grows, the wall tension increases, leading to even more dilation. The end result is an aneurysm.