Atherosclerosis is the disease that is a result of progressive narrowing and hardening of the arteries.
Atherosclerosis arises as a result of plaques building up on the inner lining of the artery wall. These plaques are also known as atheromas or atheromatous / atherosclerotic plaques. As the plaques grow larger, it occludes (blocks) the lumen of the artery to a greater extent until a point is reached where the blood flow to target organs and tissue is severely affected. This decreases oxygen supply leading to ischemia and possibly even infarct. It is often at this stage where the first signs and symptoms of atherosclerosis are noticed.
Apart from the narrowing due to the growing plaque, the hardening of the artery hampers arterial stretching and rebound relaxation which is important for keeping the blood propelled. The arterial wall becomes fragile and can rupture thereby allowing for the adhesion of platelets to the wall. This results in thrombosis, which is the formation of a blood clot. Coupled with the bulge of the atheromatous plaque, this will eventually lead to a complete occlusion of the artery.
Structure of an Artery
The wall of an artery has 3 layers :
- Tunica intima is the inner lining which is made up of a single layer of endothelium that lines the inside of the artery and supported by surrounding connective tissue.
- Tunica media which is the largest part of the arterial wall and contains mainly smooth muscle surrounded by inner and outer elastic layers adjacent to the intima and adventitia respectively.
- Tunica adventitia which is the outer lining of the artery made up of connective tissue.
Atherosclerosis tends to affect larger elastic arteries and medium size muscular arteries like the aorta or carotid artery. It may also affect the smaller coronary arteries of the heart. Athersclerotic plaques form under the endothelial lining within the underlying intima connective tissue.
How does atherosclerosis occur?
Pathogenesis of Atherosclerosis
The exact mechanism of atheroslcerosis pathogenesis is unclear. Usually a number of risk factors need to be present for atherosclerosis formation, although sometimes, just one factor is sufficient.
The current hypothesis of atherogenesis (the formation of atheromatous plaques) is known as the response-to-injury hypothesis. It is a culmination of two previous hypotheses on atherogenesis as well as new findings due to developments in medical science.
- Damage to the endothelial lining of the artery may occur for a number of reasons, particularly relating to the known risk factor for atherosclerosis.
- LDL cholesterol accumulates in the vessel wall as a result of increased vascular permeability due to endothelial damage.
- Monocytes adhere to the endothelium, enter the vessel wall where it differentiates into macrophages. These macrophages take up the LDL cholesterol and form foam cells.
- The aggregated foam cells form fatty streaks in the artery wall.
- Some of the underlying smooth muscle in the artery wall is pulled up into the intima and proliferates. This along with the fatty streaks forms an atheromatous plaque which bulges into the lumen of the artery.
- More lipids then bind to the lining of the artery wall plus enter the lining to aggregate within macrophages and even smooth muscle cells. This increases the size of the plaque.
- At this point, the bulging plaque can occlude the artery significantly. However, it also causes turbulent blood flow within the artery thereby resulting in thrombosis.
- The chemical factors and fluid dynamics that prevent blood cells from adhering to the endothelium is impaired. Coupled with the chemical mediators secreted by the macrophages, platelets begin to stick to the lining of the arterial wall. This process is explained in detail under causes of thrombosis and a blood clot.