Atheromatous plaque: Formation and development
Carotide.com :: Copyright Dr Christian Petitjean - Paris ::
An atheromatous plaque may develop until the carotid artery is occluded, without ever giving any indication of a disorder to the patient. This is what we are going to study in this chapter.
A – Normal arterial wall
|The wall of a normal artery is made up of three parts. The external part, called the tunica adventitia or externa, is thin and very strong. The middle part, called the tunica media, is thick and contains muscle fibers. The inner part, called the tunica intima, is thin and prevents blood clots from forming (figure 1).|
B – Atheromatous plaque
|Atheromatous plaque forms through the thickening of the middle layer of the arterial wall (tunica media), which then reduces the arterial lumen (channel in which blood flows) and causes a stenosis (narrowing) (figure 2).|
A plaque of moderate volume (responsible for a 70% or lesser stenosis) does not slow down the blood flow and usually has a fibrous structure. It carries only a very low risk of neurological incident.
C – Development of an atheromatous plaque
The volume increase of an atheromatous plaque most often occurs gradually under the influence of favorable factors (See the subchapter entitled: “Factors that promote stenosis” for more explanations). The volume may massively increase when an hematoma (blood leak) forms inside the plaque (figure 3).
When an atheromatous plaque becomes voluminous, several complications may occur: the tunica intima may rupture, allowing a blood clot to form. The structure of the plaque, usually fibrous, may become necrosed (liquefaction) (figure 4). As long as the necrosis or the hematoma remains localized in the atheromatous plaque, the patient does not incur any risk. But the necrosis or the hematoma may extend up to the tunica intima (inner layer of the arterial wall). The tunica intima is then the last barrier between the necrosis and the blood circulation. Should it rupture, the liquefied tissues and the debris associated with the necrosis will spill into the blood circulation and migrate toward the brain (cerebral embolism) causing a neurological incident. (See the sub-chapter entitled: “Risks” and the chapter entitled: “Diagnosis of the disease” for more explanations.)
D – Occlusion of the carotid artery
When the atheromatous plaque is so voluminous as to render filiform the arterial lumen (channel through which blood flows), the blood can no longer flow and coagulates (figure 5). It is then said that the carotid artery is occluded (clogged). Blood no longer flows. The thrombosis (blood clot) extends within the entire internal carotid artery and up to the cerebral arteries. Here, in most people, there are arteries called communicating arteries, which link the cerebral arteries together. These communicating arteries supply blood to the brain when a carotid artery is occluded (figure 6). This explains why a carotid artery may be occluded without any consequences and even without the patient being aware of it. Unfortunately, some patients do not have communicating arteries and will suffer serious disorders.