Atheromatous plaques that become extremely voluminous carry the following risks:

A – Rupture of the tunica intima

The tunica intima (inner wall of the artery preventing blood clots from forming) can rupture. Then blood clots form in contact with the plaque, detach from it and are carried away by the blood flow up to the cerebral artery where they are blocked (cerebral embolism), causing the destruction of the neurons that receive blood from that artery (cerebral infarction) (figures 1 and 2).

B – Necrosis of the atheromatous plaque

Should the atheromatous plaque become necrosed (liquefaction) and should that pocket of necrosed material rupture into the arterial lumen, necrotic debris will be carried away by the blood flow toward the cerebral arteries (figures 3, 4, and 5) with the same consequences as in the previous scenario (figure 2).

C – Insufficient blood flow

When a stenosis (narrowing) of the carotid artery becomes so extensive as to not let enough blood and thus not enough oxygen into the brain, this causes an interruption of the functioning of the neurons in certain regions of the brain or, even worse, their destruction (cerebral infarction) (figure 6).

D – Thrombosis of the carotid artery and the cerebral arteries

This is when a stenosis (narrowing) develops into an occlusion of the carotid artery (completely clogged). Such occlusion may extend to the cerebral arteries and occlude them, thereby destroying the affected neurons (figure 7).