Abstract
The major cause of human arterial thrombosis is atherosclerosis. Thrombosis over atherosclerotic plaques is either due to superficial or to deep injury. In superficial injury there is endothelial denudation with thrombi adherent to the surface of the plaque. In deep injury more major plaque disruption exposes the lipid core to the lumen. Blood enters the core and thrombus forms within the plaque expanding its volume rapidly. Later thrombosis may, or may not, extend into the lumen leading to occlusion. Plaque disruptions heal by smooth muscle proliferation. Either form of thrombosis may occur in minor forms which invoke plaque growth alone or in major forms which precipitate clinical symptoms. In large arteries, such as the carotid, plaque disruption leads to chronic ulceration with exposed thrombus acting as a nidus for distal embolisation. Plaques with a high lipid and macrophage content in which smooth muscle cell numbers are low are at the greatest risk of disruption.

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