If the endothelium of a blood vessel is damaged in some way (there are risk factors for this), then low-density lipoproteins (LDLs) enter into the intima layer of the vessel wall. The LDLs are taken up by macrophages. As more lipid accumulates, a visible fatty streak can be seen in the lumen. As this process continues, some lipid starts to accumulate outside the macrophages; at the same time, the macrophages stimulate the production of collagen and the streak becomes more fibrous - this is the stage that this patient's coronary artery is at. Eventually, the fibrous plaque weakens the endothelial wall to such an extent that the plaque often ulcerates into the lumen, providing a surface for platelets to aggregate and promoting thrombosis.