1.10—Atherosclerosis

Atherosclerosis begins when the arterial endothelium is damaged. An inflammatory response attracts white blood cells, cholesterol-rich deposits and smooth-muscle changes, forming an atheroma in the artery wall.

Endothelial damage → inflammation → low-density lipoprotein enters the wall → macrophages form foam cells → plaque grows and narrows the lumen. A rough plaque can also encourage clot formation.

If a coronary artery lumen narrows, resistance to blood flow rises and cardiac muscle receives less oxygen. A plaque that ruptures may trigger a thrombus that blocks flow suddenly.

The disease links risk factors to a mechanism: high blood pressure can damage the endothelium, while smoking, diabetes and high LDL increase the likelihood of plaque development.

A risk factor raises probability rather than guaranteeing disease. Atherosclerosis is plaque formation in the artery wall; thrombosis is a clotting event that may follow it.