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Pathophysiology of coronary artery diseases
Atherosclerosis begins as fatty streaks, lipids that are deposited in the intima of the arterial wall. Although they are thought to be the precursors of atherosclerosis, fatty streaks are common, even in childhood. Moreover, not all develop into more advanced lesions.
The reason why some fatty streaks continue to develop is unknown, although genetic and environmental factors are involved.
The continued development of atherosclerosis involves an inflammatory response. T lymphocytes and monocytes (that become macrophages) infiltrate the area to ingest the lipids and then die; this causes smooth muscle cells within the vessel to proliferate and form a fibrous cap over the dead fatty core.
These deposits, called atheromas or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood flow .
If the fibrous cap of the plaque is thick and the lipid pool remains relatively stable, it can resist the stress from blood flow and vessel movement. If the cap is thin, the lipid core may grow, causing it to rupture and hemorrhage into the plaque, allowing a thrombus to develop.
The thrombus may obstruct blood flow, leading to sudden cardiac death or an acute myocardial infarction (MI), which is the death of heart tissue.
Note;
The anatomic structure of the coronary arteries makes them particularly susceptible to the mechanisms of atherosclerosis.
As they twist and turn as they supply blood to the heart, creating sites susceptible to atheroma development.Although heart disease is most often caused by atherosclerosis of the coronary arteries, other phenomena decrease blood flow to the heart. Examples include vasospasm (sudden constriction or narrowing) of a coronary artery, myocardial trauma from internal or external forces, structural disease, congenital anomalies, decreased oxygen supply (eg, from acute blood loss, anemia, or low).