Pathogenesis of unstable angina pectoris

The pathogenesis of unstable angina involves plaque rupture, thrombosis, abnormal contraction of blood vessels and other processes.

In patients with coronary atherosclerotic lesions, the pressure in the coronary artery increases, and the structure in the plaque becomes thinner, which may cause plaque rupture. After plaque rupture, lipid nuclei may be exposed in the wall of the coronary artery, resulting in thrombosis. Thrombus contains more platelets, which may release a large number of vasoconstrictor substances, causing platelet accumulation, abnormal contraction of coronary arteries, causing myocardial ischemia and hypoxia, resulting in unstable angina.