Common pathology of ACS

Ischaemic heart disease is a complex process which develops over a number of years. A number of changes can be seen:

1. Initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia

• A number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
• Fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
• Monocytes migrate from the blood and differentiate into macrophages.
• These macrophages then phagocytose oxidized LDL, slowly turning into large 'foam cells'.
• As these macrophages die the result can further propagate the inflammatory process.
• Smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

Summary

• Atheromatous plaque formation in coronary arteries
• Fissuring/ulceration of the plaque
  • Leads to platelet aggregation
• Localised thrombosis, vasoconstriction and distal thromboembolism
• Leads to myocardial ischaemia
• Death in IHD is usually due to VF: ventricular fibrillation

This can occur in areas of low-grade stenosis which have not previously caused angina-type symptoms

Unstable angina (crescendo angina)

• Angina occurring at rest OR sudden increased frequency/severity of existing angina