It has been demonstrated that the most plausible mechanism underlying acute coronary events (acute myocardial infarction, unstable angina, coronary death) is thrombosis of a complicated atherosclerotic plaque [Davies, 1996; Virmani, 2000]. Plaque complications include:

• plaque haemorrhage with rupture of the fibrotic cap; or
• less severe damage, called a superficial erosion of the plaque, without cap rupture (see Figure 6).

 

Distinctive features (see Figure 7) of the plaque that are prone to rupture are: thinning and disorganisation of the fibrous cap; increase in intracellular and extracellular lipids (mainly cholesteryl esters); increase in macrophage number; and reduction of the number of smooth muscle cells.

Purely fibrous plaques are seldom associated with thrombosis. Recently formed, highly cellular, lipid-rich plaques are particularly unstable and prone to thrombosis, but despite this they are not significantly flow-reducing (before thrombosis occurs) (see Figure 8).

What are the effects of lipid-lowering drugs?

According to this view, the mechanism underlying the great clinical benefit experienced by coronary patients undergoing long-term lipid-lowering treatment occurs as a result of plaque stabilisation (less cholesteryl esters, fewer macrophages). An alternative possibility is that lipid-lowering treatments inhibit the formation of actively growing, new lesions, which are expected to be highly cellular and unstable.

Figure 7. Distinctive features for a plaque prone to rupture.

Figure 8. Variants of fibrous cap atheromas.