1. How to reduce the risk of plaque rupture
Figure 31 In those with established AS, reducing the risk of plaque rupture can be approached via two broad therapeutic routes:
by increasing plaque stability;
by decreasing plaque rupture-inducing factors.

2. How to reduce the risk of thrombosis
Figure 32 Thrombosis can be reduced by:
reducing platelet adhesion (via thromboxane);
inhibiting platelet aggregation (via fibrinogen and the GP IIb/IIIa receptor);
reducing thrombus formation (via fibrin).

3. ~10% Weight loss = ~30% Visceral adipose tissue loss
Figure 33 A modest loss of body weight in patients with truncal/visceral obesity is associated with substantial reductions in major atherogenic risk factors. A 10% loss of body weight roughly corresponds to a 30% loss of adipose tissue.

4. Characteristics of an unstable plaque
Figure 34 Plaques become more unstable as:
the lipid core increases as a percentage of the total plaque area;
macrophages constitute a larger proportion of the fibrous cap;
the fibrous cap loses smooth muscle density.

5. Plaque vulnerability factors Intrinsic factors
Figure 35 A major therapeutic target is to decrease the lipid core and macrophage concentration. This, in turn, reduces parietal vascular inflammation and strengthens the fibrous cap.

6. Modification of extrinsic vulnerability factors
Figure 36 Plaque stabilization is encouraged by reducing areas of low shear stress by:
reducing arterial blood pressure;
decreasing the heart rate;
reducing myocardial contractility.

7. Plaque rupture The main releasing factors
Figure 37 Common precipitants of rupture include physical effort, awakening, psychological stress and anger. Therefore, anger and stress management has a role to play in avoiding plaque rupture.