MODULE SUPPLEMENT: CARDIOVASCULAR SYSTEM
Atherosclerosis

Unlike arteriosclerosis, which may be less amenable to prevention, the process of atherosclerosis is modifiable. Plaque formation is a process that occurs over a long period of time, occurring in stages. One of the characteristics of atherosclerosis is the accumulation of cholesterol within the vessel wall (Badimon, et al, 1993). Cholesterol, like other forms of fat, is transported bound to proteins in complexes called lipoproteins.

The major two lipoproteins that carry cholesterol are the low density lipoproteins (LDLs) and high density lipoproteins (HDLs). Fats deposited in atherosclerotic lesions are mainly from the LDLs while the HDLs appear to be involved with taking cholesterol back to liver to be metabolized--a process called "reverse cholesterol transport".

The process (which is vastly simplified here) starts with LDL and other lipids entering the vessel wall (See Figure 1 below). This is facilitated if the vessel wall has been damaged by chemical irritants such as tobacco smoke or by hypertension or by high levels of cholesterol in the blood.

Figure 1

The LDL can be oxidatively modified by what are termed "reactive oxygen species" or "free radicals" (Note: This link will open in a new browser window which you can close to return here). Once these LDL particles have been modified they are engulfed by macrophage cells, which are components of the immune system (Note: This link will open in a new browser window which you can close to return here). After engulfing a large amount of LDL, these macrophage cells become foam cells, which appear to be critical to the development and subsequent progression of the plaque. Although there are many other mechanisms that are involved in this process, these basic processes provide a basis for possible prevention.

Mrs. Hazeltine, the 85 year old woman referred to in Case 1 (Note: This link will open in a new browser window which you can close to return here), was noted to have coronary artery disease, a problem generally involving the development of plaques. Given the process outlined above, what types of treatment modalities might be beneficial in preventing the progression of the atherosclerotic process? Stop and consider why and how they would work. What would your disciplines primary role be in implementing these treatment modalities?