Coronary Artery Disease and Atherosclerosis

Study Notes

Low-density lipoprotein molecules (LDL) become oxidized by oxygen free radicals.
Oxidized LDL comes in contact with an artery wall, causing damage.
The body's immune system sends specialized white blood cells (macrophages and T-lymphocytes) to absorb oxidized-LDL, forming foam cells.
These white blood cells cannot process the oxidized-LDL and eventually rupture.
The artery becomes inflamed.
Cholesterol plaque causes muscle cells to enlarge and form a hard cover over the affected area.
The hard cover narrows the artery, reduces blood flow, and increases blood pressure.

Lipoproteins: LDL and HDL
LDL: (normal level, less than 130 mg/dL)
- Primary transporters of cholesterol and triglycerides into the cell.
- Deposit these substances in the walls of arterial vessels.
HDL: (normal range in men, 35 to 65 mg/dL; in women, 35 to 85 mg/dL)
- Have a protective action.
- Transport cholesterol away from the tissue and cells of the arterial wall to the liver for excretion.
Cholesterol: (normal level, less than 200 mg/dL, High: = 240 mg/dL)
Triglycerides: (normal range, 40 to 150 mg/dL)
- Composed of free fatty acids and glycerol, stored in the tissue and are a source of energy.

Stage	Description
Healthy artery	Normal artery with no plaque build up
Plaque forms	Small deposits of plaque begin to form on the artery walls
Cholesterol deposited	Plaque starts to build up in the artery
Build-up begins	Plaque continues to build up restricting blood flow

Normal Heart and Artery	Artery with Plaque Buildup
* Normal artery wall

Advanced age
Male sex
Having close relatives who have had some complication of atherosclerosis (e.g., coronary heart disease or stroke)
Genetic abnormalities (e.g. familial hypercholesterolemia)

Depend on the degree of narrowing of the arterial lumen, thrombus formation and obstruction of blood flow.
Inadequate supply of blood leads to oxygen deprivation in muscle (ischemia).
Angina pectoris, chest pain brought about by myocardial ischemia, usually caused by coronary atherosclerosis.
If blood supply decreases significantly and for a longer period, myocardial infarction can occur.
Damaged myocardium is replaced by scar tissue, causing various degrees of myocardial dysfunction.
Inadequate cardiac output and heart failure can occur.

Non-pharmacological means (cessation of smoking and regular exercise) are usually the first line of treatment.
If non-pharmacological methods do not work, medicines are usually the next step.
Statins:
- Widely prescribed for treating atherosclerosis.
- Examples: lovastatin, simvastatin, and fluvastatin.
- Action: block cholesterol synthesis, lower LDL and triglyceride levels, and increase HDL.
Nicotinic acids:
- Another class of medications used to treat atherosclerosis.