What is Atherosclerosis?

Atherosclerosis (or arteriosclerotic vascular disease) is a condition where the arteries become narrowed and hardened due to an excessive buildup of plaque around the artery wall. Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood.
Atherosclerosis can affect any artery in the body, including arteries in the heart, brain, arms, legs, pelvis, and kidneys. As a result, different diseases may develop based on which arteries are affected. Over time, plaque hardens and narrows arteries. The disease disrupts the flow of blood around the body, posing serious cardiovascular complications. Atherosclerosis can lead to serious problems, including heart attack, stroke, or even death. Arteriosclerosis is the stiffening or hardening of the artery walls.

Causes of Atherosclerosis

Atherosclerosis can begin in the late teens, but it usually takes decades to cause symptoms. Some people experience rapidly progressing atherosclerosis during their thirties, others during their fifties or sixties. Certain factors that can damage the inner area of the artery (endothelium) and can trigger atherosclerosis include:

• High blood pressure
• High levels of cholesterol
• Smoking
• High levels of sugar in the blood

High triglycerides: Most fat in food and in the body takes the form of triglycerides. Blood triglyceride levels above 400 mg/dL have been linked to coronary artery disease in some people. Triglycerides, however, are not nearly as harmful as LDL cholesterol.

Diabetes: Patients with poorly controlled diabetes, who frequently have excess blood glucose levels, are much more likely to develop atherosclerosis.

Genetics: People with a parent or sibling who has/had atherosclerosis and cardiovascular disease have a much higher risk of developing atherosclerosis than others.

Obesity: Excess weight increases the strain on the heart and increases the risk of developing atherosclerosis even if no other risk factors are present.

Pathophysiology of Atherosclerosis

Very low density lipoprotein (VLDL) is produced by the liver and is changed into LDL by means of lipoprotein lipase. This process removes triglycerides from VLDL by hydrolysis, releasing fatty acids and leaving greater numbers of cholesterol, thus increasing the density of the molecule. The LDL crosses the endothelium and moves into the extracellular matrix where it is oxidized (by the aforementioned steps above), and forms oxidized LDL (OxLDL). OxLDL is a cause of inflammation and signals monocytes (white blood cells) to enter the arterial wall to fix the inflammation. As monocytes enter the arterial wall, they transform into macrophages. As this process continues, more and more LDL becomes trapped within the tunica intima (the innermost layer of the arterial wall) creating a pool of cholesterol called a fatty streak. The major atherosclerosis causing plaque has a fibrous cap, which sticks out into the artery, causing vasoconstriction, and blocking blood flow (the plaque always forms in the lumen, which is between the intima and the musculature of the wall.

Symptoms of Atherosclerosis

Carotid Arteries: These arteries provide blood to the brain. When the blood supply is limited, patients can suffer stroke.

Coronary Arteries: These arteries provide blood to the heart, when the blood supply to the heart is limited, it can cause angina.

Heart attack: If one of the plaques in coronary arteries ruptures, it could create a blood clot. If the blood clot blocks the supply of blood to heart, it will cause to have a heart attack.

Aneurysm: If atherosclerosis weakens the walls of blood vessels, it can lead to the formation of an aneurysm (a bulge in a blood vessel).

Renal arteries: These supply blood to the kidneys; if the blood supply becomes limited, there is a serious risk of developing chronic renal failure.