Arteriosclerosis

Arteriosclerosis literally means “hardening of the arteries” and is a broad term used to describe many diseases that cause thickening and loss of elasticity of the walls of arteries. Arteries are the vessels that carry oxygenated blood full of nutrients from the heart to organs throughout the body. Blood leaves the heart through the aorta, the largest artery in the body, and travels through arteries and then arterioles, the smallest arteries, to different organs. The arterial wall is made up of three distinct layers—an outer layer of tissue (adventitia), a muscular middle layer (media), and an inner layer of epithelial cells (intima). There are three recognized types of arteriosclerosis: atherosclerosis, arteriolosclerosis, and Monckeberg medial calcific sclerosis.

Atherosclerosis is the most common and most important pattern of arteriosclerosis because its end result can be a harmful clot in the blood that may cause a heart attack, stroke, or disease of the peripheral blood vessels. How the entire process occurs is not entirely understood, but most scientists agree that it begins when the inner layer of a blood vessel, or the endothelium of the intimal layer, becomes injured. Some things that cause mechanical damage to the endothelium are high cholesterol and triglycerides, high blood pressure, and cigarette smoke. People who have an abnormally large amount of cholesterol or other lipids (fats) in their blood are often treated with lipid-lowering medications to prevent or slow the process of atherosclerosis.

Once damage has occurred, platelets, cholesterol, other cells and debris accumulate over time in the damaged endothelium. These cells release chemicals which attract still more cells to the site of the injured layer. Fat deposits and builds up in and around these cells. The cells at the impaired area produce connective tissue that also deposits there. This conglomeration of cells, fat, debris, and connective tissue is called an atheroma, or fatty plaque. If we imagine an artery as a round tube and the blood flowing through the tube, it is easy to see that the bigger a plaque is, the more it affects the size of the lumen, or area that the blood has to flow through. If the wall of the vessel is thickened enough from a large atheroma or multiple atheromas, there will be decreased blood flow, which decreases oxygen supply to the body's [Page 161]organs. If blood flow is cut off to the heart, this can cause a myocardial infarction, or heart attack. If the blood supply to the brain is blocked, this can cause a stroke. Similarly, if the blood flow to the extremities is stopped, gangrene may occur. Often what blocks blood flow to these vital organs is a clot.

Fortunately, atherosclerosis does not produce symptoms until the vessel's luminal diameter has been decreased by 70 to 80 percent. Angina pectoris, or chest pain brought on by exertion, can be caused by this blockage of the lumen. In this situation, a person's arteries may still have enough room for blood to travel when the person is at rest, but when he or she works hard and the heart pumps more blood, all of this extra blood cannot fit and causes chest pain. Interestingly, acute (sudden) events such as a heart attack, stroke, or sudden death are typically caused by rupture of plaques that only decrease the lumen by 50 percent. This happens because the plaque rupture releases several chemicals that aid in coagulation or are “proclotting.” The most important of these is tissue factor, which initiates the pathway of clotting. This leads to the formation of a clot in situ, right on top of the preexisting fatty plaque. So the long-standing, slowly accumulating process of atherosclerosis (which is going on inside all of us all the time) may cause symptoms such as angina pectoris if severe, but the life-threaten-ing events such as heart attack or stroke are usually associated with this sudden plaque rupture on top of an already somewhat narrowed lumen.

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