Narrowing of Artery.
When pipes get clogged, it is usually because something gets stuck in them – a greasy mass of bone bits or a hair ball. But when arteries are narrowed by atherosclerosis, the damming-up process occurs from the inside out: The walls of the vessels thicken and then protrude into the vessel lumen. Once this happens, it does not take much to close the vessel completely. A roaming blood clot or arterial spasms can do it.
Although all blood vessels are susceptible to this serious degenerative condition of the blood vessel walls, for some unknown reason the aorta and the coronary arteries serving the heart are most often affected. The disease progresses through many stages before the arterial walls actually become hard and approach the stages of the rigid tube system described in the text, but some of the earlier stages are just as lethal or more so.
What triggers this scourge of blood vessels? According to the response to injury hypothesis, the initial event is damage to the tunica interna caused by bloodborne chemicals such as carbon monoxide (present in cigarette smoke or auto exhaust); by bacteria or viruses; or by physical factors such as a blow or persistent hypertension. Once a break has occurred, blood platelets cling to the injured site and initiate clotting to prevent blood loss. The injured endothelium sets off the alarm summoning the immune system and inflammatory process to repair the damage. If it is a one-time injury, when it’s over, it’s over. But most plaques grow slowly, through a series of injuries that heal, only to be ruptured again and again. As the plaque grows, the injured endothelial cells release chemotactic agents and chemicals that increase the permeability of the endothelium to fats and cholesterol, allowing them to take up residence just deep to the tunica interna. Monocytes attracted to the area migrate beneath the endothelium, where they become macrophages that gorge themselves on the fat. Soon they are joined by smooth muscle cells migrating from the media of the blood vessel wall. The result is the so-called fatty streak stage characterized by thickening of the tunica interna by greasy gray to yellow lesions called atherosclerotic plaques. When these small, fatty mounds of muscle begin to protrude into the vessel wall (and ultimately the vessel lumen) the condition is called atherosclerosis.
Arteriosclerosis is the end stage of the disease. As enlarging plaques hinder diffusion of nutrients from the blood to the deeper tissues of the artery wall, smooth muscle cells in the tunica media die and the elastic fibers deteriorate and are gradually replaced by nonelastic scar tissue. Then, calcium salts are deposited in the lesions. Collectively, these events cause the arterial wall to fray and ulcerate conditions that encourage thrombus formation. The increased rigidity of the vessels leads to hypertension. Together, these events increase the risk of myocardial infarcts, strokes, and kidney failure.