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It is worthwhile to reflect on atherosclerosis vs. arteriosclerosis because of some confusion in the meaning and use of the two terms. Arteriosclerosis is a general term. Atherosclerosis is a more specific one.
Etymology and similarities
Arteriosclerosis derives its name from the combining of the word elements ‘sclerosis’ and ‘arterio.’ Sclerosis is a Greek word meaning hardening of tissue. Arterio is the Latinized form of the word ‘arteria’ meaning arteries. Therefore, in the broadest since of the word arteriosclerosis means hardening of arteries.
Atherosclerosis derives its name from combining the Greek word element ‘athere’ which means accumulation, with the word element ‘sclerosis’. Thus atherosclerosis means hardening of arteries with the accumulation of lipid.
Types of arteriosclerosis
In the general sense of the word there are three patterns of arteriosclerosis. They are:
- Atherosclerosis which affects large and medium-sized vessels
- Monckeberg medial calcific sclerosis which affects the muscular layer of arteries
- Arteriolosclerosis which affects small arteries and arterioles
Atherosclerosis is thickening, hardening and loss of elasticity of the walls of an artery or arteries. But more importantly, it is also the presence of an atheroma – a deposit or accumulation of lipid-containing plaque(s) on the inner layer of the vascular wall. It most commonly affects medium-sized and large arteries and can affect one or more arteries in a given person. It can affect arteries almost anywhere in the body. But it causes the greatest and most frequent morbidity and mortality in the heart, brain and lower extremities.
The arteries most commonly involved and the complications are the following:
- Coronary arteries → coronary artery disease; angina; heart attack
- Brain arteries and carotid arteries → ischemic stroke; TIA
- Arteries of the lower extremities → peripheral arterial disease; claudication
The earliest characteristic finding is fatty streaks composed of foam cells. They are located in the tunica intima of an affected artery. Foam cells are macrophages filled with lipid material they have engulfed. They appear to form at a very early age. In fact, some studies have revealed this finding in children. Other studies have detected it even in unborn fetuses. Many of the streaks progress to form atheromatous plaques.
An atheromatous plaque is a raised lesion within the intima of an artery. It consists of foam cells and other debris surrounded by immune system cells, smooth muscle cells, calcium deposits, and newly formed blood vessels. A cap of fibrous tissue often covers the plaque. In addition to being a part of the plaque, the immune system cells play a role in causing chronic inflammation which is a part of the overall process. There is narrowing of the lumen of the affected artery(s), often in conjunction with thrombus formation upon the fibrous cap if there is damage to the cap.
Atherosclerosis is a complex disease process involving several factors and interactions. The full process is not well known. But there is agreement among medical and scientific scholars worldwide that the earliest event is damage to the endothelium. Some of the presumed sources of that damage are the following:
- Physical stress from direct trauma or hypertension
- Hypercholesterolemia (high blood LDL or VLDL)
- Chronically elevated blood glucose levels (diabetes mellitus)
- Cigarette smoking
- Circulating air pollutants
- Turbulent blood flow, such as at branching points of arteries
- Free radicals (unstable atoms with at least one unpaired electron)
- High concentrations of homocystine (a natural amino acid in blood)
In addition to the above presumed sources of damage to the endothelium, other risk factors for atherosclerosis are the following:
- Family history of heart disease at an early age
- Increasing age
- Physical inactivity
Despite only partial knowledge of the events and their sequence following initial injury to the endothelium, there are a number of theories. A commonly held oversimplification of what happens is the following:
Injury to the endothelium causes the adhesion of monocytes and T-lymphocytes to it. That adhering results in loosening of the junctions between the endothelial cells. The loosening of the cell junctions causes the endothelium to become more permeable. The monocytes subsequently differentiate into macrophages and easily passed through the endothelium into the intima where they begin engulfing LDL cholesterol particles and forming foam cells. Many of the foam cells evolve into atheromatous plaques.
T lymphocytes in the intima then secrete cytokines which induce the migration of smooth muscle cells from the media to the intima. Under the influence of growth factors the smooth muscle cells also began to multiply. T-lymphocytes, macrophages and the endothelium release other chemicals that mediate a number of processes involved in the completion of the plaque formation. Those processes include the incorporation of fibrous connective tissue and calcium.
Foam cells eventually die over time, but their death promotes inflammation and contributes to the vascular disease. The growing plaque composed of lipid, smooth muscle cells and fibrous elements progressively accumulates in the intima and eventually begins to raise the endothelium and cause narrowing of the lumen of the artery.
Secondary medical conditions caused by atherosclerosis depend on the site of involvement; the degree of reduced tissue blood flow caused by the blockage; and how fast the blockage develops. Even though the process of plaque formation is chronic an acute event can complicate it. That event is plaque rupture.
Plaque rupture is the splitting open of an atheromatous plaque due to injury to the fibrous cap. The mechanism of the injury is not well-understood, but once the blood stream comes in contact with plaque material the triggering of clot formation takes place. If the clot is large enough it can cause sudden occlusion – total blockage – at the site where it forms. If the clot breaks and travels downstream it can cause sudden occlusion of a smaller vessel. In either case, the end result can be severe ischemia ± tissue death. Heart attack and stroke are the most common dreaded consequences.
In the purest sense of the word arteriosclerosis is hardening of arteries due to calcium deposits in the middle layers of artery walls, not plaque buildup. But that use of the term for the most part has become obsolete. The reason is the pure form of the disease rarely exists. Thus, in addition to atherosclerosis, it now also refers to three other patterns of disease that cause hardness and stiffness of arteries. They are:
- Arteriosclerosis obliterans – is atherosclerosis of the arteries of the lower extremities. It can cause narrowing that ranges from partial blockage to total occlusion of blood flow to the legs and feet. The term is now equivalent to PAD.
- Medial calcific sclerosis (Monckeberg’s calcific sclerosis) – is hard stiff arteries due to calcium deposits in the middle layers of the walls of small and medium-sized arteries. There is no thickening of the inner layers of the artery walls and thus no narrowing of the lumen. It commonly involves arteries of the limbs. It occurs primarily in elderly people. Other risk factors for it are diabetes mellitus and chronic kidney disease.
- Arteriolosclerosis – Non-atheromatous arteriosclerosis involving small arteries and arterioles. There are two subtypes of this disease. They are:
- Hyaline arteriolosclerosis – Is thickening of walls and narrowing of the lumen of arterioles. It is due to the buildup of hyaline – a plasma protein which leaks through the endothelium into the intima and sometimes the media. It mainly affects arterioles of the kidney. Age, hypertension and diabetes mellitus are the presumed risk factors.
Atherosclerosis vs. arteriosclerosis in summary
In light of what atherosclerosis is and the different forms of arteriosclerosis as discussed, the table to the right summarizes the important distinctions between the two terms. It bears noting that all three types of arteriosclerosis can be in the same person but in different vessels.