March 30, 2015
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A New Way of Looking at Atherosclerosis
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A New Way of Looking at Atherosclerosis

Drs. Andreotti, Ikonomidis, Sdringola, and Nihoyannopoulos are all associated with the Divisions of Cardiology at Catholic University, Rome; Patras University, GR; University of Texas - Houston; and Imperial College, London, UK, respectively.

Atherosclerosis, which comes from the Greek words for "gruel" or "goo" and "hardening," is defined as the presence of atheromas, or lesions, on the inside walls of arteries. The lesions, also known as plaque, consist of fatty deposits and other substances.

What makes atherosclerosis particularly dangerous is that it seems to have a special attraction for the large important arteries — those that supply blood to the heart ("coronary") and brain ("cerebral"). When pieces of a plaque-filled lesion break off (rupture) from the inside wall of these large arteries, the fatty material flows downstream into smaller arteries that directly supply the heart and brain, where they become stuck, preventing blood rich in nutrients and oxygen from reaching these vital organs. If total blockage occurs, the result can be a heart attack or stroke.(1)

What Causes Atherosclerosis?
Exactly how and why atherosclerosis occurs is not known for certain, although we are learning more and more about the processes involved. Most people are familiar with the various risk factors associated with the disease; these include high blood levels of LDL ("bad cholesterol") and a substance called homocysteine, hypertension, cigarette smoking, obesity and diabetes.

Recent research, however, suggests that the cause of atherosclerosis may lie in the body's immune system, perhaps as a response to injury caused by an unidentified infection.(2) This raises the exciting possibility that some future treatment may be developed that targets the underlying infection or aspects of the immune system response.

So far, no one has been able to pinpoint the exact type of injury that begins atherogenesis. We do know, though, that the body's response to injury or infection ("inflammatory response") can become chronic, creating its own set of health problems.(3)

Whatever its origin, there is little question that atherosclerosis starts with the formation of fatty patches or streaks in the inner lining of the arteries (endothelium). With the arrival of so-called "scavenger cells" (macrophages) and lymphocytes, a type of white blood cell, that move into the tissue behind the artery walls, production of growth factors(4) is stimulated — smooth muscle cells build-up and connective tissue, a kind of scar tissue, is produced. The end result of this process is the formation of a fibro-lipid plaque that effectively narrows the artery and limits blood flow through the artery.

Figure 1.
Macroscopic View of a Severe, Eccentric, Coronary Atherosclerotic Plaque.
Note the thick fibrous cap and the large crescent-shaped core.
By kind permission of Professor Eloisa Arbustini (University of Pavia, Italy).

What the Macrophages and T-Lymphocyte Do
The role of macrophages is to act as scavengers to remove what the body perceives as foreign substances. Once lodged in the inner lining of the artery (endothelium) they produce growth factors and cytokines, both of which are involved in the human immune response. These substances bring in more macrophages and cause the proliferation of smooth muscle cells.(5) Part of the job of macrophages and smooth muscle cells is to produce connective tissue. Macrophages also produce collagen-degrading enzymes, which can cause the fibrous cap of the plaque to rupture, leading to possible blockage of blood flow in the artery.(6)

Another member of the body's immune system, T-lymphocytes, have been shown to be present at all stages of atherosclerosis. Their presence provides further evidence of a connection to the immune or autoimmune response.(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)

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