Atherosclerosis Starts Early In Life
POSTED BY: Steve Parker | April 28, 2009 | 5:00 AM
The first heart attack in a 57-year-old is the culmination of a lifelong process. Atherosclerosis, sometimes called hardening of the arteries, has its origins in childhood and adolescence.
The American Journal of Medicine in January this year (volume 122, number 1A) published a supplement entitled "Management of Atherosclerosis: A Practical Guide in 2008." A chapter by William Insull, Jr., M.D., provides a nice discussion of atherosclerotic plaque development.
Think of arteries as pipes through which blood flows, providing nutrients and oxygen to all living tissues. Atherosclerosis is a common cardiovascular problem characterized by blockage of blood flow in arteries. It causes most heart attacks, about half of all strokes, and impairs blood flow to legs (peripheral arterial disease). The blockage is caused by build-up of plaque in the wall of arteries. Plaque is composed of fatty deposits and inflammatory/necrotic debris.
You can see artists' renditions of an atherosclerotic artery here and here.
The first step on the journey to atherosclerosis is early fatty streak development, which begins in childhood and adolescence. It's an accumulation of lipids in the wall of the young artery. If enough fatty deposit is present, it's visible to the naked eye.
Next is early fibroatheroma, starting in the teen years and early 20s. Along with increased lipid deposits, we see macrophages, inflammatory cells, fibrous tissue, and necrotic (dead) debris. Eventually a fibrous cap forms over a lipid-rich necrotic core within the wall of the artery. This starts to reduce the amount of blood that can flow through the artery because the developing plaque expands into the middle, or inside, of the artery where blood is flowing.
The process continues over the years, with variable degrees of arterial obstruction. At about age 55, the fibrous cap thins out, producing the thin-cap fibroatheroma. These thin caps are prone to rupture, which is often associated with a blood clot that may obstruct the artery completely, or break off and flow downstream to get lodge elsewhere, stopping the flow of blood.
This is when our 57-year-old shows up in the emergency room with a heart attack, or suddenly dies without benefit of medical care. On the other hand, many of these plaque ruptures seem to be clinically silent. That is, they just happen without anyone noticing anything.
Plaques at the thin-cap fibroatheroma stage are also prone to hemorrhaging (bleeding) within themselves, leading to additional fibrous tissue formation.
The final stage of the atherosclerosis process is complex lesion development. Repetitive cycles of plaque rupture, clotting, hemorrhage, and healing result in additional build-up of fibrous tissue and debris which obstructs arterial flow. Calcium deposits also occur in the arterial walls over the years, contributing to the "hardening" of the arteries.
The good news is that the underlying disease process can be significantly modifed, for the better, by attention to atherosclerosis risk factors such as smoking, poor diet, physical inactivity, diabetes, and high blood pressure.
-Steve Parker, M.D.
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