280 The Heart
BOX12–1 CORONARY ARTERY DISEASE
Other predisposing factors for atherosclerosis
include cigarette smoking, diabetes mellitus, and
high blood pressure. Any one of these may cause
damage to the lining of coronary arteries, which is
the first step in the abnormal deposition of choles-
terol. A diet high in cholesterol and saturated fats
and high blood levels of these lipids will increase
the rate of cholesterol deposition.
A possible chemical marker of risk is a high blood
level of homocysteine. Homocysteine is a metabolic
product of the essential amino acid methionine,
and may be converted back to methionine or fur-
ther changed and excreted by the kidneys. A high
blood level of homocysteine may indicate inflam-
mation of the walls of arteries. Yet another chemical
marker of inflammation is C-reactive protein (CRP).
There is still much to learn about the role of inflam-
mation in atherosclerosis, but simple blood tests for
chemical markers may someday provide a diagnosis
before heart damage occurs.
When coronary artery disease becomes life-
threatening, coronary artery bypass surgery may be
performed. In this procedure, a synthetic vessel or a
vein (such as the saphenous vein of the leg) is
grafted around the obstructed coronary vessel to
restore blood flow to the myocardium. This is not a
cure, for atherosclerosis may occur in a grafted vein
or at other sites in the coronary arteries.Coronary artery disease results in decreased blood
flow to the myocardium. If blood flow is diminished
but not completely obstructed, the person may
experience difficulty breathing and angina, which is
chest pain caused by lack of oxygen to part of the
heart muscle. If blood flow is completely blocked,
however, the result is a myocardial infarction
(necrosis of cardiac muscle).
The most common cause of coronary artery dis-
ease is atherosclerosis. Plaques of cholesterol form
in the walls of a coronary artery; this narrows the
lumen (cavity) and creates a rough surface where a
clot (thrombus) may form (see Box Fig. 12–A). A
predisposing factor for such clot formation, one that
cannot be changed, is a family history of coronary
artery disease. There is no “gene for heart attacks,”
but we do have genes for the enzymes involved in
cholesterol metabolism. Many of these are liver
enzymes that regulate the transport of cholesterol in
the blood in the form of lipoproteins and regulate
the liver’s excretion of excess cholesterol in bile.
Some people, therefore, have a greater tendency
than others to have higher blood levels of choles-
terol and certain lipoproteins. In women before
menopause, estrogen is believed to exert a protec-
tive effect by lowering blood lipid levels. This is why
heart attacks in the 30- to 50-year-old age range are
less frequent in women than in men.Normal artery Atherosclerotic arteryA B
Box Figure 12–A (A) Cross-section of normal coronary artery. (B) Coronary artery with
atherosclerosis narrowing the lumen.