Chapter 12
Coronary Artery Disease
and Heart Attacks
We have seen that the myocardium does not extract oxygen
and nutrients from the blood within the atria and ventricles,
but depends upon its own blood supply via the coronary arter-
ies. In
coronary artery disease,
changes in one or more of
the coronary arteries cause insuffi cient blood fl ow
to the heart. The result may be myocardial damage in the
affected region and, if severe enough, death of that portion of
the heart—a
myocardial infarction,
heart attack
patients with coronary artery disease experience recurrent
transient episodes of inadequate coronary blood fl ow, usually
during exertion or emotional tension, before ultimately suf-
fering a heart attack. The chest pain associated with these epi-
sodes is called
angina pectoris
(or, more commonly, angina).
The symptoms of myocardial infarction include pro-
longed chest pain, often radiating to the left arm, nausea, vom-
iting, sweating, weakness, and shortness of breath. Diagnosis
is made by ECG changes typical of infarction and by measure-
ment of certain proteins in plasma. These proteins are present
in cardiac muscle and leak out into the blood when the muscle
is damaged; the most commonly checked are the enzyme cre-
atine kinase (CK), particularly the myocardial specifi c isoform
(CK-MB), and cardiac troponin.
Approximately 1.1 million Americans have a new or
recurrent heart attack each year, and over 40 percent of them
die from it. Sudden cardiac deaths during myocardial infarction
are due mainly to
ventricular fi
an abnormality in
impulse conduction triggered by the damaged myocardial cells.
This conduction pattern results in completely uncoordinated
ventricular contractions that are ineffective in producing fl ow.
(Note that ventricular fi brillation is fatal, whereas atrial fi bril-
lation, as described earlier in this chapter, generally causes
only minor cardiac problems.) A small fraction of individuals
with ventricular fi brillation can be saved if emergency resus-
citation procedures are applied immediately after the attack.
This treatment is
cardiopulmonary resuscitation
repeated series of mouth-to-mouth respirations and chest com-
pressions that circulate a small amount of oxygenated blood to
the brain, heart, and other vital organs when the heart has
stopped. CPR is then followed by defi nitive treatment, includ-
a procedure in which electrical current is
passed through the heart to try to halt the abnormal electri-
cal activity causing the fi brillation.
Automatic electronic defi
are now commonly found in public places.
These devices make it relatively simple to render timely aid to
victims of ventricular fi
The major cause of coronary artery disease is the pres-
ence of atherosclerosis in these vessels (
Figure 12–66
is a disease of arteries characterized by a thick-
ening of the portion of the arterial vessel wall closest to the
lumen with plaques made up of (1) large numbers of abnormal
smooth muscle cells, macrophages (derived from blood mono-
cytes), and lymphocytes; (2) deposits of cholesterol and other
fatty substances both in these cells and extracellularly; and (3)
dense layers of connective tissue matrix. Such atherosclerotic
plaques are one cause of aging-related arteriosclerosis.
Atherosclerosis reduces coronary blood fl ow through
several mechanisms. The extra muscle cells and various depos-
its in the wall bulge into the lumen of the vessel and increase
resistance to fl ow. Also, dysfunctional endothelial cells in
the atherosclerotic area release excess vasoconstrictors (e.g.,
endothelin-1) and lower than normal amounts of vasodila-
tors (nitric oxide and prostacyclin). These processes are pro-
gressive, sometimes leading ultimately to complete occlusion.
Total occlusion is usually caused, however, by the formation
of a blood clot
coronary thrombosis
in the narrowed ath-
erosclerotic artery, and this triggers the heart attack.
The processes that lead to atherosclerosis are complex
and still not completely understood. It is likely that the dam-
age is initiated by agents that injure the endothelium and
underlying smooth muscle, leading to an infl
ammatory and
proliferative response that may well be protective at fi rst but
ultimately becomes excessive.
Cigarette smoking, high plasma concentrations of cho-
lesterol and the amino acid homocysteine, hypertension, dia-
betes, obesity, a sedentary lifestyle, and stress can all increase
the incidence and severity of the atherosclerotic process. These
are all termed, therefore, “risk factors” for coronary artery dis-
ease, and prevention of this disease focuses on eliminating
or minimizing risk factors through lifestyle changes and/or
medications. In a sense, menopause can also be considered a
risk factor for coronary artery disease because the incidence of
heart attacks in women is very low until after menopause.
A few words about exercise are warranted here because
of several potential confusions. While it is true that a sudden
burst of strenuous physical activity can sometimes trigger a
heart attack, the risk is greatly reduced in individuals who per-
form regular physical activity. The overall risk of heart attack at
any time can be reduced as much as 35 to 55 percent by main-
taining an active rather than sedentary lifestyle. In general, the
more you exercise the better the protective effect, but any exer-
cise is better than none. For example, even moderately paced
walking three to four times a week confers signifi cant benefi t.
Regular exercise is protective against heart attacks for a
variety of reasons. Among other things, it induces: (1) decreased
myocardial oxygen demand due to decreases in resting heart
rate and blood pressure; (2) increased diameter of coronary
arteries; (3) decreased severity of hypertension and diabetes,
two major risk factors for atherosclerosis; (4) decreased total
plasma cholesterol concentration with simultaneous increase
in the plasma concentration of a “good” cholesterol-carrying
lipoprotein (HDL, discussed in Chapter 16); and (5) decreased
tendency of blood to clot and improved ability of the body to
dissolve blood clots.
Nutrition can also play a role in protecting against heart
attacks. Reduction in the intake of saturated fat (a type abun-
dant in red meat) and regular consumption of fruits, vegetables,
whole grains, and fi sh may help by reducing the concentration
of “bad” cholesterol (LDLs, discussed in Chapter 16) in the
blood. This form of cholesterol contributes to the buildup of
atherosclerotic plaques in blood vessels.
Supplements like
(a B vitamin; also called folate or folacin) may also be pro-
tective, in this case because folic acid helps reduce the blood
concentration of the amino acid
one of the
risk factors for heart attacks. Homocysteine, cysteine with an
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