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The name angina pectoris refers
to a strangling or pressure-like pain caused by cardiac ischemia.
Angina is the most common condition involving tissue ischemia in
which vasodilatordrugs or cardiac depressants are used. The pain
may be located substernally, radiating to the neck, in the left
upper extremity, occasionally in the right upper extremity, or in
the epigastrium. However, not all cardiac ischemia is associated
with pain. Clinical conditions exist, such as silent myocardial
infarction, in which myocardial ischemia or necrosis may occur without
pain. Anginal pain is often atypical in women.
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This chapter reviews the pathophysiology of angina and the therapeutic
strategies for its treatment. Pharmacologic treatments are divided
into vasodilators and cardiac depressants (Figure 8–1).
In addition to the drugs discussed in this chapter, patients with
angina are often treated with lipid-lowering drugs to minimize additional
lipid plaque formation and antithrombotics or anticoagulants to
control thrombosis at the site of these plaques. These drugs are
discussed in Chapters 11 and 26.
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The pharmacologic treatment of coronary insufficiency is based
on physiologic factors that control the myocardial oxygen requirement.
A major determinant of oxygen requirement is myocardial fiber tension.
The higher the tension, the greater the oxygen requirement. Several
variables contribute to fiber tension (Figure 8–2).
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Among the diastolic factors, venous tone determines the capacity
of the venous circulation and controls the amount of blood sequestered
there versus the amount returned to the heart. Venous tone is maintained
by sympathetic activity and increases when sympathetic activity
increases. Venous tone and blood volume together determine preload, and
preload is the major diastolic determinant of myocardial oxygen
requirement.
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The systolic factors include afterload, heart rate, contractility,
and ejection time. Afterload is the pressure that the ventricle
must overcome to eject blood into the arterial system. Afterload
is determined by arterial blood pressure and large artery stiffness.
Heart rate contributes to time-integrated fiber tension because
at fast heart rates, fibers spend more time contracted at systolic tension
levels. Because coronary perfusion is maximal during diastole,
faster heart rates lead to decreased myocardial perfusion; that
is, faster rates abbreviate the time spent in diastole and decrease
myocardial perfusion. Systolic blood pressure and heart rate may
be multiplied to yield the double product,
a measure of cardiac work and, therefore, of oxygen requirement.
In patients with atherosclerotic angina, effective drugs reduce
the double product. Force of cardiac contraction is another systolic factor
controlled mainly by sympathetic activity to the heart. ...