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U N I T 5
Circulatory Function
Silent Myocardial Ischemia
Silent myocardial ischemia occurs in the absence of
anginal pain. The factors associated with asymptomatic
ischemia appear to be the same as those responsible for
angina: impaired blood flow from the effects of coro-
nary atherosclerosis or vasospasm. Silent myocardial
ischemia affects three populations—persons who are
asymptomatic without other evidence of CAD, per-
sons who have had a myocardial infarct and continue
to have episodes of silent ischemia, and persons with
angina who also have episodes of silent ischemia.
21
The
reason for the painless episodes of ischemia is unclear.
The ischemic episodes may be shorter and involve less
myocardial tissue than those producing pain. Another
explanation is that persons with silent angina have
defects in pain threshold or pain transmission, or an
autonomic neuropathy with sensory denervation. For
example, asymptomatic ischemia is observed in persons
with diabetes mellitus, probably the result of autonomic
neuropathy, which is a common complication of diabe-
tes.
21
Silent myocardial ischemia makes up a significant
proportion of all STEMIs in the elderly.
Variant (Vasospastic) Angina
Variant angina, also known as
vasospastic
or
Prinzmetal
angina,
is caused by coronory artery spasm. The causes
of variant angina are not completely understood, but
a combination of pathologic processes may be respon-
sible. Endothelial dysfunction, hyperactive sympathetic
nervous system responses, defective handling of cal-
cium by vascular smooth muscle, or altered nitric oxide
production may all contribute.
21
In some persons it is
associated with hypercontractility of vascular smooth
muscle, as well as with migraine headaches or Raynaud
phenomenon. Unlike stable angina that occurs with
exertion or stress, variant angina usually occurs during
rest or with minimal exercise and frequently occurs noc-
turnally (between midnight and 8
am
).
Rhythm disturbances often occur when the pain is
severe, and most persons are aware of their presence dur-
ing an attack. Electrocardiographic changes are transient
and include ST-segment elevation or depression, T-wave
peaking, and inversion of U waves. Persons with variant
angina who have serious arrhythmias during spontane-
ous episodes of pain are at a higher risk of sudden death.
23
Diagnosis andTreatment
The diagnosis of chronic ischemic heart disease is based on
a detailed pain history, the presence of risk factors, inva-
sive and noninvasive studies, and laboratory studies. It is
important to rule out non-coronary causes of chest pain,
such as esophageal reflux or musculoskeletal disorders.
Noninvasive testing for chronic stable angina includes
ECG, echocardiography, exercise stress testing, nuclear
imaging studies, computed tomography (CT) scan, and
possibly cardiac magnetic resonance imaging (MRI).
Because the resting ECG is often normal, exercise testing
is important for evaluating persons with angina. Although
noninvasive testing is valuable in the diagnosis of chronic
stable angina, cardiac catheterization and coronary arteri-
ography are often needed for a definitive diagnosis.
21
The treatment goals for stable angina are directed
toward symptom reduction and prevention of myocar-
dial infarction through nonpharmacologic strategies,
pharmacologic therapy, and coronary interventions.
Nonpharmacologic methods are aimed at symptom
control and lifestyle modifications to reduce risk factors
for coronary disease. They include smoking cessation in
persons who smoke, stress reduction, a regular exercise
program, limiting dietary intake of foods high in cho-
lesterol and saturated fats, weight reduction if obesity
is present, and avoidance of cold or other stresses that
produce vasoconstriction. Immediate cessation of activ-
ity often is sufficient to abort the onset of anginal pain.
Sitting down or standing quietly may be preferable to
lying down because these positions decrease preload by
producing pooling of blood in the lower extremities.
Pharmacologic agents used in the treatment of chronic
stable angina include nitrates, beta blockers, and calcium
channel blockers.
22
Nitrates, both short- and long-acting,
are vasodilators used in the treatment of chronic stable
angina and in silent myocardial ischemia. Nitrates exert
their effect mainly through a decrease in venous return
to the heart with a resultant decrease in intraventricu-
lar volume. Arterial pressure also decreases. Decreased
intraventricular pressure and volume are associated with
decreased wall tension and myocardial oxygen require-
ment. Although they are not vasodilators, beta blockers
are extremely useful in management of angina associated
with effort. The benefits of beta blockers are due primar-
ily to their hemodynamic effects—decreased heart rate,
blood pressure, and myocardial contractility—which
decrease myocardial oxygen requirements at rest and dur-
ing exercise. The calcium channel–blocking agents, also
called
calcium antagonists,
block activated and inactivated
L-type calcium channels in cardiac and smooth muscle.
The therapeutic effects of the calcium channel blockers
result from coronary and peripheral artery dilation and
from decreased myocardial metabolism associated with
the decrease in myocardial contractility. Percutaneous
coronary intervention relieves symptoms for patients with
chronic stable angina, but does not appear to extend the
life span. Coronary artery bypass grafting is usually indi-
cated in patients with double- or triple-vessel disease.
22
SUMMARY CONCEPTS
■■
Coronary artery disease is a disorder of
impaired coronary blood flow, usually caused by
atherosclerosis.
■■
The acute coronary syndromes (ACS) include
unstable angina/non-ST elevation myocardial
infarction (UA/NSTEMI) and ST elevation
myocardial infarction (STEMI), which differ
in severity based on the absence or presence
of electrocardiograph ST segment changes.
