Thoracic Imaging 2003 - Society of Thoracic Radiology

neuronal damage to the myocardium. The resultant myocardial
denervation could result in functional abnormalities, arrhythmias
or silent anginal episodes. Patients with diabetes have an
increased incidence of coronary artery disease, as well as diabetic
neuropathy, resulting in one of the major causes of silent
myocardial ischemia. This has been demonstrated with
decreased I-123 MIBG uptake which occurs mainly in the inferior
wall. Myocardial denervation also results in a hyperreaction
to dobutamine stress which may explain the higher incidence
of sudden death in advance stage diabetics. Patients with
hypertrophic cardiomyopathy demonstrate autonomic dysfunction,
which is thought to be directly related to disease progression
and heart failure. Quantative PET studies with C-11 HED
and C-11 CGP have shown that the cardiac pre-synaptic catecholamine
reuptake is impaired in hypertrophic cardiomyopathy,
resulting in reduced postsynaptic beta adrenoreceptor density.
Patients with arrhythmagenic right ventricular dysplasia have a
form of fibrolipomatous degeneration of the right ventricular
myocardium and are predisposed to dangerous arrhythmias and
sudden cardiac death. It is believed that the abnormal sympathetic
innervation is responsible for the arrhythmogenesis. I-
123 MIBG imaging and C-11 HED PET Imaging have shown a
reduction in the postsynaptic beta adrenoreceptor density in the
right ventricle as well as the left ventricle.
Infarct/Injury Avid:
Imaging of acute myocardial necrosis has been accomplished
in the past with Tc-pyrophosphate (PYP) utilizing planar and
SPECT imaging. It is reported to have a 90% sensitivity and is
generally imaged at least 12-24 hours post infarction. The peak
level of uptake occurs at 48-72 hours and will slowly revert to
negative within 4 weeks post injury. Most recently Tc-glucarate
has also been reported for imaging acute myocardial infarction.
Indium-111 antimyosin antibody also is utilized for “hot spot”
imaging of acute myocardial infarction. This occurs directly
after exposure of the myocytes allowing a sensitive and specific
antibody to label the area of injury. Indium-111 antimyosin has
also been used to detect myocarditis, transplant rejection, and
doxyrubricin cardiotoxicity. Myocardial apoptosis has also been
imaged utilizing technetium annexin, which is still being evaluated.
Myocardial Perfusion Imaging:
Most nuclear cardiology studies are currently being accomplished
with SPECT imaging utilizing thallium or technetium
agents. Perfusion tracers are utilized to detect coronary artery
stenosis. Lesions less than 50% stenosis demonstrate no flow
limitations at rest or stress and are generally not identified with
myocardial perfusion imaging. Lesions greater than 50% stenosis
will be flow limiting at high flow rates during exercise or
pharmacologic stress testing. Critical stenosis or lesions with
greater than 85-90% stenosis may result in decreased perfusion
even under rest conditions. With slow progression of stenosis,
myocardium may remain viable even with lesions up to 100%
stenosis, due to development of collateral blood flow. With
ECG gating, myocardial SPECT imaging can also now provide
information concerning left ventricular function, wall thickening,
wall motion, and left ventricular ejection fraction. Most
recently, it is felt that prognastic assessment and risk stratification
utilizing myocardial perfusion imaging may be just as
important as evaluating coronary artery disease itself.
Exercise Tolerance Testing:
Non-imaging exercise tolerance testing is noted to have poor
sensitivity and specificity of approximately 60-65% respectively.
Utilizing radiotracers delivered at peak stress, ETT SPECT
imaging has demonstrated an average sensitivity of 87% and
specificity of 73%. Most physicians would prefer MPI-SPECT
be accomplished in association with exercise tolerance testing,
since this provides additional functional and physiological information
over pharmacological stress testing. However, many
patients are not able to complete the exercise stress testing due
to physical limitations or due to inability to reach 85% of maximum
predicted heart rate.
Pharmacological Stress Testing:
Most pharmacological stress testing is currently accomplished
utilizing dipyridamole, adenosine, or dobutamine.
Dipyridamole and adenosine are potent coronary vasodilators
which increase myocardial blood flow by approximately 5
times, thus allowing detection of myocardial perfusion abnormalities
resulting from fixed stenosis. For stress imaging, 0.56
mg/kg/min of dipyridamole is injected intravenously over 4
minutes to a maximum total dose of 60 mg. The radiotracer for
stress imaging is administered at 7 minutes (3 minutes after
completion of infusion). Dipyridamole blocks the reuptake of
adenosine which is the direct coronary vasodilator. The dipyridamole
therefore increases the extracellar concentration of
endogenously produced adenosine. The effects of the dipyridamole
can be reversed at 11 minutes with aminophylline. In
18 studies utilizing 1,272 patients with thallium-201, the overall
sensitivity was 87% and specificity was 81% for detecting
CAD, similar to those studies accomplished with exercise stress
testing.
Adenosine can be directly infused at a rate of 140
mcg/kg/min over 6 minutes with the radiotracer injected at 3
minutes. The flow rate must be carefully controlled utilizing a
computerized pump to achieve a consistent rate of infusion and
pharmacologic effect. Shorter adenosine infusion protocols
have also been utilized. In general, the adenosine protocol produces
more symptoms than the dipyridamole protocol, however
due to its ultra short half life (less than 10 seconds) the effects
are quickly reversed when the infusion is terminated. The
patients should also be screened 2 nd degree and 3 rd degree AV
nodal block, because of the known AV node blocking effects of
adenosine.
Caffeine and food products or beverages containing caffeine
should be withheld for 12-24 hours prior to dipyridamole or
adenosine testing. Beta blockers, anti-hypertensive medications,
and other cardiac medications should not be withheld for adenosine
or dipyridamole stress testing. However, beta blockers do
need to be withheld for exercise tolerance testing. Dobutamine
infusions have also been utilized for pharmacologic stress testing
and are used most frequently with echocardiography and
infrequently for MPI SPECT imaging. Dobutamine’s main
mechanism of action is stimulation of beta 1 receptors, thus
increasing contractility, workload, heart rate, and myocardial
blood flow. One commonly used protocol is a step approach
beginning with low dose infusion at 5 mcg/kg/min over 3 minutes
and increasing in steps up to 40 mcg/kg/min. Some centers
inject a higher dose rate at 50 mcg/kg/min and administer
atropine if the 85% maximum predicted heart rate is not
achieved.
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