4 major types of Radiopharmaceuticals:
1. Myocardium Perfusion: used to demonstrate myocardial ischemia, \
2. |\MI, and hibernating and stunned myocardium
Single photon emitters:
N-ammonia (nitroglycerin 13 ammonia)
3. Blood Pool:
For MUGA, RVG, ERNA or RNA (same things, different names)
Tc-pertechnetate labeled RBC’s
RE: Must use Sn, and denature the RBC’s
4. A.M.I. (acute myocardial infarction)
2 weeks later its no longer acute, it becomes chronic
Another word for acute is avid
5. Myocardial Metabolism:
I fatty acids
C-labeled fatty acid/polmatate
Planar vs. SPECT (define and describe)
Planar: It’s best to use planar imaging when studies have a low count rate or when data must be
recorded with in a short interval. Planar images can sample the major surfaces of the left ventricle (usually
SPECT: SPECT imaging should able used when high count rates or longer imaging times are
available. Images done with single/multi head camera with extrinsic resolution better than 5mm FWHM.
Typically recorded with 64x64 or 128x128 matrix for a large field detector.
Acquisition: 12-19mm Planer vs.5mm FWHM SPECT
Angular Sampling: Acquisition Angle
3 degrees angular sampling (greater than 6 can result in an artifact resembling spokes)
180 degree sampling with a 2 detector head
360 degree sampling with a 3 detector head (not preferred due to back and spine attenuation)
Projection Acquisition Time: Sampling Time:
Step and shoot – greater resolution, but more time b/c it takes 1-2 seconds to incrementally
move and come to full stop
Supine (some clinics prone) for 20-30 min
Filters: Cutoff Frequencies. When filtered back-projection is used, the filter should have sufficient
spatial resolution to permit visualization of the myocardial borders. A frequency of .2-.4 cycle/cm is
used. (u pick the cutoff frequencies)
Slices: # & pixels thickness
o Between 6-8 common amount of slices
o 1-3 pixels in thickness
NM Imaging Studies
Acute/Avid Infarct Imaging: (rarely done) (also IND agent: 111In-antimyosin/Myoscint Know agent is
an antibody; picks on page 426 Early/Sodee Infarction has changed cells of the heart and therefore the cell
membrane now allows antibodies to be picked up)
Clinical procedure steps:
99m-Sn-PYP: IV dose given; pt asked to force fluids
Begin images at 2-3 hours up to 4-6 hours post injection
Best positive results occur at 24-48-72 hours after the trauma occurs
Should not image sooner than 6-12 hours
Uptake is increased for 2 weeks and then decreased beyond 2-3 weeks
IV dose given after onset of signs and symptoms of AMI
Images taken at 18-24 hours after injection and 48 if needed
Pt positioning – anterior, 45 LAO or 30-70 degree LAO, L. Lateral for 500K – 1M counts/image
Pitfalls – with PYP the timing of the study to the occurrence of the infarction is a disadvantage
Should have emergency equipment and supplies ready
Normal – PYP uptake only seen in bone, not between ribs or ribs and sternum
Abnormal – diagnostic accuracy 90-95% with transmural infarcts (transmural means all the way through)
Image grades 0-4 with increasing myocardial uptake / concentration vs bone
0 = no myocardium uptake / normal
1 = diffuse uptake, less than the ribs
2 = focal- diffuse uptake, ribs
3 = uptake – sternum
4 = uptake greater than sternum
Tc-PYP, use 15-25mCi (as also in bone study) The PYP is the only one approved, but u can really use
any bone agent.
Image findings: heart can shows up on bone scan because there are calcifications in the heart
o Amount of Ca++ ions that influx to the damaged cells mitochondria / dense bodies form
increased uptake and concentration
o Peak uptake occurs 48-72 hours after infarction (not injection)
o May be seen as early as 6-7-10-14 days after inarction with decreasing uptake beyond this
Do anterior then LAO’s at a 45-700 angle, then left lateral
Normal vs. Abnormal:
Technical Considerations: Time related uptake: 24-72hr up to 7-10 days
Myocardial Perfusion Imaging:
Main use is for the diagnosis of myocardial ischemia due to CAD (coronary artery disease)
The study is > 85% sensitivity and 90% specificity to finding ischemia
Tl or 99mTc heart perfusion agents for ―cold spot‖ scan study (cold spot represents ischemia)
Studies performed at stress and redistribution or rest; results depend on ischemia, reversible or
myocardial infarction, irreversible; with a question of myocardial viability
Normal results show even distribution / concentration / uptake
Abnormal shows areas of decreased regional perfusion
Tl study usually performed without a gating device because in order to have gating image u
should have high counts; may more often include gated study with the 99Tc heart agents to improve
the quality of the imaging and quantitate heart function
SPECT / tomographic vs planar study increases sensitivity by 10-25%
Treadmill Exercise Testing: 12 lead ECG; 85% max predicted heart rate
1. Screen for CAD regional Myocardial Ischemia, reversible w/ stress vs redistribution or rest
a. To evaluate cardiac arterial blood flow patency
2. Assessment of angina pectoris or with positive ECG as a screen for CAD
3. MI localization may be positive w/ in ~ 6hrs for acute; rest only study;
to determine chronic MI(scar tissue) vs viable myocardium, hibernating vs stunned
4. Screen patients prior to cardiac catherization as a complimentary / correlative study
5. Baseline in asymptomatic patients with pre-disposing factors:
to determine risk stratification: % chance infarction w/in a year; normal < 1%
Stelio – if you’re doing a patient who may or may not have ischemia and study shows normal, they
still have some risk they will have problem with in a year, but it’s less than 1%
6. Screen patients prior to or evaluate post-op coronary by-pass graft evaluation
201Tl chloride solution, as a K+ analog, biorouting similar to Na+ / K+ w/ ATPase pump for active
transport into cells. (know its active transport AND diffusion)
201Tl is cyclotron produced, but its expensive CF, Tp = 73 hr, EC decay, w/ 201Hg x-rays = 60 -
99mTc-sestamibi (Cardiolite) (know spelling)
99mTc-teboroxime (Cardiotec) (not available, but have to know, also know spelling)
99mTc-tetrofosmin (Myoview) (know spelling)
To do a 201Tl Viability, its best to give a stress / exercise injection e.g. 201TlCl dose: ~ 3 mCi &
obtain redistribution delayed images or w/ a second 1 mCi re-injection IV at rest.
99mTc agents: ~ 10 - 30mCi. One day or two day protocols used for separate stress & rest
Other agents: 133Xe or 85Kr gases.
Mechanisms of Localization:
201TlCl = active transport & ion exchange cell concentration directly relative to coronary blood
flow or perfusion. Not age dependent, i.e. C.O. e.g. liver, GI organs, spleen, renals, large muscles.
o Ion exchange is a diffusion process
There is ~ 88% extraction efficiency w/ first pass & w/ ~ 3 - 4% in the myocardium.
Coronary artery affected by segment stenosis shows decreased uptake beyond the stenosis w/ stress.
A ~ 3 - 4hr redistribution or rest shows increase uptake w/ decreased washout in the affected area.
Normal myocardium = ~ 25% decrease concentration / washout @ ~ 2.5 hrs after the dose compared
to ischemic areas = relative increase in concentration & longer clearance times.
99mTc heart agents: unclear mechanisms; no or little redistribution w/ sestamibi & tetrofosmin;
Rapid washout w/ teboroxime / Cardiotec.
Target or critical organs
201TlCl – myocardium is target, kidneys is critical
99mTc agents – myocardium is target, large bowel is critical
Pt Prep / Concerns and considerations
NPO for 3-8 hours to decrease GI and liver uptake; determine if diabetic, if so, do in morning
Discontinue beta blockers, calcium antagonist, and nitrates if possible. No glucose or stimulants
No caffeine (xanthene), theobromine (chocolate), theophyline / Aminophyline for 24 hours
No nicotine for 12 hours.
Instruct patient to wear comfortable clothes if patient is to exercise
Drugs that Affect Response:
Drug Discontinue before test
Digitalis (strengthens the contractions 1-2 weeks
of the heart muscle, but there is a
narrow therapeutic range because it
can be toxic)
Antihypertensives 4-7 days
Diuretics 4 days
Beta blockers 2 days
Anti-arrhythmic 2 days
Tranquilizers/Sedatives 1 day
Nitrates 1 day
Nitroglycerine 1 hour
Morning of the study; immed. prior to:
Interview / confirm patient followed prep; obtain signed written consent for procedure
Obtain baseline blood pressure & EKG.
Establish patent IV access. Start a slow drip saline Infusion or use a heparin med-lock or use a 3-
way stop-cock w/ a saline flush & butterfly.
Stress immediately prior to or during exercise perfusion study.
High resolution, all-purpose, converging low energy collimator.
Ancillary equipment = treadmill exerciser or ergometer. Monitoring device = EKG monitor.
1. Start slow drip saline infusion or use 3-way stop-cock w/ saline flush or a heparin med-lock or connector.
2. Use a treadmill or ergometer to stress patient to ~ 85% or higher of maximum predicted heart rate;
Re: max predicted = 220 - age (.85) = target heart rate or until angina occurs.
May use vasodilator drugs as stressors instead.
3. Treadmill Bruce protocol: most common, advances every 3 minutes w/ increase in % grade / slope &
faster speed. Modified Bruce protocol used for those w/ some difficulty walking, increase in grade
4. Inject the ~ 3m Ci 201TlCl IV, flush with saline; have patient continue to exercise ~ 30 - 60 seconds more.
5. Begin imaging ideally within 3 – 5 minutes (Tl); redistribution begins ~ 10 - 15 minutes after
obtain the images within 30 minutes after injection; greatest redistribution > 45 minutes after injection.
Patient Positions / Views:
Planar views: (in order of preference) stress / exercise include most of LV: 45 degree LAO & / or 30-60-70
degree LAOs; ANT; L. Lateral; uptake is seen as a "doughnut" or "horseshoe" shapes w/ decreased central
Repeat these views / images at redistribution ~ 3 - 4 hr or more later or at rest.
SPECT study: increases sensitivity over planar by ~ 10 - 25%.
Patient must lie still, with patient's arm up out of the field of view.
Primarily uses 1800 = 450 LPO to 450 RAO vs 3600 orbits: circular; or elliptical or body contouring.
Technical Points / Pitfalls: Re: Heart lies in an oblique body position.
Cardiac monitoring used; life support & CPR trained NMTs & physician present.
EKG stress abnormalities noted; may need to cancel study.
If rest only images obtained, may have patient stand & inject ~ 15 minutes prior to imaging.
Some MD's prefer to have stress and rest on two separate days.
Shield body bckgnd. useful w/ uptake to all major organs & muscles. Have female patients remove
Acquisition & Processing:
64x64 or 128x128 matrix acquired. Optional = circumferential profile analysis
myocardium divided into sectors by usually 60 radii @ 6 degrees each;
Count rate derived from stress & rest studies are shown graphically.
64x64 or 128x128 matrix acquired. Total Imaging time = ~ 20 - 40 minutes.
Orbits usually 1800 w/ ~ 3 - 6 degrees angular sampling @ ~ 15 - 60 sec per angle / stop.
First images obtained are planar images non-gated or gated. Review frames of study for patient
Processed reconstruction images: raw projection data reconstructed into transverse images, by
backprojection & ramp filtering techniques.
Filters e.g. Butterworth used to increase contrast resolution @ frequencies ~ 0.2 - 0.4 cycles/sec.
First cuts are transverse body planes, then with proper determination of heart location (with cursor
above and below), vertical & horizontal long axis slices; last reconstruction of short axis slices.
Optional: bullseye analysis (aka polar display) coordinate plot based on short axis slices of the stress
concentration vs the redistribution / washout .
Gated SPECT: Gating of 99mTc-heart agents imaging. Includes additional information like obtained
Exercise Protocols: Bruce protocol = speed and elevation increases per 3 min
Modified Bruce protocol = usually elevation Not speed increases per 3 min
Pharmacological Stress Agents: Dipyridamole, Adenosine, and Dobutamine:
Interventional Drugs Administration Protocols:
Dipyridamole / IV Persantine: (used to be called Dipyridamole challenge) indirectly increases level of
exogenous adenosine in pt.s blood by deactivating adenosine deaminase. The increased blood level of
adenosine results in vasodilatation of the coronary arteries, increase blood flow by 2-5 times greater
Steal phenomenon or Robin hood effect – adenosine activates the A2 receptors on the cell membrane
of smooth muscle, and that creates this phenomena/effect. It diverts blood away from the myocardium that
is fed by stenotic coronary arteries, resulting in an increased uptake in myocardium supplied by healthy
arteries and decreased or absent uptake in myocardium that receives its blood supply from artherosclerotic
or stenotic coronary arteries
A common chemical stess agent
Heart does NOT need to reach 85% max predicted heart rate
Patient history Prep: Thorough history, NPO for min of 4min hrs. No xanthene derivatives
(Aminophylline, Theophylline, caffeine, etc.) must be discontinued for 12-24 hours prior b/c they compete
with adenosine for binding sites on the walls of the coronary arteries and may result in a false-negative
Resting Administration Protocol:
Dose is based on weight chart, i.e. .56mg/kg diluted in 50ml of saline
Inject IV over a 4 minute period with the rate of administration being .142/mg/kg/min.
Inject 201TlCl 2-5 minutes after the infusion (he says 2 min. elsewhere)
Scan should begin within 10 minutes
Must have Aminophylline available; use immediately as an antagonist if the patient has a
Persantine’s T1/2 = 20-30 minutes—so give an antagonist to stop it before they go home
Baseline heart rate, b.p., and ECG obtained before infusion begins.
Parameters acquired continuously during admin, and recorded every minute.
Pt should be monitored abt. 15 min, until hr, b.p, and ECG have returned to baselines
Exercise Administration Protocol: low level exercise to increase heart rate and stress, therefore u
should see more uptake, this isn’t required, it’s an option
Must assess if patients breathing is compromised prior to or during the test
History of bronchospasms or pulmonary disease, active wheezing, hypotension (systolic <90
mmHg), and severe mitral valve disease. Also MI with in 2 days, unstable angina with in 48 hrs.,
severe aortic stenosis, severe obstructive hypertrophic cardiomyopathy, and severe orthostatic
Does pt have any know sensitivity to Persantine?
Bronchospasms are most critical thing to worry about with Persantine, which is why we ask about
the pulmonary history
Has pt had any Persantine with in the last 48 hours?
If there are adverse reactions give 1-2mg/kg of Aminophyline
Adenosine (Adenocard): directly increases the level of adenosine in pt.s blood (adenosine is a potent
vasodilator) directly effects cells of myocardium and cause vasodilatation
Agent that is the natural vasodilator substance of the body
Directly increases the levels of adenosine in the CVS to produce increased vasodilatation
Short biological half life of (2) – 10 seconds; reactions may be controlled by shutting off infusion
pt not expected to reach 85%
Pt. Prep: same as Dipyridamole
240ug/kg administered @ a rate of 140ug/kg/min for 6 min
Tl injected @ 3 min into infusion
Continuous infusion required due to adenosines short plasma half-life of <10 sec
Base line hr, bp, and ECG obtained, continuously monitored, recorded every min during infusion
Monitor @ least 5 min after cessation of infusion or until pt.s hr, bp, and ECG have returned to
Pts @ increased risk can get a 7 min titrated dosage
Contraindications and Side Effects: same as listed for Dipyridamole, as well as a second or third degree
AV block (without a pacemaker) b/c of the negative dromotropic (SA and AV node) effect that occurs w/
the infusion of adenosine
Adverse effects are flushing, chest pain, dyspnea, ST segment depression, dizziness, nausea, and
hypotension. Side effects usually dissipate with in 1-2 min.
If adverse reactions occur, they will be more severe with adenosine than Persantine, although its not
as common for adverse reactions with adenosine—don’t give Aminophyline routinely
Dobutamine: (Dobutrex- trade name-) – a positive inotropic (responsible for increasing myocardial
contractions) and chronotropic pharmaceutical. Enhances force of hearts contractions and increases hr, thus
increasing myocardial oxygen demand. Stimulates beta-1 receptors in myocardium, resulting in increase
in force and frequency of contractions, and most closely mimics effects of physical exercise on heart.
Drug with effects most similar to exercise
Indirectly causes coronary vasodilatation by increasing the myocardium contractility which causes
increased oxygen demand
May be used on COPD pts, where as Dipyridamole and adenosine its contraindication
Patient Prep: no beta blockers 24-48hrs and anti-hypertensives 4-days prior
Administration Protocol: Titration –(meaning start off at small amount and increase gradually in
increments) start at 5-10mg/kg/min for 3 min up to a max of 40ug/kg/min. The Dobutamine is diluted in
50ml of normal saline or 5% dextrose/water. Stepped increases follow at 3 minute intervals to infusion rates
of 10,20,30, and 40 ug/kg/min. At the beginning of the last stage, the 201TlCl is injected (1 minute after
Contraindications & Side Effects: Recent MI (<1wk), unstable angina, hemodynamically significant
left ventricular outflow tract obstruction, critical aortic stenosis, and atrial tachyarrhythmias w/ uncontrolled
ventricular response, ventricular tachycardia, uncontrolled hypertension, aortic dissection, or large aortic
Side Effects: chest pain, palpitations, headache, flushing, dyspnea, paresthesia, and ischemic ST segment
depression, as well as nausea and vomiting
Atropine: (according to Bryan) – third choice for cardiac stress imaging, it increases heart rate and is used
for Dobutamine studies when you can’t get heart rate up enough. 1mg limit. Can cause drowsiness,
confusion and a contra is beta blockers
Radiopharmaceuticals Administration Protocols:
201Thallium Chloride: an analog of potassium, which is used by the heart during contractions.
Used for Thallium heart perfusions
Redistribution does occur (not exact equivalent of rest images) get this stuff
Images can be done planar, SPECT, and gated, but its difficult for gated with Thallium
After injection u should start imaging w/I 10 min
Can do circumferential profile
Hard to image the obese patient due to thallium’s attenuation problems, and the fact that u can use
very little thallium, its not weight based.
Kidneys are critical organs with Thallium
Stress vs. Rest Image Acquisition vs. Redistribution:
Stress and Delay (standard) – Inject 2-4mCi at peak stress and wait 2-4 hr (3 preferred) for rest
imaging. Waiting time is only 5-10 min. after stress 1.5mCi may be re-injected. Imaging and re-
imaging may be done again up to 24 hr later (if u don’t give second injection its called
redistribution, which is for detec)
Planar Imaging vs. SPECT Imaging:
Planar – begin 10 min after admin of 2-4 mCi. 30% window centered over 72 KeV, and second 20%
window centered on 167KeV. Images acquired w LEAP coll, matrix of 128X128. Minimum of
6000,000 counts in total field of view for 8 min
o Anterior (u will get an angular horseshoe shape)
o 45 degree LAO, and 70 degree LAO (donut shape for 45 degree and horseshoe for the 70
degree with the apex more rounded)
SPECT – LEAP coll. Each image acquired 40 sec. SPECT 45 degree RAO up thru 45 degree LAO
Rest Imaging Protocols:
To assess the pt that may have suffered acute MI, defects indicative of necrotic tissue. NPO 4 hrs,
dose – 2.5-3mCI IV. Image begins @ 10-15 min, followed by acquisition of delayed images at 3-4
Rest ONLY images would be for acute MI, u definitely don’t want to stress these pts
Contraindications: none if ur using just thallium Delay should be avoided, because redistribution occurs
Normal vs. Abnormal Results: Stress – looking for cold areas, Redistribution- looking to see if its even
compared to stress, if it is, your done. If Stress shows with cold area and later it’s filled in u, have
proven a true ischemic area. If its still cold - -be careful its not always infarction so wait 12-24 more
hours to see if its still viable or if u don’t want to wait, give a re-injection of about 1mCi of thallium, if
its really infarction it will still be cold
Tc-sestamibi / Cardiolite: or 99mTc-tetrafosmin / Myoview:
They have very little if any redistribution
Sestamibi / Cardiolite
Undergoes redistribution at a slow rate and remains fixed in the myocardium for hours (unlike 201Tl)
Major disadvantage is its hepatobiliary clearance
Planar: asses extent / severity of acute myocardial infarction
20-30 mCi injection IV (1rst pass/wall motion possible)
Imaging 1-3 hours after injection to clear lung/hepatic background
Light fatty meal 45-60min after injection (to reduce gall bladder contraction)
High resolution collimator (high photon flux)
Images – 45 degree LO and 70 degree LO
300-400seconds per image, shielding to block GI activity
Reproduce angles exactly
Patient Prep: NPO min. 4 hours
Rest Protocol: imaging begins 60-90min after rest injection (can get images up to 4 hrs due to slow
redistribution) If its only rest, pt may have had an MI
Stress Protocol: imaging begins 15-20 min after stress injection
Two-Day Stress: both injections are 20-30mCi
Planar/ SPECT imaging 60-90 min after injection
Rest preformed the next day
One-Day Stress-Rest Protocol: 5-10mCi for the first dose and 25-30mCi for the second dosage
5-10 mCi iv injection 1 minute before exercise termination
Imaging 45-90 minutes after tracer injection
After 4 hours, 25-30mCi injected
Imaging at 60-90 minutes post injection
One-Day Rest Stress Protocol: the first injection is the low dosage—8-12mCi, and the second injection is
the high dosage---25-30mCi
5-10 mCi iv injection
Rest images 45-90 after injection
stressed after 3-4 hours later
25-30 mCi administered
Dual-Radionuclide Protocol: 3 mCi 201Tl for rest imaging begin imaging 10-30 minutes later, then 20-
30mCi Tc agent --Sestamibi / Cardiolite or Myoview second and then wait 60-90 minutes before imaging.
Cross talk occurs between the energies of thallium and Tc, however, when imaging is done in this sequence,
the energy spill is minimal compared with imaging thallium after technetium
High detection of coronary stenosis with sorter time
3 mCi IV injection Tl with patient at rest
Imaging 10-30 minutes later
Contraindications & Side Effects: taste perversion
Tetrafosmin / Myoview
Taken up rapidly by the myocardium, and It is theorized that it localized in the mitochondria of the
Clears from the liver and the lung faster than sestamibi, but like sestamibi, it remains in the
myocardium for several hours after injection – resulting in the need for separate injections at rest and
Acquisition and processing time same as sestamibi except due to rapid uptake and background
clearance, u can image as early as 5 minutes after injection.
Heart perfusion interpretations:
L. ventricle = even uptake / conc’n at stress & resdistribution = perfusion & tissue viability.
Recall that myocardium normally metabolizes primarily fatty acids; then abnormally primarily
Area of focal decreased uptake. Further delayed > 3 - 4 hrs up to 24 hr or
Re-injection may help differentiate the viability.
Ischemia, reversible: cold normal = viable tissue
Infarction, irreversible: cold cold = probably non-viable tissue
Differential diagnosis is usually possible observing the washout pattern.
However, if a cold area is seen on redistribution, and if no necrosis is present, viable tissue may
be very hypoperfused & revascularization of stenotic area would be beneficial.
Seen during myocardial stun = short term greater decrease in blood flow: rest = cold, stress
normal or cold;
During hibernation = chronic decrease in blood flow = long term pattern of rest = cold, stress =
High correlation w/ cardiac catherization i.e. ~ 73 - 95% vs. only ~ 60% with conventional
Our studies show relative perfusion not anatomy.
Rest images only w/ patients too ill to be stressed e.g. within ~ 6 - 24 hr after recent MI.
Study is positive in ~ 90% cases of transmural MI.
Rest only images obtained ~ 15 minutes after injection; patient standing if possible.
Slow Tb = # rads/mCi 201Tl dose = critical organs = kidneys ~ 2.5 rads vs heart ~ 1.1 rads
Breast tissue attenuation artifacts may be seen. Computer acquisition should be standardized.
Processing should = reproducible results w/ quantification by
Circumferential profile, tomographic slices, washout rates, & bulls eye analysis.
Dynamic Quantitative Functional Imaging of the Heart / R-N Angiography:
MUGA (multigated blood pool acquisition) AKA:
Radionuclide ventriculography (RVG)
Equilibrium radionuclide angiography (ERNA or RNA)
Equilibrium Gated R-N Ventriculogram
Gated (Heart) Blood Pool
This test involves labeling RBC’s with 99mTc-pertechnetate and imaging blood pool in the heart using a
gated acquisition technique. An equilibrium (meaning stability with in the CV space) study requires the
radionuclide agent to remain in the vascular space up to 4 hours.
Able to assess regional wall motion; LVEF; CO; ventricular volume at rest and stress for ischemia
Requires 8-10 min. per view
Looking at the heart cycle as it dilates and contracts, not looking at the myocardium
Divide heart cycle into 16 frames / segments for few hundred cardiac cycles
Myocardial evaluation LVEF, regional wall motion or CO in cases of CAD: ischemia (stress
ischemic) vs. Myocardial infarction (don’t stress). Ischemia or chronic MI with or without stress;
acute MI rest only
Ventricular aneurysms, rest only; seen as area of paradoxical motion (Dyskinesis)
Cardiac failure (rest only) with Congestive Heart (ventricular) failure
o Drug toxicity effects and follow- ups (chemo)
Main criteria is that the Rphx remains tin the CVS in equilibrium w/o leakage for up to 4 hours
The agents of choice for single injection and multiple images:
99mTc-Sn-RBCs – 15-25 mCi
99mTc-HSA – 15-20 mCi
99mTc tagging of pre-tinned RBCs may be done in-vivo, modified in-vivo/invitro, and invitro
Requires use of 500ug-1mg Sn+2
Incubation of RBCs for 15-30 min (to allow tinning b/c tinned RBCs get the tag) prior to use of the
It has been found that as little as .02 mg/kg of weight has the ability of altering the RBCs for up to 2
The amount of SN-PYP recommended is .2mg/kg of weight for adults
A vial containing lyophilized stannous chloride
Two syringes – one containing sodium hypochlorite and other with citric acid / sodium citrate
One to three milliliters of patients blood is added to vial, followed by the contents of both syringes
When blood is obtained from patient a small amount of heparin or ACD anticoagulant should be
present to prevent clot formation
Gently invert vial after each step
Use 19-21 gauge need so that RBCs aren’t damaged
From 10 – 100 mCi of 99mTc-NaTcO4 is added to the mixture
After 20 minute incubation period, the labeled cells are ready for injection
95% or greater results
Requires the preparing of a ―cold‖ pyrophosphate kit (which contains 14mg of SnPYP with 1-3mg
SN+2 available as SnCl2, and made with rphx quality saline – 3-5ml
Shake vial gently for 1 min and let stand for about 5 minutes
Inject about half of the ―cold‖ PYP IV into patient
Wait 15-20 minutes and inject 20-25 (up to 30-35) mCi of pertechnetate (first pass is an option here)
Wait 15-20 minutes to begin images
Labeling efficiency 90%
Modified In-vivo method
Requires IV injection of ―cold PYP into patient
Butterfly infusion set used with a 3-way stop cock; a syringe with 1 ml of ACD solution (heparin
would interfere) and 20-25 mCi of pertechnetate is attached in which (after 15-20 min) 5-8 ml of the
tinned RBC / WB is with drawn.
During an 10-20 min incubation period, this syringe is rotated; after which the tagged RBCs are re-
injected, followed by a saline flush from another attached syringe
Mechanism / method of localization – compartmental in CVS
Target and Critical Organs – Heart, Blood
Patient Prep: ECG/EKG get before. (required as input to the gating device)
3 leads minimum if your not doing stress
Options – use 3 leads or with augmented uni-polar leads: AVR, AVL, AVF; chest leads V1-
Must know we used to use 5 leads
2 leads – shoulders, supraclavicular, one each above the mid-clavicle (left arm right arm)
2 leads – midline (below the mammaries) between ribs (left leg and right leg)
1 lead – between the ribs, placed at area right to the sternum near the heart
NPO for 2-4 hours
No stimulatants including caffeine or nicotine
Anger camera w a LEAP, HS, HR, or Converging collimator
A SFOV camera is better with SMALLER area for MUGA
LFOV with pre acquisition ZOOM for best magnification and resolution
Ancillary / Monitoring Equipment / Devices
An ECG physiological synchronizer used as a gating device with the R wave as the physiological
trigger to synchronize the data storage directly related to specific sequence points of the heart cycle
The MUGA study results in a statistically high count density study in which count changes reflect
volume changes; may be used to accurately assess heart function
An older method is a dual gated geometric / plamimetry study with a manual outline or ROI of the
LV chamber with the disadvantage of decreased accuracy due to analysis in only 2 points of the
Relationship of counts and volume are directly proportional
Detector angled @ 35-450 LAO image with a slight 15o caudal (tilt) angulations for separation of
left ventricle from right ventricle and to further move detector away from atria for best temporal
Best angle for imaging is obtained by observing when the left ventricle may be isolated from the
Optional views – 700 LAO, 35-450 LPO, 300 RAO and anterior for right ventricle wall motion
The study images are obtained for > 300-500 (higher these days) minimum heart cycles. Image in
format of > 16 frames
Each image is a high count density image of 200-300K counts per frame; each view takes 10-15
minutes to acquire
LVEF determination is the best indicator of overall heart function as a pump
Primary disadvantage is inexperienced camera-computer system operators (that’s us)
Indication to terminate study include:
o Abnormal ECGs, hypotension, severe angina, stress to > 85% max predicted heart rate,
severe fatigue, leg pain, breathlessness, monitor failure
Cina’ can be produced only if the RR intervals are of appx equal length, so this is a problem with pts
with severe arrhythmias.
o Arrhythmias more than 10%, there will be a problem with acquisition
Proper tagging or tag quality
Excess free pertechnatate may obscure cardiac chambers and make it difficult to identify ventricular
Red blood cells of pts on high doses of steroids or heparin may be difficult to label
Stress as you are imaging (which cant be done on treadmill—has to be an ergometer bike or
The increase in stress with the ergometer has to be at different initial workload @ 20-25 watts, with
increments every 3 minutes. EF should increase normally (abnormal would be EF decrease)
Gated blood pool is recorded during the last 2 minutes of each stage because we don’t want to image
the first minute while the pt. Is still increasing the workload
RPM must be maintained by the pt through out
Rest Imaging: Septal separation
Acquisition and Processing
Timing – is everything! Use the fastest mode possible for the time/frame
Format usually – 64 x 64 matrix, acquired in byte mode (8 bits deep) mode for 4.5mm/pixel spatial
Optional 128 x 128 matrix for LFOV cameras
List mode may be used, but not recommended, not as flexible in retrieving images
Chamber Overlap – because it’s a type of dynamic and with proper positioning to see only LV
Wall Motion / High Count
Multiple Views – most important. About a 450 angle for a standard size pt
Total or global EF – of the entire left ventricles
Segmental or regional EF – a part of the divided left ventricle
EF normals are greater > 50-55%
Keep in mind you have to look at the patient, 50 may be normal for and elderly but not a young
healthy looking person.
Anything less than 50 is abnormal for anyone
EF can go as high as 75-83% before being considered too high
Phase amplitude analysis -
Manipulation of data requires the operator to enclose the L ventricle in a proper ROI
Must choose proper background! One that is greater than what it should be will give a false
increase of EF
The operator should observe each frame, possibly adjust for proper edge detection / wall
delineation based on a threshold of counts determined, an verify that the background is
acceptable by proper ROI
The MUGA program starts its analysis from the centroid of the chosen LV ROI; moving out to till it reaches
a matrix point / pixel analyzing for the threshold point where:
1. It reaches a point of the second dimension second derivative
2. The number of counts at the matrix point is < the threshold value
A time vs activity curve is reconstructed based on the change in counts / volume vs change in time.
Normal: LVEF = > ~ 50 - 55%; ~ 55 - 75( -83)%; i.e. ~ 50 - 55% = borderline, individual dependent
With exercise increase SV,CO, & decrease ESV w/same EDV = increase EF
Abnormal: LVEF = < 50%
With exercise: ischemia increase EDV & possible increase ESV, same SV = decrease EF.
The time vs activity / counts curve is directly related to ED & ES volume changes with time.
ED & ES points indicated on graph (Text Fig.) w/ ED seen 2x @ first & last points / endpoints of the
Computer methods allow critical background subtraction, counts/pixel = essential for each image.
Recorded multiple images = segments of the average heart cycle.
Acquired as >16 to 64 frames/points dividing the heart cycle; w/ > 300 cycles, 600 cycles ave, up to
MUGA = best study for regional wall motion / kinesis assessment.
Easy quantification of LVEF w/ ~ 90 - 95% correlated accuracy vs cardiac catherization = "gold
May assess exercise effects on heart function especially with ischemia present.
Multiple views w/ single Rphx. Dose.
High count density images w/ hundreds of heart cycles in multiple frames.
High resolution (because its about spatial and temporal resolution) images obtained at the various
points of the heart cycle; usually with 64x64 matrix byte mode.
Computer processed to construct a cine / movie mode display for visual inspection in real-time or w/
High correlation w/ cardiac catherization & other studies, non-invasively.
Reproducible results within a short study time with confidence.
Quantification at rest or w/ stress or exercise.
ROI allow edge detection/display for wall motion & assessment of EF, CO & other ventricular
Time vs activity curve generation display by computer accurate with counts directly related to
Easily accessible & integratable equipment & techniques.
Pre-cardiac catherization or surgery screen procedure.
Baseline study with follow-up comparisons e.g. effects from chemotherapy drugs.
First Transit / Pass Analysis or Radionuclide Angiography Study AKA Radionuclide
A dynamic camera-computer acquisition and processed analysis cardiac blood flow, function and
anatomy. A gating device may be needed with a single crystal scintillation camera only (u don’t have to do
a gating device, you would when the efficiency is low). Study is best performed with a multi-crystal, high
efficiency scintillation camera
Principles and Purposes:
Study is completed or acquired in less than 1 minute; tracer bolus is seen from vena cava through
Records the Tc agents with High Specific Activity initial pass through the major vessels and heart
Provides accuracy of about 95% and determines RVEF and LVEF
Quantitates LVEF normal at >50-55% (u have to look at the pt) The best indicator for overall
Study requires a very high efficiency camera that will count more than 200K – 400K per minute. This is
a problem because most Anger cameras are from 60K-200K, which will give decreased study reliability an
decreased dead time loss and decreased linearity. The study is best done with a camera of 450K cps
efficiency. Also, a bad bolus injection or concentration will give deceased counts and a hard to calculate
ECG should be done prior to study acquisition and requires <10% arrhythmias or your have major study
Especially ideal with patients who are allergic to iodine contrast and those with congenital defects like
1. Measures / calculates RVEF (40-45% is norm for right) and LVEF from a beat by beat analysis vs.
the equilibrium study which is an average
2. Assesses regional wall motion / kinesis (but better with equilibrium study), SV, CO, EDV, ESV, etc.
a. AKA type of ―Biventriculography‖ study – because you can assess wall motion as well as
the ejection fractions of both ventricles
3. Screen study pre-surgical or post chemo therapy. An example of some chemotherapeutic drugs
that cause toxicity to the heart are Doxorubicin and Adriamycin
4. Evaluate defects like septal / intracardiac shunt quantification , vena cava defects, a-v
malformations, aneurysms, or pericardial effusion (seen as a decreased halo of activity)
5. Evaluation with exercise or pharmacological intervention to screen for CAD; Normal E.F. seen to
increase >5% (after giving interventional agent) vs. Rest; abnormal shows a decreased in E.F. with
induced ischemia and hypokinesis
Rphxs: (agents for FIRST PASS) in order of preference:
Ultra short Tps Rphxs: Rare (don’t worry about Tp’s, recognize these as used for first pass studies)
OS / 199mIr - Tp 4.8 seconds 195(m)
Hg / 195mAu - Tp 30 seconds
Rb / 81mKr – TP 13 seconds 198
Ta – Tp 9.3 minutes
Doses and Administration:
Average dose range is 20-25 mCi of the Tc agents, total shouldn’t exceed 35 mCi
o give as a compact <1ml bolus IV injection
If doing a first pass in a series of 2 or 3 injections- Use 8-20 mCi doses of multiple agents with
different clearance if multi-studies are needed, but not more than 35 mCi. DTPA would be used
before sulfur colloid
Bolus Injection Set-Up:
This is a big deal, it REALLY needs to be REALLY bolus, so not your usual set-up
3 way stop cock
Large—like 18 gage or bigger bore needle (horrible monstrous things!)
Good vein – a good choice would be the basilica in the anti cubital fossa
Mechanism / Method and area of Localization:
Compartmental specifically to the study
Target and critical organs:
Critical Organs, basis is the radiopharmaceutical agent. Heart is always the target.
prefer high sensitivity, but if u don’t have it, just use all purpose
electronic gating device optional
Patient History & Prep:
Baseline ECG Determines CO, Rt or LV EF, Wall Motion, Cardiac Shunt Evaluation Imaging, and
pulmonary transit time
If using Pertechnatate – a thyroid blocking agent is required
Patient Procedure / Technique
Entire study done in less than a minute with sequential imaging on film at 1 second per frame for a
Imaging acquisition with computer < .1 second per frame for less than a minute
Radiotracer from the injection site is imaged as it enters the right heart, pulmonary circulation, left
heart, enters the systemic circulation
Patient position is supine and accurate anterior views of the entire heart to include the great vessels;
critical for temporal and spatial resolution and separation
After the < 1 min dynamics, 500K static images may be obtained for blood pool images @ 1, 5, 10,
or 20 minutes after injection if needed
Data Processing / Computer Acq, processing / image format
A heart rate of 70 bpm = cardiac cycle of 800 msec e.g. requires frame rate should be 25 frames or
about 40 msec / frame
A bolus of activity requires 15 sec to travel through the right heart, pulmonary circulation, and left
A 60 second acquisition would result in 1500 frames. Acquisition should be < .05 sec / frame for
Frames required are minimally 25-50 frames; also includes a minimum of > 5-15 heart cycles
Processing may need to reformat to 1 sec / frame for static images of thes dynamic study
Review of study frame by frame for display in cene continuous loop format to observe wall
Computer program may generate time vs. activity courses with max counts = ED and min counts =
ROI drawn over right ventricle, lungs and/or left ventricle or non-pulmonary background region.
Number of frames per second are 25 or more. Another way to state the same thing is
acquiring each frame at < 40usec/frame
Subtract properly for background
%EF = EDV (gross cts. – bkgd cts ) – ESV (Gross cts. – bkgd cts)
EDV (Gross cts. – Bkgrd cts) X 100
LVEF > 50 – 55% RVEF 40-50% With exercise the normal pt the EF increase > 5%
If no pericardial effusion is present, no separation of the blood pools between the heart and the
lungs, liver and spleen
If pericardial effusion is present visual comparisons of the diameters of the cardiac chambers blood
pools show a light shadow or halo of decreased activity seen as an abnormal separation of heart and
body blood pools and that indicates more than 100 ml of fluid
Detection and quantization of cardiac shunts with stress exercise screens patients with induced
reversible ischemia. At rest = normal but as stress = hypokinesis or Akinesis
a regular rhythm without ectopic beats or premature ventricular contractions is essential for a
accuracy of the study depends on the quality of the bolus and imaging system
Venography: Dorsal Vein Procedure
Purpose: To visualize the deep venous system of the lower extremity as well as the internal iliacs. By
using Tc-MAA or Tc-HAM, the lung may also be imaged to help rule out pulmonary embolization
S-camera with 140 KeV parallel-hole collimator
MAA – 2-3 mCi each
Two or three way stop cocks
Butterflies 20-21 gauge
Prep – nothing special, explain.
Contraindications: inadequate tourniquet application
Butterfly into dorsal vein of each foot.. flush.
Connect stopcocks, MAA syringes, saline, and tubing
Place feet center of camera
Set scan controls
Set area scan speed, or u will do a certain number of statics (3 lower extremities, 1 pelvis)
Apply tourniquets at ankles and below knees
Start camera, wait a few seconds for it to start imaging, then inject MAA then saline
If not doing statics, when camera reaches knees, slow speed
Spend more time imaging pelvis, static or not
If assessing lungs, perform a 1000K anterior view, with pt. Supine
Repeat legs, remove butterflies
Venography: Equilibrium 99mTc Red cell procedure
Using Tc-tagged red cell images of lower extremities, show depiction of deep and superficial venous
system without being invasive.
20 mCi of Tc pertechnetate, 1.0 ml of stannous pyrophosphate for in vivo labeling of pts red
Prep – no special, explain.
Inject pyrophosphate, wait 20-30 minutes
Position pts lower extremity for study
Inject 20 mCi of Tc pertechnetate
60 one second sequential images
Area scan speed 15 – 20 cm counts/min
Statics – 1000K each. Anterior, posterior of femoral, popliteals, calves, and feet
Gives excellent resolution of the deep venous system and collateral circulation
Shows info as to amount of inflammation in the region
Helpful in establishing diagnosis of acute thrombophlebitis
Superficial and deep venous systems are demonstrated
Thrombi are not visualized; however, the decrease in flow in the venous system or the
obstruction to the deep venous system is apparent and comparable to radiographic
Normal variations in FDG Localization
Myocardial activity ranks as the most noticeable normal variation.
Most fasting patients demonstrate little or no left ventricular activity, which is an advantage in the
search for tumors, especially in the left lung base. (therefore, they need to be NPO to ―starve the
However, intense left ventricular activity can occur normally in fasting patients
Also, heterogeneous activity frequently appears in diabetic patients even with blood glucose levels
less then 120mg/dl (which is the cut off for normal). Glucose clamping protocols are used when
myocardial PET imaging is performed in these patients
FDG accumulates in many places; this is usually ok if the accumulation is symmetrical:
Salivary glands, all 3
Labial or buccal muscles
Laryngeal and anterior spinal muscles
Muscles of mastication
o Diffuse uptake:
Complementary muscle pairs
Muscles of an or both eyes
Normal variations frequently cause diagnostic problems or misdiagnoses b/c they mimic cancer:
o Muscular or fat activity in the neck and shoulders, especially:
Subclavius muscle groups
GI tract activity
PET perfusion tracers
Positron emittin r-ns are used for the assessment of reginal perfusion in two groups: tracers only
partly extracted by myocardium and freely diffusible
R-N Tp Tag and studies
C (carbon) 20 min C-palmitate myocardial metabolism
C-acetate myocardial metabolism
N (nitrogen) 10 min N-NH3 myocardial perfusion
O (oxygen) 2min O-CO myocardial blood volume
O-H2O myocardial perfusion (most accurate)
Above is labeled water which is freely diffusible so extraction is
100% - doesn’t depend on flow rate
F (fluorine) 110 min Common organic molecules
18F-fluorodeoxyglucose myocardial glucose metabolism
R-N Tp Tag
Rb 1 ½ min Rb-Rb+ myocardial perfusion
Acts like 201Tl
82Sr 75 sec
Myocardial perfusion is done most accurately with 15O water
PET and SPECT have sensitivities ranging from 80-90% depending on pt population
PET has higher energy of annihilation radiation and improved correction for attenuation, its
specificity tends to be about 10 – 15% higher
Glucose / insulin clamp – continuous infusion of glucose and insulin is administered at the time of
FDG injection. The infusion is maintained during the interval of FDG blood clearance.
Deoxyglucose is an analog of glucose
Palmitate is a naturally occurring fatty acid
Other stuff on prep
Coronary Artery Disease – coronary insufficiency or ischemia with fibrosis or stenosis or rheumatic
(valve) heart stroke or myocardial infarction
Atherosclerosis – build-up of deposits in artery walls (usually fat)
In our society, this begins at a very early age
If coronary arteries are partially occluded then pt gets angina chest pain
If sudden occlusion of blood, M.I., there is damage and necrosis which turns into non-fx scar tissue.
Begins with fatty streaks small lipid vessel with wall deposits
Becomes ischemic myocardium with decreased perfusion and contraction
Arteriosclerosis – type of arthrosclerosis with primarily calcium deposits instead of fat.
For flexibility, narrowing vessels = b.p. = danger, stroke (CVA) from ruptured vessel
Group of diseases with thickening and decreased elasticity of arterial walls with calcium deposits
Angina pectoris – due to decreased blood flow (ischemic areas)
Peculiar, severe anterior chest pain with exertion, stress, intense cold is a sign of inadequate or
decreased O2 blood supply to the myocardium due to atherosclerosis of coronary artery
Pain usually radiates from inner left arm
Treatment – rest or vasodilators like nitroglycerin
Angina pectoris is the medical term for chest pain or discomfort due to coronary heart disease. It is
a symptom of myocardial ischemia. It occurs when the myocardium doesn’t get as much blood (hence as
much oxygen) as it needs. This usually happens because one or more of the hearts arteries is narrowed or
Decrease in blood supply by partial to complete stenosis. Occlusion of coronary artery branches
With decreased blood flow and efficiency of contraction of ischemic areas called hypokinetic areas
with stenotic vessels, stress increased blood flow to the normal areas
Ischemia is a lack of blood or inadequate supply of blood to a part of the body (in this case the
heart) caused by a partial of total blockage of an artery (in this case coronary arteries)
Reversible – there are things that can be done to re-open the arteries therefore reverse the problem.
Due to arthrosclerosis – a form of arteriosclerosis with plaques of cholesterol and lipids that form
within inner arterial walls or vessel walls; and that causes fibrotic, or calcified narrowed lumens, and
then decreased blood flow to organs.
o This is caused from diet excesses, non-exercise, aging, obesity and with hypertension and
M.I. (myocardial infarction) – due to sudden occlusion of blood flow
Acute sudden occlusion of coronary artery branch by atherosclerosis or thrombosis / emboli
Necrotic area results in myocardium injury or death of myocardium which is fibrosis or scarring
Heart attack: the death of a segment of heart muscle, caused by a blood clot in the coronary artery
interrupting the blood supply
Irreversible – this cannot be fixed and is not reversible because the tissue is already dead / necrotic /
Stelio - a wide variety of conditions that leads to abnormal heart function, and most of this can be
seen as decreased function / decreased ejection fractions, and the heart is often times enlargement.
(enlargement of the heart, does not mean the myocardium is thick)
Wikipedia – literally means “heart muscle disease”; the deterioration of the function of the
myocardium for any reason. People with cardiomyopathy are often at risk of arrhythmia and/or
sudden cardiac death.
Hypertension: ONE of the most common causes of underlining heart disease!
Pt is asymptomatic even with increased blood pressure > 140/90
Etiology – no single cause; increased risk from:
o Increased sodium levels
o Family history
o Other diseases
Aldosternonism – too much aldosterone being produce (from adrenal gland / the
Cushing’s disease – abnormal function of adrenal gland
Glomerulonephritis – kidney issues
Dx – if blood pressure becomes greater than 140/90 measured several different occasions; with CAD
or Cerebral vascular disease more prone to disability or death
Treatment – Antihypertensives, diuretics, vasodilators, sympathetic NS depressants and inhibitors,
ganglionic blocking agents
Types of hypertension:
o Essential – develops with out apparent cause; the primary type
o Malignant – rapidly progressing with severe vascular damage – death
o Benign – slow rate of increasing blood pressure
o Renal – secondary type due to renal disease e.g. renovascular, renal artery stenosis with
increased renin production
Hyperlipoproteinemia – large group of inherited and acquired disorders
Abnormal lipoprotein metabolism with greater than normal cholesterol and lipoprotein levels
including things like triglycerides and phospholipids
Treatment – weight loss with diet and exercise. Medication if its of metabolic origin
Hibernating myocardium – severely ischemic.
Myocardial Stunning – temporary contractile dysfunction after episodes of myocardial ischemia
Reverse Redistribution – associated with significant stenosis, presence of collateral circulation
Digitalis glycosides – digoxin or digitoxin: action – increased C.O. decreased HR; Toxicity – arrhythmias
Cardiac Tumors – mets from breast, bronchus, lymph, melanoma
Wall motion Abnormalities:
Hypokinesis – area of abnormally low wall motion
Akinesis – area of no wall motion
Dyskinesis – area of paradoxical (asynchronous) wall motion
Eukinesis – normal wall motion
Tetralogy of Fallot – (congental problem) anomaly of heart with pulmonary stenosis, Interventricular
septum defects, dextraposed aorta, blood received from both ventricles and right ventricle
Parietal layer - has about 1-10 ml (less than 10 ml) between, abnormal if there is more than 10-15. We can’t
see pericardial effusion until it reaches 100 ml.
Major vessels and chambers for first pass?
Main blood vessels: Heart and great vessels
IVC and SVC with de oxygenated blood to the right atrium through the tricuspid valve to the right
Pulmonary semilunar valve to the pulmonary artery to pulmonary circulation
Oxygenated blood to pulmonary vein to left atrium through bicuspid valve to artic semilunar valve
Systemic circulation to aorta then ascending aorta, aortic arch, descending aorta