Nuclear Cardiology Flashcards
Perfusion Imaging Overview
LV perfusion imaging evaluates _________ to the myocardium.
If a perfusion abnormality is present, what 5 questions help characterize the perfusion abnormality?
What are the two components of each perfusion test?
How is the stress component of perfusion imaging is accomplished?
All perfusion imaging uses radionuclides with _____ imaging.
What are the other types of stress tests?
- Left ventricular perfusion imaging evaluates the blood flow to the myocardium.
- If a perfusion abnormality is present, the following five questions help to characterize the perfusion abnormality:
- Is the perfusion abnormality reversible during rest, or is the defect fixed at both stress and rest?
- How large is it: Small, medium, or large?
- How severe is it: Mild (subendocardial), moderate, or severe (transmural)?
- Where is it: In which coronary artery territory?
- Are there any associated abnormalities, such as right ventricular uptake, ischemic dilation, or wall motion abnormalities?
- Each perfusion test has two components: An element of stress, and a method of imaging.
- The stress component can be physical (treadmill), pharmacologic-adrenergic (dobutamine), or pharmacologic-vasodilatory (dipyridamole or adenosine).
- All perfusion imaging commonly performed uses radionuclides with SPECT imaging. Some protocols include gated SPECT (gSPECT) as well.
- Other types of stress tests performed by cardiologists (EKG stress tests and echocardiographic stress tests) can be performed in lieu of imaging. These non-imaging tests can only detect secondary signs of perfusion abnormalities, such as ischemic EKG changes or wall motion abnormalities.
Clinical Applications of Myocardial Perfusion Imaging
Name them all.
Role in evaluating acute CP? A normal myocardial perfusion exam is assocated with a ___% annual rate of cardiac events
What are the findings that would classify a patient as high risk after an MI?
How do you calculate EF?
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Evaluation of acute chest pain. Myocardial perfusion imaging is often the gatekeeper to further cardiac workup in patients where there is clinical ambiguity for cardiac ischemia (e.g. chest pain with negative EKG and troponins). A negative myocardial perfusion exam allows safe discharge.
- A normal myocardial perfusion exam is associated with an annual rate of a cardiac event of 0.6%, even among patients with a high pretest likelihood of coronary artery disease.
- Evaluation of hemodynamic significance of coronary stenosis. Even with coronary artery stenosis seen on angiography or CT, patients with a normal nuclear cardiac perfusion exam have a relatively low risk for cardiac events.
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Risk stratification after MI. Findings that would classify a patient as high risk include:
- Significant peri-infarct ischemia.
- Defect in a different vascular territory (suggesting multi-vessel disease).
- Significant lung uptake, suggesting left ventricular dysfunction.
- Left ventricular aneurysm.
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Low ejection fraction (less than 40% seen) on gSPECT.
- Ejection fraction is calculated as EF = (EDC - ESC)/(EDC - BC)
- EDC = end diastolic counts; ESC = end systolic counts; BC = background counts
- Preoperative risk assessment for noncardiac surgery.
- Evaluation of viability prior to revascularization therapy.
- Evaluation of myocardial revascularization status-post CABG.
Viability Imaging Overview
Why is it important to know if hypoperfused myocardium is viable?
Hypoperfused myocardium that is viable is known as __________ mycoardium.
What are two ways viability imaging can be done? Which one is the gold standard? Does this gold standard method evaluate perfusion?
Can a pure perfusion scan distinguish between hibernating myocardium or scar? How do these look like on both stress and rest images?
What type of perfusion defect suggests viability? Which kind of defect suggests scar?
What does an FDG mismatch between FDG PET and perfusion imaging mean and what is the contrary mean?
- Prior to a revascularization procedure (e.g., CABG or coronary angioplasty/ stenting), it is important to know if the hypoperfused myocardium is viable, as the revascularization of scar tissue would not provide a clinical benefit. Hypoperfused myocardium that is viable is known as hibernating myocardium.
- Viability imaging can be performed with rest-redistribution thallium-201 perfusion imaging or F-18 FDG PET. F-18 FDG PET is the gold standard for evaluation of myocardial viability, although unlike thallium FDG-PET does not evaluate perfusion.
- Static SPECT images from a pure perfusion exam (such as Tc-99m sestamibi, rubidium-82 PET, or N-13 ammonia PET) cannot distinguish between hibernating myocardium or scar. Both of these entities appear as a fixed (present on both stress and rest images) myocardial perfusion defect.
- Evaluation of gated SPECT (gSPECT) functional data can suggest either hibernating myocardium or scar.
- Normal or nearly normal wall motion and wall thickening in the area of the perfusion defect suggests viability (hibernating myocardium), while a large defect with abnormal wall motion suggests scar.
- If the region of the perfusion defect takes up FDG (a “mismatch” between FDG PET and perfusion imaging), that region of the myocardium is viable and may benefit from intervention (either CABG or percutaneous intervention).
- In contrast, an FDG PET “match” of a photopenic region corresponding to the perfusion defect is consistent with a non-viable scar, and the best treatment is medical therapy only.
What are the radionuclides used in nuclear cardiology?
- Thallium-201
- Technetium-99m sestamibi (Cardiolite)
- Rubidium-82
- Nitrogen-13 ammonia
- F-18 FDG
Thallium-201
How is this produced? 1/2 life? How does it decay? What does it emit?
The relatively low energy characteristic X-rays does what to chest wall soft tissues?
Why it is necessary to administer fairly low doses?
How does thallium physiologically act like?
Myocardial uptake is directly proportional to myocardial ________.
A __% stenosis will produce a perfesion defect upon maximal exercise.
What does postredistribution images show for defects in ischemic but viable myocardium? Contrast this to a scar.
- Thallium-201 is a cyclotron-produced radionuclide with a half-life of 73 hours. It decays by electron capture and emits characteristic X-rays of 69-81 keV.
- Relatively low energy characteristic X-rays increase attenuation artifact from chest wall soft tissues.
- It is necessary to administer fairly low doses due to its long half-life, with resultant lower count densities.
- Physiologically, thallium acts like a potassium analog, crossing into the cell via active transport through the ATP-dependent sodium-potassium transmembrane pump.
- Myocardial uptake is directly proportional to myocardial perfusion.
- A 50% stenosis will generally produce a perfusion defect upon maximal exercise.
- Thallium undergoes redistribution with simultaneous cellular washout and reextraction of blood-pool radiotracer. Since ischemic myocardium progressively extracts thallium but washes out more slowly than normal myocardium, postredistribution images will therefore show normalization of defects in ischemic but viable myocardium. In contrast, a scar will show a persistent defect.
Technetium-99m Sestamibi (Cardiolite)
Contrast this to thallium - difference? Similarity?
How does sestamibi enter the myocardium and where does it bind to?
- Unlike thallium, Tc-99m sestamibi does not undergo redistribution and remains fixed in the myocardium.
- Sestamibi enters myocardium via passive diffusion and binds to mitochondrial membrane proteins. Similar to thallium, myocardial uptake of sestamibi is proportional to myocardial perfusion.
Rubidium-82
Is a ________-emitting PET perfusion agent that is generated from ________-__.
Half life? What does this half life allow us to do? What does it preclude us from doing? What is used instead?
Physiologically how does Rubidium-82 act?
- Rubidium-82 is a positron-emitting PET perfusion agent that is generated from strontium-82. A very short half-life of 76 seconds allows high doses to be administered, although such a short half-life precludes the use of exercise stress. Pharmacologic stress is used instead.
- Rubidium-82 acts as a potassium analog, similar to thallium.
Nitrogen-13 Ammonia
Is a _______-emitting PET pefusion agent (like ______-__)
Half life? How is this radionuclide made? Why would it need to be made on-site?
What does N-13 have excellent imaging characteristics?
Compare to rubidium-82.
- Nitrogen-13 ammonia is a positron-emittngPET perfusion agent(like rubidium-82) that has a half-life of10 minutes. Unlike rubidium-82, N-13 iscyclotron-produced and the cyclotron must be on-site due to its short half-life.
- N-13 has excellent imaging characteristics. N-13 positrons have low kinetic energy and don’t travel very far in the tissue before annihilating, which allows relatively high resolution. The short half-life also allows large doses to be given for high counts.
- Like rubidium-82, a relatively short half-life makes use with exercise stress logistically challenging, and N-13 perfusion is almost always coupled with a pharmacologic stress.
F-18 FDG
What else is this radiotracer used for?
_______-emitting agent with half life of ________.
Can this be used for perfusion imaging?
What is F-18 FDG PET images correlated with and for what reason?
Explain how you can tell between hibernating myocardium and scar with F-18 FDG?
- F-18 Fdg, the same radiotracer used for oncologic imaging, is a positron-emitting PET viability agent with a half-life of 110 minutes. Unlike rubidium-82 and N-13 ammonia, FDG cannot be used for perfusion.
- F-18 FDG PET images are correlated with a sestamibi perfusion study to evaluate viability. A defect on sestamibi rest perfusion with discordant FDG uptake represents viable hibernating myocardium that could potentially be revascularized. In contrast, a sestamibi perfusion defect correlating to lack of F-18 FDG uptake is a scar.
What are the types of exercise and pharmacologic stress tests?
- General exercise
- Dipyridamole stress - pharmacologic vasodilator
- Adenosine stress - pharmacologic vasodilator
- Ragadenoson - vasodilator
- Dobutamine stress - pharma stress
What is the general protocol for exercise stress component of cardiac perfusion imaging and why?
Food?
Meds?
How is exercise performed? What must be achieved for the study to be diagnostic? How is this calculated?
- Prior to undergoing a myocardial perfusion study, the patient should be NPO for 6 hours to decrease splanchnic blood flow and therefore reduce liver and bowel uptake.
- Calcium channel blockers and b-blockers should be held to allow patient to reach target heart rate.
- Exercise is performed with a multistage treadmill (Bruce or modified Bruce) protocol. The target heart rate, which is calculated as 85% of maximal heart rate, must be achieved for the study to be diagnostic. The maximal calculated heart rate is 220 bpm - age.
Dipyridamole Stress
What is dipyridamole? What does it do?
How does this show perfusion?
Does this stress test increase cardiac or O2 demand?
What must be held for 24 hours before this test?
What is the antidote?
- Dipyridamole is an adenosine deaminase inhibitor that allows endogenous adenosine to accumulate. Adenosine is a potent vasodilator, increasing coronary blood flow by 3-5 times.
- A critical coronary artery stenosis cannot further dilate in response to adenosine. That coronary artery territory will appear as a relative perfusion defect on stress imaging.
- Unlike physical stress, dipyridamole stress does not increase cardiac work or O2 demand.
- Caffeine and theophylline reverse the effects of dipyridamole and must be held for 24 hours.
- The antidote is aminophylline (100-200 mg), which has a shorter half-life than dipyridamole, so the patient must be continuously monitored.
Adenosine Stress
Physiologic mechanism?
What is this pharmacologic stress physiologically identical too?
What is the half-life? What is the antidote?
- Pharmacologic vasodilator
- Adenosine has identical physiologic effects to dipyridamole but a more rapid effect.
- Adenosine half-life is approximately 30 seconds and thus does not require a reversal agent.
Regadenoson
Pharmacologic mechanism?
Half-life?
Compare to adenosine.
- Pharmacologic vasodilator
- Regadenoson is an adenosine receptor agonist with a 2-3-minute half-life. It is easier to administer than adenosine with a convenient universal-dose intravenous injection.
Dobutamine Stress
What is the mechanism of action?
When is this used?
- Dobutamine is a b1 agonist that increases myocardial oxygen demand.
- Dobutamine is usually reserved for when adenosine is contraindicated (severe asthma, COPD, or recent caffeine) - however, we just use regadenoson now, which doesn’t have those contraindications.