Nuclear Medicine: Cardiac Imaging Part 2
Part 2 Q&A review of nuclear cardiac imaging for board review. Check out www.theradiologyreview.com for other podcast episodes and free board preparation resources.
Show Notes/Study Guide:
By which mechanism does Thallium enter into a cell?
Thallium enters a cell using a Na/K pump in a manner related to blood flow.
What happens after Thallium enters into a cell?
Unlike Tc-sestamibi and Tc-tetrofosmin, Thallium is able to redistribute among viable cells in the myocardium. So initial Thallium imaging provides information about blood flow to the myocardium and delayed imaging evaluates for redistribution.
How does Thallium distinguish between normally perfused, ischemic, and dead (infarcted/scarred) myocardium?
Thallium can show areas of ischemic but viable myocardium. Ischemia: perfusion defect on initial imaging but uptake is seen on delayed imaging as Thallium redistributes into the viable but hibernating myocardium. Scar/prior infarct: perfusion defect on initial imaging that persists on delayed imaging (redistribution requires functional Na/K pumps—which won’t be functioning in case of myocardial scarring). Normal perfusion: No defect on initial imaging. Delayed imaging would typically not be performed as ischemia and/or scar is already excluded if initial imaging is normal.
On a myocardial perfusion study with Tc-sestamibi or Tc-tetrofosmin, how does imaging distinguish between scar/prior infarct and ischemia?
The key to differentiate between scar and ischemia on a myocardial perfusion study is to compare uptake between the stress and rest portions of the examination. A fixed defect on both stress and rest is consistent with scar from prior infarct. A reversible defect, meaning a defect seen on stress imaging only, with no defect on rest imaging, is a manifestation of stress-induced ischemia. Sometime a fixed defect is seen with reversible components around the fixed defect (in other words the defect is distinctly larger on stress images and smaller on rest images) and this suggests a component of scar with peri-infarct ischemia.
True or false: A thallium lung to heart ratio study with decreased lung uptake suggests multi-vessel coronary artery disease.
False. Multi-vessel coronary artery disease would show increased uptake in lungs as the reduced blood flow through the lungs due to cardiac disease is not sufficient to clear the tracer from the lungs.
What are imaging manifestations and clinical implications of transient ischemic dilation?
Transient ischemic dilation (TID) is identified on a myocardial perfusion scan when the left ventricular cavity appears larger on stress imaging compared to rest imaging. Note that perfusion can appear otherwise normal—the finding of interest is simply apparent left ventricular enlargement on stress imaging that is not seen on rest imaging. The significance of this finding is that this correlates with left main and/or 3-vessel coronary artery disease that causes diffuse subendocardial hypoperfusion. This diffuse subendocardial hypoperfusion means that less radiotracer is delivered to the subendocardial myocardium, therefore causing a diffuse subendocardial perfusion defect on stress imaging that causes the appearance of left ventricular enlargement on stress imaging, not seen on rest imaging (therefore transient dilation as in the name), thus showing diffuse reversible subendocardial ischemia related to left main and/or 3-vessel coronary artery disease.
How might dilated cardiomyopathy without ischemia manifest on a myocardial perfusion scan?
In comparison to transient ischemic dilation, dilated cardiomyopathy would be expected to present with left ventricular dilation that is fixed on both stress and rest images.
What is the significance of seeing increased right ventricular activity (right ventricle uptake similar to left ventricle uptake) on rest imaging?
If the right ventricle shows higher than normal uptake on rest imaging which would manifest as right ventricle uptake similar to left ventricle uptake this is a sign of right ventricular hypertrophy.
What is the difference between stunned and hibernating myocardium?
Stunned myocardium is seen in the acute phase following ischemia that resolves with reperfusion injury but not frank myocardial infarction/scarring and manifests as normal perfusion with impaired contractility of the heart. As the name suggests this stunning is temporary and typically resolves within a few weeks.
Hibernating myocardium results from chronic decreased perfusion to the heart from chronic severe coronary artery disease and manifests as areas of decreased perfusion and decreased contractility in myocardium that is not infarcted and is still viable. A key to remember for board exams is that hibernating myocardium is viable heart tissue that is chronically hypoperfused, and therefore poorly contractile but if the perfusion is improved through intervention such as coronary stenting or angioplasty, cardiac contractility can recover to normal or else be significantly improved.
How can one assess for viability of cardiac tissue using FDG PET/CT and/or Thallium?
Another way one could phrase this same question is as follows: how can one differentiate between infarcted myocardium and viable myocardium using FDG PET/CT and/or thallium imaging? With FDG-PET/CT hibernating myocardium is chronically hypoperfused and therefore very hungry for nutrients such as glucose—therefore FDG uptake is sometimes more intense in hibernating myocardium compared to normal myocardium. The key however is simply the finding of FDG uptake in the region of perfusion defect (whether increased, normal or slightly decreased compared to normal myocardium) proving that there are viable cells in the region of decreased perfusion/ischemia. With thallium imaging the key for viable myocardium is that thallium will redistribute into viable myocardium but not scarred myocardium. In hibernating myocardium on initial imaging with thallium one will see a perfusion defect related to the chronic hypoperfusion but on delayed imaging thallium will use functional NaK pumps to redistribute into any myocardium that is viable but will not redistribute into any myocardium that is scarred as scarred myocardium will not have functional NaK pumps.
Summary of imaging for:
Hibernating myocardium: myocardial perfusion scan will show decreased perfusion and decreased contractility, FDG PET/CT will show uptake equal to higher than normal for myocardium, thallium will show redistribution on delayed imaging. Hibernating myocardium is chronically hypoperfused myocardium that is still viable.
Stunned myocardium: myocardial perfusion imaging will show normal perfusion but decreased contractility. This is temporary and is the result of a recent, transient ischemic insult to the heart but not frank infarction.
Ischemic myocardium: myocardial perfusion scan will show less tracer uptake on stress compared to rest imaging (reversible defect) and poor contractility in ischemic segments on stress imaging.
Scar/infarcted myocardium: No tracer uptake on stress or rest images in the infarcted/scarred myocardium and no contractility in that infarcted segments as the myocardium is simply dead in that region. No redistribution with thallium and no uptake with FDG PET/CT.
