I'm going to talk about ammonia, cardiac PET, myocardial perfusion imaging cases. I don't have any disclosures. So the learning objectives for this talk are describe the PET rest stress myocardial perfusion imaging protocols, and to detail the findings from ammonia and 13 PET images to effectively assess myocardial blood flow, to identify how to use gated information effectively, describe the application of quantitative flow assessment, explain how to read and interpret PET MPI studies, and describe the advantages of PET myocardial perfusion imaging studies. PET rest stress myocardial perfusion imaging protocols, you're going to discuss about ammonia protocol here, but I'm also going to mention about rubidium so that we know the two most commonly used myocardial perfusion imaging protocols available for stress testing with the cardiac PET. So A is ammonia. So the first thing what we do is we do a scalp scan, and after the scalp scan, we do the transmission scan with the CT, or you can do a coronary artery calcium score with the new cameras. You can use that as the transmission scan. The only difference between doing a CT for attenuation correction or the coronary artery calcium score is that one is non-gated, which is for attenuation correction, and the radiation is a little bit less with the coronary artery calcium score is gated with breath hold image. So the radiation is slightly more because the MAs which are used for coronary artery calcium score are higher than the ones which are used for attenuation correction, but the information which you get from coronary artery calcium score is very important for the study and also for prognostic indication. So after this, we give ammonia injection, and after the ammonia injection, a 20-minute rest scan is acquired, and then there is a delay of about five half-lives. So ammonia half-life is about 10 minutes. So we wait about 50 minutes before doing the stress portion, and then stress is done with either ragadenosine, adenosine, or dipyridamole, and then a second injection after the stress of ammonia is given. With ragadenosine, it's given after about 30-40 seconds. With adenosine, we usually give the injection after two minutes of adenosine, and then we continue it four minutes after that, and for dipyridamole, it's about between seven and nine minutes after the dipyridamole is started. Now with the ammonia injection, it's always good to use a pump instead of just giving a bolus, because giving a bolus without a pump interferes with the flow measurements. Then again, after the injection, we require a 20-minute scan. Now with ammonia, the last 17 and a half minutes of acquisition are used for static summed images, and also for gated images, and the whole 20-minute acquisition is used for the coronary flow reserve for measurement of that. For the rubidium, which is B, the protocol for rubidium, we do a scalp scan, and then an attenuation map or a transmission scan is done with CT, and then coronary artery calcium score if that is needed, and then a rubidium injection is given. So the dose of rubidium varies between whether you're using a 2D system or a 3D system. For a 2D system, the dose is higher, and 3D system, the dose is lower. For ammonia, the dose is 10 to 20 millicuries, which is used for both by the same dose for 2D or 3D system. So here we give the rubidium injection, acquire the images for seven minutes. The half-life is short for rubidium, so just after the rest images are done, about a minute and a half after that, we do the stress. And after the stress, we inject a second dose, which is the stress rubidium dose, and then scan the patient, acquire the images for seven more minutes. And then these images, just like ammonia, are unlisted, and the last five and a half minute is used for some static images and also for gated images. And the whole seven-minute acquisition is used for the flow, for the quantification of the flow. So now we'll do the cases. So this is a 48-year-old female who was admitted to the hospital after a 20-minute episode of chest tightness. There is no association with exertion or shortness of breath. Patient was under a lot of stress. She had lost her husband to COVID-19 four months ago. Arrest ECG had nonspecific T wave abnormality. Troponin were less than 0.02 times three. Her past medical history was COVID-19 and also gastroesophageal reflux disease. The only medication she was on was protonics. So the first thing we do when we read the scan is always look at your transmission scan, then look at your emission scan, and then look at the fused images. So if you look at the upper image, you can see the first row is your emission scan. And then this is the transmission scan, which is the CT attenuation scan. And then you have the fused images. Very important before we start reading any study to look at these, to make sure that they are properly fused or not. And then after that, if you have not doing the coronary artery calcium score, it's important to also look at the calcium on your low-dose CT, which is done for attenuation correction, and see if you have any calcium in LAD, CERC, or RCA, and to look at, you know, visually if there is calcium there or not. And you can even give it a visually estimated coronary artery calcium score. So if you look at these images on top, which is A, you can look at the top two, which, in fact, the first four rows, which you can see over here, the top one is the stress, and the bottom one is the rest. So if you look at the stress images, it looks like there is decreased perfusion in the anterior or intralateral region, and which improves at rest. But when you look at your fusion images, see the fusion, you can see that the anterior wall is not properly fused with the emission and the transmission images. And that's giving you this false positive perfusion defect on stress images. Then when you fuse them properly, then you look at your scan, which is in the B, you can see the scan looks completely normal. So that defect, which was there, completely disappears. And that defect was because it was not properly fused, your emission and transmission images. The good thing is you don't have to require the study on these patients. You can fuse them at the processing station and then reprocess the scan, and you can get your image. So very important to look at your fusion and to look for transmission and emission misalignment. After looking at your fusion images, it's good to look at either visually estimated, coronary artery calcium, or coronary artery calcium score. And that helps with the prognosis and also helps while you're reading the scans. Because if you see a study which has significant calcium, over 400 or over 1000, and when you're looking at the scan, you're going to see if you're not missing any ischemia in these patients. There was one study which had shown that if you have over 400 calcium, about 30% of these patients would have ischemia on myocardial perfusion imaging. So then we look at the scan, you can look at the top four rows. And on that the top, we are looking at short axis images starting from the apex, going down towards the base. The upper one is the stress and the bottom one is the rest. And the stress extending from the apex going all the way down towards the base. You can see there's a uniform distribution of the tracer on short axis. And don't see any defect on short axis. And looks like that it's a normal perfusion study by looking at the counts from apex to the base on short axis. Then we look at the horizontal long axis, which starts inferiorly towards the left and goes on the right from inferior to anteriorly. And this is just like an apical four chamber view which we have on the echo. And here again, this uniform distribution of the tracer and don't see any defect. This is an ammonia study. So with ammonia study, you're going to see that the lateral wall counts are less than the septum. If you're used to reading SPECT studies, in SPECT, the lateral wall is harder than the septum. The ratio of lateral wall to septum is 1.2 to 1. So in PET, especially ammonia PET, it's reversed. Septum is harder than the lateral wall. So if you're used to reading SPECT, when you look at the lateral wall decrease counts, you tend to call these as defects. But just remember with ammonia, it's different. Lateral wall counts are slightly lower than the septum. Then if you look at the bottom image, which is the vertical long axis, so vertical long axis starting from the septum going down towards the lateral wall. And this is like the two chamber view on echo. And again, here you see uniform distribution of the tracer and don't see any perfusion defects. So the perfusion study looks normal. Now, if the perfusion study is normal and you have no coronary artery calcium score, so the event rate is 2.5% or less in some studies, which it has shown. But if the same patient who has normal perfusion, but the coronary artery calcium score is greater than 1000, the event rate is 12.3% over a year. So very important that if you have coronary artery calcium score, even if your perfusion study is normal and coronary calcium score is high, that helps you with deciding whether the patient needs any treatment or not. Then after that, what we do is we look at the gated images. Gated images are very important in cardiac PET. In SPECT, when we look at the gated images, those are basically two rest images we are looking at. We look at the rest after the rest gating on SPECT, and then we are looking at rest, which is post-stress, because it's about hour and a half or more after the peak stress when you do the gated images on SPECT. So it's basically two rest images on SPECT. On PET, you're doing it at the time of stress. So if there is any wall motion abnormality or any stunning, you're going to see that more on cardiac PET. So the cardiac PET on gated images, what we look at is wall motion, and we also look at wall thickening. And the other thing we look at is the cavity size. Cavity size with ungated images is smaller with stress and a little larger at rest. And also the stress EF is more or equal to rest EF. So in this case, you can see wall motion is normal. The LV ejection fraction is 54%. LV is mildly dilated and diastatic volume was 169 ml on this patient, but the wall motion, wall thickening looks normal. And then below here, they compare it with the normal database computer and tells you as compared to normal database, if the study is normal or not. So after perfusion, we look at the flow in cardiac PET. So if you look at this image, the yellow arrows are for perfusion and the green arrow tells you the flow. So we do the flow at rest and then flow at stress and then calculate the coronary flow reserve to see if there is a decreased flow in any region of the myocardium. So if you look at this image on the flow at the bottom, the flow is with the milliliter per minute per gram. So the rest flow ranges between 0.6 to 1.10 ml per minute per gram. And the stress flow depends on what tracer you're using. It's, you know, if we're using dibutamine or ragadenosine, that increases your flow about two and a half times your resting flow. If you're using adenosine or dipyridamole, that increases the flow about three to four times the resting flow. But again, if you have a flow reserve, which is greater than 2.5, it's normal. Flow reserve less than two is abnormal and less than 1.5 is severely abnormal. And the flow between two to 2.5 is the gray area. So what we do is we look at the flow in all the regions. So you can see that flow, which is at rest stress on the 17-segment model. And then we divide it according to the vascular distribution. That what's the flow in LAD, at rest and stress, and what's the flow in CERC, RCA, and then the global flow or the total flow we look at. So below those flow numbers, what you can see is time activity curves. So these are the ones which are used to calculate or quantify your blood flow. And if you see these time activity curves, and if you see that the curves are off, then you know that the numbers which you're getting, the flow numbers are not correct. So it's important to look at these time activity curves when you are looking at the flow numbers, rest and stress. So in this patient, the rest flows are normal. I always start by rest flows, because if the rest flows are off, that means if you're getting a rest flow of three or getting rest flow, which is completely off, then I'll be very careful in commenting on coronary flow reserve. Because if the rest flow is between 0.6 to 1.10, I know this is the normal range, so then I feel more comfortable looking at the stress flows and then commenting on the flow reserves. So this is just a little history about cardiac PET and coronary flow reserve. So here in picture, you can see in the middle is Dr. Paul Cannon, and then on the right is Dr. Lance Gold, and then Dr. Shelbert and Dr. Wolfgang. And this is in 1979 at a meeting in Germany, where they first presented the data on dog. A is the top is the dog data, in which they used ammonia, and you can see it's in the RV, then LV, and then in myocardial tissue. And at that time, they looked at the time activity curve and said that you can quantify flow with good accuracy with cardiac PET. And then C is the first clinical study, which was shown in patient who had normal at baseline, and then with stress with diapretamol had LAD ischemia. So quantification is important for diagnosing balanced ischemia, for diagnosing diffuse disease, and also microvascular disease, and also looking for coronary spasm and endothelial dysfunction. So it's very helpful in all these conditions. So what are the characteristics of a normal myocardial perfusion PET study? So on perfusion, you're going to have uniform distribution of tracer. And LV cavity at peak stress is equal to or smaller than at rest. And on gated images, you're going to see uniform and normal wall thickening, and uniform and normal regional wall motion. And peak stress LVEF is either greater or equal to rest left ventricular EF. So what are the cardiac PET CT advantages? So the advantages of cardiac PET are that it's a low radiation exposure. So it's about three times less than the SPECT scan. So for the whole PET study, it depends what tracer you're using is, and if you're doing the coronary artery calcium score or not, but the radiation dose varies anywhere from three to five millisieverts. Compare that to SPECT, it's about eight to 12. So it's three times less than the SPECT. And it's improved efficiency, it's a faster protocol. As you know, if you're doing rubidium, the protocol is about 17 minutes, you're done with the study. And if you're doing ammonia, it's about 90 minutes, you're done with the study, as compared to SPECT where it would take about three hours to do a study. It has improved spatial, temporal, and contrast resolution. So the spatial resolution with cardiac PET is about four millimeter at eight centimeter distance, as compared to with SPECT is about 10 millimeter at eight centimeter distance. And temporal and contrast resolution are also better with PET as compared to SPECT. It has higher system sensitivity, and it's a straightforward and high quality attenuation correction. And the most important benefit is measurement of coronary flow reserve. And also it's used for assessment of viability, inflammation, and infection, which I'm not going to talk about today, but those are important indications for cardiac PET scan. So we'll do the case two, it's a 72 year old female admitted to hospital after a 60 minute episode of chest tightness. There's no association with exertion. Her risk factors were, she was type two diabetic and had essential hypertension. Her resting ECG showed nonspecific T wave abnormality. Her troponins were within normal limits times three. And her past medical history, she had osteoarthritis, and also had anxiety and major depression. And her current medications were lisinopril and metoprolol. So patient underwent PET rest stress, adenosine myocardial perfusion imaging with ammonia. So immediately following the adenosine infusion, she experienced chest pain and dyspnea. But there was no change in blood pressure. There was no change in the heart rate. And the ECG did not show any ischemic changes. So this was her perfusion study. So the top four rows are short axis. Again, starting from the apex, going down towards the base. And we look at it, it's the uniform distribution of tracer on stress images, and also at rest images. And then when we look at the vertical long axis, we see the same uniform distribution of the tracer on stress and rest. And then when we look at the horizontal long axis, again, we see it's a uniform distribution of the tracer. So it's a normal perfusion study. And the TID, transient ischemic dilatation ratio was 1.06, which is normal. And on gated images, the wall thickening was normal. The wall motion was normal. And on the left side, you can see the stress. Stress, left ventricular ejection fraction was 66%. And on the right side, you can see the rest. Rest LVEF was 64%. So stress EF is slightly higher than the rest EF. And the wall motion and wall thickening were normal. So on the Adenosine stress test, we didn't see any change in heart rate or blood pressure. So what would that imply? Number one, patient had inadequate vasodilation with Adenosine. Number two, adequate vasodilation with Adenosine. Number three, possible caffeine ingestion. Number four, any of the above. So would you call it a normal study? Abnormal study? Are you going to say you're uncertain because you didn't see any heart rate, the heart rate didn't rise and blood pressure didn't fall with Adenosine? So just to show you, so this was a nice study by Mishra and group in which they looked at 348 patients without any known coronary artery disease. And they did ammonia with six minute Adenosine study. And look at your Delta heart rate and Delta mean arterial pressure and its relation to myocardial blood flow. So it's all over. So there's really no relation. So having a increase in the heart rate or decrease in the blood pressure really doesn't tell you whether patient had any response to the stress test or not. So for quantification, so ammonia gives you an excellent image. Same thing with rubidium gives you an excellent image. For quantification, the gold standard is O15 water. With water, because it's freely diffusible, the image quality which you get is not as good, but you get absolute quantification with that. So then what we do is we look at the time activity curve and then we use a two compartment mathematical model to calculate the myocardial flow reserve or coronary flow reserve. So what we do is if you look at this, you can see the tracer is in the RV, then in LV, and then you see the uptake in the myocardium. At the base of the LV, at the level of the mitral valve, we draw the ROI and take the counts from there and then take the counts from all the myocardium with multiple ROIs on the myocardium and then apply the two compartment mathematical model to calculate the flow at rest and then the flow at stress. So here you can see on the left, you can see the myocardium, the tracing is not that good. You can see they're missing part of the lateral wall on the tracing over here, but the top image is the stress and the bottom one is the rest. And here, then when you look at down in that table, you can see that the LAD stress was 1.06 with ML per minute per gram, and then CERC was 1.08 and RCA was 0.47. So if you look at the flow, flow is really down in all the vessels, the stress flow. And when you look at the rest is 0.87, 0.93, 0.70. And if we look at the difference between the stress and rest, you can see the significantly down on stress in the RCA distribution. There's also down on CERC and LAD. And when we look at the myocardial flow reserve, you can see LAD is 1.21, severely decreased. Anything less than 1.5 is severely decreased. CERC is 1.13 and RCA is 0.65. So we know that there's significant disease, which is in all the vascular distribution. And then you look at the time activity curve on this, and then the polar plots. So just to show you a couple of examples. So on the top, you can see this, the perfusion image looks completely normal, short axis, vertical long axis, horizontal long axis, uniform distribution of the tracer, no defects present. And then when you look at the myocardial flow on the right side on the table, you can see that the LAD stress flows are good, rest flows are within normal range, and flow reserves are normal, over two is normal. Then when you look at down here, the second image, you can see the perfusion looks completely normal with uniform distribution of the tracer on short axis, vertical long and horizontal long axis. But when you look at the flow, you can see the rest flows are within normal range, but the stress flows are significantly reduced in all LAD, SIRC and RCA distribution. And the flow reserve is severely reduced in all vascular distribution. So again, if you look at A, you can see the perfusion images look normal. Then when you look at the B, what you're looking at is the stress flow. And if you look at the stress flow, red is normal, green and light blue is moderately reduced. And the dark blue is severely reduced and black is absent flow. So if you look at the stress flow, you can see that they're moderately reduced flows. You can see green or light blue. And then on the rest flows, you can see it's completely normal. And then when you look at the flow reserves, again, those are also at the range of about 1.5. So when you look at the calculation, the calculated rest flow was with the normal image, stress flow is significantly reduced and myocardial flow reserve is significantly reduced. So if you were just relying on this, we would call it a normal study. But once you have the information from flow, you know the patient has severe triple vessel disease. So this patient, when you cap the patient, you can see severe proximal LAD disease, CERC disease and RCA disease. So very important. So this is an example of balanced ischemia because you're going to have completely normal perfusion study and flows would help in diagnosing balanced ischemia in these patients and diagnosing severe triple vessel disease. Coronary flow reserve also has a prognostic significance. So it doesn't matter with male and female, there's not a huge difference. So we just use the same flow reserve cutoff points for male and female. So if the coronary flow reserve is greater than two, your major adverse cardiac events are significantly less as compared to the coronary flow reserve, which is less than two. Same thing with the, so it has incremental effect with this if you're looking at some stress score. So if you look at some stress score, some stress score goes up and your percentage of major adverse cardiovascular events go up. Same thing with coronary flow reserve. The coronary flow reserve goes down, you can see more major adverse cardiovascular events. And it's also, if you have a higher, some stress score, which is greater than eight or even greater than four, you're going to see if your flow reserve is less than 1.5, that percentage of your major adverse cardiac event is significantly high. So it's very helpful combining these two to look at the prognostic significance of the PET step. So for the application of quantitative flow assessments, it's help for diagnosis of coronary artery disease to assess balance ischemia. Detection of microvascular disease and endothelial dysfunction. It's very important, especially in female patients who have typical angina. And even if you do their cath is completely normal and their symptoms are very typical angina and those patients looking for microvascular disease with flow assessments with cardiac PET is very helpful. And same thing looking for coronary spasms with cardiac PET is very helpful. So assessment of flow when perfusion may be disordered, but homogenous is important, especially in patient with transplant vasculopathy, patients with cardiac transplant. And to diagnose these patients early, flow assessment is very helpful. And delineation of interventional strategies, surgical, mechanical, or pharmacological. So we'll do a case three, 69-year-old male with exertional chest pain, relieved with rest. His risks are essential hypertension, mixed hyperlipidemia, type two diabetic, and his past medical history of paroxysmal atrial fibrillation. He is on enalapril, metoprolol, torvastatin, and aliquis. He underwent rest, dipyridamole, N13 ammonia stress, myocardial perfusion PET study. Now with this patient, he has, if you look at the pretest likelihood of having coronary artery disease, so you still follow the diamond and Forrester table, which is from like early 80s, 1980s, or late 1979. You can see that this patient comes up to almost high risk of pretest probability of coronary artery disease, or high pretest probability of coronary artery disease. So remember, whenever we are reading any stress study, the things which are important are to see if the patient had any symptoms during the test. Patient complained of chest pain or not. What was the blood pressure response? Did patient have hypertensive response to stress? Or did the blood pressure fall during the stress? And then looking at the EKG changes. Now, if you look at this patient, look at the first EKG on the top left, is normal, low voltage EKG, but it's normal, no STT wave changes. Then you look at, on the top right, this was the second ECG done at the time of stress. You can see that the ST elevation in one, and AVL, mild ST elevation, and you can see there's some ST depression in three and AVF. Then at peak stress, you can see the ST elevations in one and AVL, and with ST depression, significant ST depression in three and AVF. And then this was during recovery. This was patient scan. So here, if you look at the top four are the short axis, and on the top four, you can see the infralateral wall and basal inferior wall. You can see that there's decreased counts of the tracer and on stress images, and which normalizes at rest. So this is a large area, extends to mid lateral wall, then basal lateral, and then basal inferior wall. So more than four segments involved, and the intensity is severe. So we're going to call it a large size, severe intensity, infralateral and inferior wall defect extending from base to mid. And it's a reversible defect because it normalizes at rest. So then the other thing, which is very important in PET is to look at the cavity size. So if you look at the cavity size on your stress, and then look at the cavity size at the rest, significant difference. And then when you look at the TID ratio, which is the transient ischemic dilation is 1.41. Now with PET, you can have a high TID ratio, even with the single vessel disease. It's not like SPECT with triple vessel disease, you're going to see TID ratio of greater than 1.3 or 1.21. But in PET, you can see that sometimes with a single vessel disease also. Then we look at the gated images. On gated images, we look at the wall thickening and also look at the wall motion. So this patient on peak stress, the wall thickening was not good in the basal lateral and also basal inferior wall, and was severely hypokinetic on wall motion. LVEF at stress was 46%. And at rest, the wall thickening and wall motion were normal and LVEF was 62%. And when we looked at the flows on LAD, the flow, the resting, the first thing I always look at is resting flows. Resting flows are normal. So on LAD, the stress flow is normal, three, and coronary flow reserve was 2.90. RCA was 1.02, and the stress flow was normal with 2.69, but your CERC flow reserve were decreased, were 1.86. So patient underwent coronary angiography, which showed 90% stenosis of proximal left circumflex coronary artery. So we'll do case four. This is a 58-year-old male who was admitted to hospital after four hours of central chest pain and exertional shortness of breath. So after two hours of central chest pain and exertional shortness of breath. His hospital course, his chest pain resolved when he came to the hospital. His troponins were within normal limits, times three. He had past medical history of hypertension, hyperlipidemia, and tobacco use. And on ECG, he had normal sinus rhythm, and there were no ischemic SDT abnormalities. So this was his perfusion study. On perfusion study, you can see that there is, the counts are not uniform. There's decreased counts in the anterior wall, and there are decreased counts in the septum, and there are decreased counts in the inferior wall, extending all the way towards the base. So inferior wall is from base to apex. Anterior wall is from mid-anterior wall, and then apex, there are no counts in the apex. So it looks like this is the distribution of proximal LAD and RCA. And the cavity size, we look at the cavity size, there's a significant difference between the cavity size of the stress and the rest images, and the TID ratio, transient ischemic dilation ratio, was 1.48. On wall motion, the thickening of the wall was reduced in the apex, intraapical, septal, and intraapical walls, and the wall motion was also hypokinetic in that region, and the LVEF was 56%. Rest ejection fraction was normal, and the rest wall motion was normal, and wall thickening was normal, and LVEF was 65%. So the stress LVEF is reduced compared to the rest LVEF. And when we look at the coronary flow reserve, so we always start with looking at the resting flows, resting flows are normal, stress flows are significantly reduced. So a stress flow should be greater than two, and they're reduced, and then when we look at the coronary flow reserve, they are also significantly reduced. So this patient looks like by the flows that has significant trypovascular disease. So the other thing which is important with flows is that if you have on your perfusion study, a defect which is a single vascular distribution, so like on this patient, you can see that this patient has inferior wall severe defect, which is reversible, and which is inferior wall and extends a little bit to the basal septum, and it's a reversible defect. But when you look at the flow reserve in these patients, you see in this patient with flow reserve, your myocardial flow reserve is significantly reduced and inferior, and also moderately reduced in LAD distribution, and also mildly reduced in CERC distribution. So when we look at the angiogram in this patient, you can see significant left main disease, and also significant RCA disease, proximal RCA. So flows also help you, even in patient with a defect in single vascular distribution, the flows can help you to see if the patient has significant disease in other vascular distribution. So coronary angiography showed 90% stenosis of LAD, and 80% stenosis of mid-RCA, and 90% stenosis of large obtuse marginal branch. So patient underwent CABG times three, LIMA to LAD, SVG to OM, and RCA. So we'll do a last case, is a 69-year-old female admitted to hospital with chest pain, which lasted for 45 minutes, and she had mildly elevated troponins. She had past medical history of hypertension and type two diabetes. She underwent REST and LexiScan stress N13 ammonia, myocardial perfusion PET study. So first thing when we look at, is to see if the patient images are fused properly. The second thing which we are going to look for is coronary artery calcium score. In this case, you can see the coronary artery calcium score is 62, and you can see some calcium in LAD, and RCA is not visible over here, but RCA had a 21 calcium score. So total score was 62. And then we look at the fused images, which are pretty well fused, so everything looks good with this. And then when we look at the scan, it looks like slightly decreased counts in the lateral wall, which is normal with ammonia, and mildly decreased counts in the inferior wall on both stress and rest images. But the wall motion was normal on the inferior wall and the other regions, and wall thickening was normal. Ejection fraction was 60% mildly less than the rest of LVEF, and rest wall motion and wall thickening were normal. Then when we looked at the coronary flow reserve on this patient, again, you look at the perfusion on the left, the polar plots, and then the flow. So we look at all the 17 segment models, and then look at the vascular distribution. You can see that the flows, rest flows were normal, and the stress flows were also normal, all greater than three, and the flow reserves were normal. So even with patient with slightly decreased counts in the inferior wall and lateral wall, when you look at the flow reserves, which are completely normal, reassures you that this is a normal study. So coronary angiography showed a non-obstructive coronary artery disease on this patient. So in summary, cardiac PET, myocardial perfusion imaging has higher diagnostic accuracy to detect coronary artery disease as compared to SPECT. The sensitivity and specificity are over 90% with cardiac PET as compared to cardiac SPECT, which are in around 80% with cardiac SPECT. Cardiac PET, myocardial perfusion imaging has lower radiation exposure as compared to SPECT. It's about three times lower than SPECT radiation exposure with cardiac PET. Quantitative flow assessment is useful in diagnosing of balance ischemia. And quantitative flow assessment helps with the detection of microvascular disease, endothelial dysfunction, and transplant vasculopathy. Thank you for your attention.

myocardial perfusion imaging

coronary artery disease

image fusion

cardiac PET

SPECT

quantitative flow assessment

diagnostic accuracy

viability