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And thanks for the introduction. So my name is Shannon. I'm one of the T five doing Cardio Economic Ology. Um My camera is not working anymore, so I've just given up. So we're just gonna have to roll with a green screen, I'm afraid. So I was asked to do this second part of the cardiac side because we kind of rushed through the cardiac because the thorax takes a lot longer. And ultimately, the thorax is probably more important because it's the higher yield um percentage that you'll get in your exam. But it's still important to go through high yield easy cardiac stuff. Um So we're going to go through constrictive versus restrictive cardiomyopathy, which is a common um exam scenario because a lot of people get mixed up patterns of LG coronary artery territories and viability looking at anomalies and which one's a higher risk? Um Quick chat about prospective versus retrospective cardiac ct gating as that's big right now. Um And then we'll go through cardiac chamber enlargement with different shunts and then go through anomalies again. So, as well, last time I'm going to just do it through questions because ultimately, the exam is question based. And my personal opinion is that you learn the most from just doing questions. So let's crack on no need to waste any time. So 82 year old male with a recent diagnosis of multiple myeloma presents to cardiology, outpatient with worsening shortness of breath and peripheral Adema. His echo shows severe by a child irritation L V normal in size with a concentric LVH and preserved ejection fraction. His myocardium is noted to have a speckled appearance that patient undergoes a cardiac MRI. And there was difficulty in knowing the myocardium during the T I scout based on the most likely diagnosis, which of the following is at least likely to be seen on the cardiac MRI. So I'll give you a moment to answer. There should be a pole that should cop up in your chart um which you should be able to on. So I can then see the response is. So I think there's about 20 of you. So there's five responses so far. So if we'll give it another minute or so, remember, this is all anonymous. So if you get it wrong, no one's going to know what you said. And plus that's not the aim of this to catch you out. So just answer what you would in the exam given this coming up relatively soon. So it's a good opportunity to just try out what you would have said, God. Okay. So the majority are going with diffuse sub epicardial enhancement and you would be absolutely correct. So the reason for that is, so let's look at the question and see what they're trying to tell you. Remember every part of the question, the description has to have meaning. So they're not going to say things unnecessarily. So just bear that in mind, 82 year old old man, multiple myeloma. So you have to say, why is he saying multiple myeloma that's obviously linking to something and in the heart, if you see multiple myeloma and heart, just automatically you think amyloid. So we've kind of already got a diagnosis of amyloid, um worsening shortness of breath and edema again fitting with Amyloid, his echo shows severe by atrial debilitation. So then you're thinking, okay, I know that two things commonly caused severe by a child irritation or a few things. You've got cardiomyopathy, which is either constrictive or restrictive. And I've got a uncontrolled af so they're your three common things that would cause by HDL debilitation for this exam. Okay. So you've got three differential. So far LV is normal in size with concentric LVH and preserved ejection fraction. His myocardium is noted to have a speckled appearance. So this is a buzzword. So in your exam, if you see speckled LV on echo, the answer is Amyloid, obviously, we don't do echo, but they could easily put echo findings in because cardiac imaging, you're expected to have an understanding, basic understanding of echo. The patient then undergoes a cardiac MRI. And the this is the key really difficulty in mulling. The myocardium is basically the most sensitive uh sign for cardiac amyloid on late gadolinium enhancement. So all of those features are guaranteed to give you amyloid. So now you have to think okay based on that, which of the following is least likely to be seen on cardiac MRI. So let's start with the normal thickness pericardium. So we would expect to see a normal thickness, pericardium. What we wouldn't expect to see is so um diffuse subepicardial enhancement because remember the cardinal feature of cardiac amyloid is diffuse subendocardial enhancement that doesn't fit a coronary territory. And I've got a nice picture of it that's coming up in a second. Um dilated dilated IVC and hepatic veins implies that you've got back flow of blood. So remember if you're unable to pump blood through a stiff ventricle, you're basically both of your atrial going to get bigger. And then the backflow from the atrium is either the lungs which gives you Pommery Dema or the IV C and S V C. So that's why you get debilitation and reduce global longitudinal strain is basically any patient who's got any restrictive or constrictive cardiomyopathy is likely to have reduced global longitudinal strength. So that's why the answers be. So the next question, 63 or female plan to cardiology, outpatients with progressive shortness of breath on examination. Her JVP is raised with shifting dullness in the abdomen and peripheral edema. Her echo shows restricted filling of both ventricles and mild by atrial delegation. There is septal bounce which is accentuated with inspiration. LVEF is 58% and R V E F is 61%. There are small bilateral pleural effusions and no pericardial effusion. What is the most likely diagnosis? So I'll give you a minute or so again. Just remember everything that's mentioned. There's pathognomonic uh feature in the question that will tell you the diagnosis. So seven responses, bit of a mixed bag, but the majority of going with B so split between B and E. Okay. So the answer is B so let's go through it again. So 63 year old female cardiology, outpatients, progressive shortness arrest, that couldn't be anything right? That doesn't really help us but implies there is something that's symptomatic JVP is raised with shifting dullness in the abdomen. So shifting dullness is ascites peripheral edema. So in the content, this is a cardiac question because they've told you that the patient is in cardiology, outpatients. So the chances are it's gonna be a cardiac problem. They've got right sided heart failure and you know that because they've got shift ascites and peripheral edema, right. So right sided heart failure causes the edema. Left sided heart failure causes pommery edema. So the cough, the shortness of breath, etcetera. Her echo shows restricted filling of both ventricles and mild by actual delectation. So this line gives you two possible diagnoses, either constrictive cardiomyopathy or restrictive. Remember, anytime they mentioned, restricted filling of the ventricles with by atrial delectation, you're either gonna think restrictive cardiomyopathy or constrictive cardiomyopathy. And then it's your decision to decide which one of those is going to be correct. So then there has to be something else. If there's questions stopped here, you wouldn't really be able to decide whether it's A or B. So now they said there is septal bounce which is accentuated with inspiration. So that is pathognomonic for constrictive cardiomyopathy. So, if you ever read septal bounce, which is accentuated with inspiration, there is no alternative. The answer is constrictive cardiomyopathy and the way they could word that as an alternative is what anatomical abnormality would you look for in this patient? And you're going to look for a thickened pericardium or a calcified pericardium. The reason why it's not C is because you're told that the left ventricular ejection fraction is 58% and the right ventricle ejection fraction is 61%. And congestive cardiac failure generally, by definition would imply that those would be reduced to less than 55%. So it can't be seen acute pericarditis shouldn't present with remodeling of the ventricle cause it's an acute process, right? So this is there's restricted filling with by atrial irritation. So that implies that something is kind of relatively long standing and there's no pericardial effusion, which is the most common imaging manifestation of pericarditis that we see on imaging dilated cardiomyopathy. Again, there's nothing here that says that the left ventricle is dilated. Remember, dilated cardiomyopathy isn't referring to the atria. You don't if the atrial dilated, but the left ventricle is normal, that is not a dilated cardiomyopathy. So nothing in the question says it's a dilated cardiomyopathy just as normal ejection fraction, restricted feeling. So it can't be. So again, your answer would have been between A and B and because of the septal bounce, your answer is B and we'll go through why? In a second. So let's just talk about L G because this is exam fodder so easily a question could be on their timings and what's the appropriate timing. So remember what is L G? Basically, you're giving gadolinium and then you're waiting because gadolinium distributes itself in the interstitial and extracellular space. And remember everything that takes up gadolinium will shorten T one. So the relative contrast enhancement of normal and diseased myocardium depends on when imaging occurs. So in the early stages, so like 1 to 3 minutes. So in this section here, gadolinium will predominantly be within the blood poor and normal myocardium. So you can see normal myocardium and blood pool, higher concentrations of gadolinium, which implies that they will be brighter. Whereas in abnormal myocardium, the gadolinium levels will be lower as you get in towards the later phases. So we're looking at 5 to 20 minutes. Gadolinium then washes out of normal tissues quicker but is retained by the pathological ones. So, for example, in myocardial infarct, you can see the purple line, it's very slow to take up gadolinium, but it's also very slow to wash out. So if we image any time around 10 minutes, we will see that the concentration of gadolinium is going to be much higher in the diseased myocardium compared to the normal myocardium. And that's why we say it's late gadolinium enhancement because there is going to be a relatively higher percentage of gadolinium in the diseased tissue than there is in the normal tissue. And that's why it's important to do imaging at 10 minutes. As you can see if you did it two minutes, it would just be a mixed, it would be the opposite and then it can become confusing. Remember 10 minutes is the optimal time. And then there's this principle of my cards, your Knowling, which is what we said is the key sense to feature to differentiate amyloid from the other cardiomyopathies. So what is called, what is myocardial mulling? So that is basically it's a specific pulse pattern which you don't really need to know about. But the idea is that they use a specific M R physic physics pulse that nell's signal from a specific tissue to accentuate pathology. So in cardiac M R, they will use a specific pulse to null the signal from normal myocardium during delayed imaging. So that means that they're normal my card, it will be dark and the abnormal myocardium will be really bright and therefore, you've got a good contrast between disease and normal. Um These inversion recovery passes have a parameter called an inversion time. So to null normal myocardium, the MRI technician will basically do MRI pulses at multiple inversion times and then we'll find the time when the myocardium is dark. When normal myocardium is dark, the diseased myocardium will be relatively bright and that's all you need to know. So for the sake of your exam, the question will be which of the following is the most sensitive uh parameter for diagnosing amyloid on L G and it will be an inability or a difficulty in Knowling the myocardial blood poor or a very prolonged inversion time. Okay. Um So that's that this is cardiac amyloid on imaging. So what you can see is this is all abnormal. Remember, normal myocardium is dark disease. Myocardium is bright because we did it in the later stage. So 10 minutes. So you can see all of this is abnormal sub endo car deal. So the closest layer to the to the blood is the subendocardial. This lay on the outside is the sub epicardial layer. So remember, amyloid is diffusely involving the sub endocardium. If it was a coronary, imagine if this was an in fact, you wouldn't have an in fights that affect all three coronary artery territories. So that's what makes this more likely to be amyloid rather than an in foot, which also results in sub endocardial uh announcement. So constricted versus restrictive cardiomyopathy. So, clinical presentations are similar. So that doesn't really help you. So they both present with right sided heart failure or left sided heart failure or both, they both have buy actual debilitation. Although if they say severe, the chances are you're more like to be looking at restrictive pathology and now they're differentiators. So if they say septal bounce, then it's a constrictive cardiomyopathy, and then the answer will be to look at the pericardium from doing a CT um to look at pericardial calcification. If they say equilibrate a shin of diastolic pressures, that's classic for constrictive pericarditis or constrictive physiology. And they're not expecting you to know what that really means. I mean, you can dive into it um and understand it. But ultimately, this exam isn't trying to make you a specialist at cardiac imaging. The idea is to understand the bread and butter and this is the basic overview of what you need to know. So, septal bounce, constrictive pericarditis, um constrictive cardiomyopathy, equilibrate Asian of diastolic pressures, constrictive cosmo opathy, inability to null the myocardium restrictive cardiomyopathy, diffuse subendocardial enhancement that doesn't fit a coronary artery territory, restrictive cardiomyopathy. And they are the two main ways that you're going to be able to differentiate the two. Uh because most of you will be left with either a constrictive or restrictive as your choices in your, in your single best answers. So next question. So 42 year old male is brought in by ambulance with acute central chest pain with a raised troponin. He has non regional S T N T wave changes. He has taken for a catheter angiogram which shows unobstructed coronary arteries. He has a cardiac MRI which shows raised t two values in the basal to mid lateral wall and a thin rim of sub epicardial enhancement in the basal lateral wall. What is the most likely diagnosis? Yeah. So remember just all give it a go, just answer it and see what happens. I got nothing to lose. So for everyone's gone with viral myocarditis, one person's one for sarcoid, I'll give you all a couple of minutes. Yeah. So the correct answer is fire myocarditis. So it's a split and I I understand why a lot of you would say sarcoid because Sarcoid technically does everything but this is classic. So let's go through the question and we'll try and understand why. So this is the key. I would just learn this. There's only four things to learn. So if you see chest pain, acute chest pain and erase troponin, your answers are going to be acute M I or myocarditis or the non cardiac stuff I E acute P or acute aortic dissection. Now, that is very basic, but that is actually the truth. Um your, this is what they're testing. Let's be honest, we're not cardiologists and neither are we like in A and E. So we for SBA type questions based on clinical scenarios. This is kind of what it's going to be like acute chest pain with a race troponin. You're either looking at an MMI which could be embolic or myocarditis or the non cardiac causes of chest pain like a Q P or aortic dissection. So let's go back to the question. So he's brought in, he's got chest pain. He's got a race troponin. He's got non regional S T and T wave changes. So basic interpretation of E C G, if they say non regional, there's probably not an acute ST elevation M I that's fitting into a Coronary church. It's not a proximal led or circumflex or RCA touch. In fact, he's taken for a Cath angio which shows unobstructed coronary arteries. So that doesn't exclude be because remember there can be calcified disease that's not seen on angio. So it doesn't mean it's not to be. So you from, for me, at this point, my answers would be either a viral my colitis or B I don't think it's C D or E based on what we just said before that your main differentials for acute chest pain with, with raised troponin is either acute my or my colitis. Then you do an MRI which shows raised T two values in the basil to mid lateral war, raise T two values. What does that mean? So, what causes an increased T two that goes back to your physics, which is edema. So you've got focal edema in the basal to mid lateral and you've got a thin rim of subepicardial enhancement in the basal lateral or so taken together. So if we stopped at this point, and then we only had a patient with cardiac MRI which shows edema in the basal to mid lateral war with subepicardial enhancement. I agree. You could argue that maybe it is sarcoid because Sarcoid can technically do everything. But in the context of the rest of the question, Sarcoid is not correct. Um And the only correct answer in this situation is viral myocarditis. Um So, does that make sense? Um Just remember, sarcoid is classically multifocal involvement of the L V sub epicardium classically, it will tell you there's a thick layer of subepicardial enhancement involving the basil septum and extending around the RV free wall there. The words that you're looking for to get classical sarcoid in a question, remember that when they write an S B A, you have to get agreement between multiple clinicians and everyone has to agree that that answer is can only be a the chance of you getting a question where everyone agrees that the only diagnosis is sarcoid is unlikely. So if it is going to be Starkwood, they're gonna mention specific things like multifocal subepicardial involvement, basil septum and RV free wall, then you can say sarcoid and it shouldn't present acutely with chest pain like this. Why is it not D so I think one of you put dee um So ARVC is or arrhythmogenic right ventricular cardiomyopathy is basically fibro fatty infiltration of the right ventricle. So, they're either going to say that they're going to say there is fatty infiltration of the right ventricle of the interventricular septum or they will covertly say there is reduced T one in the RV free wall or in the interventricular septum. Okay and reduce T one in cardiac either means fat infiltration or it means iron. So there you're to differentials for reduced T one in the myocardium um and they have to give you something else. So for ARVC, there's a strict criteria which involves regional right ventricle, right ventricle, regional wall motion abnormality or disc in easier a dilated right ventricle. Uh in addition to micro aneurysms of the RV, free war, so they will have to give you a history of arrhythmias because remember the first line in this condition is arrhythmogenic. So if they don't say arrhythmias and they don't say there's a family history, the chance of them asking you the chance of that being the right answer is pretty low. Okay, remember they're trying to test the common things that you should encounter. So the chance of getting a question where ARVC is the correct answer is unlikely. The only reason I'm talking about it is because if you actually know what it is, you will then be able to dismiss it in your exam. Remember, acute chest pain, raised troponin for the sake of the exam. Acute M I including embolic. In fact, remember, even if, if they say the question could easily say he's 60. Here comes in with acute chest pain where they raised troponin, they do an angio, there was nothing obvious. His cardiac MRI shows a subendocardial in enhancement in the mid anterior wall. So you've got subendocardial abnormality involving a single coronary territory. That could still be an embolic. In fact, just remember that you don't just don't let the unobstructed coronary arteries fool you. Um or it can be viral, my colitis or A Q P or dissection like we spoke about this. You just need to learn. Um I would take a picture of this. I think this is from Radio Pedia um or radiology assistant and just learn it. There's not that many to learn. Um I think I've got a picture of the high yield stuff. So this is L G is gonna come up so late. God is going to come up in this scenario, dilated LV with septal mid wall enhancement. DCM. No questions dilated LV with a combination of transmural and subendocardial LG, ischemic cardiomyopathy. It's going to be uh cory artery related a nondilated LV with subepicardial G E in the basal lateral wall, most likely viral myocarditis, nondilated LV with concentric LVH and mid wall LG in the basal lateral walls. Remember, basal lateral comes up multiple times, but it's the rest of the secondary findings that will point you towards different diagnosis. So this one's got concentric LVH with mid wall LG in the basal lateral wall that's fabrics and then again, nondilated LV with asymmetrical septal LVH with mid wall LG in the hypertrophy, septum hypertrophic cardiomyopathy. And then at the end, just remember anything with reduced T one is either fat. So that's ARVC or A L V C fab berries or iron deposition. Remember fabrice is basically fiber fatty infiltration, which is why it's also reduces Taiwan if I'm going to quickly or you want me to rephrase something, just pop a message in the chat and then Jordan will alert me hopefully. So next question, 86 year old female has been referred for an urgent outpatient to VCT for preoperative planning for an aortic valve replacement due to severe aortic stenosis. Bedside investigation shows sinus rhythm, heart rate of 90 and BP of 100 over 60. She has had a previous stroke in 2019. You were asked by the radiographer to prescribe the necessary medications, which of the following is recommended. Just give that guy. So I'll just give you a minute. Uh That's that. So this is a big split basically um between A C B actually. So it's basically just a big split. Um The actual answer is a which is fine. I think it's really important. This is for if I was setting a question. And if I think a lot of my consultants, if they were setting a question, I think they would very happily write a question on this because uh um cardiac CT is booming, right? It's massive. It's now in the curriculum as having to be independent. So it's really important that everyone who's coming through uh to a and to be now or should be familiar with cardiac CT. And that includes prescription of basic meds and knowing the side effects and the contraindications as a rule of thumb. If they say to V and they say severe aortic stenosis, the chances are you don't give drugs because why? Because think about it, if you're able to evolve is tiny and not much is getting through. If you give G T N, you're gonna vase a dollar everything. Remember, your cardiac output is already probably reduced because your valve is tiny. So there's not really much getting through your uh your aortic valve. If you then give G T an invasive dollar, everything, you're gonna result in a massive BP drop. So you don't give G T N. And again, remember your um equation for cardiac output is heart rate, time stroke volume. If your stroke volume is reduced, a lot of these patient's are reliant upon an increased heart rate to provide cardiac output. If you then have low stroke volume and then you artificially lower the patient's look heart rate by giving a beta blocker, they're cardiac output is going to drop and fall and they might have a syncopal episode. So the answer is E so to V with it and they mentioned specifically severe aortic stenosis, no medications. And just remember this table, right. So, remember you can see severe aortic stenosis is contra indication to bleeds blocker and severe aortic stenosis are contra indication to G T N. So it's one of the only ones that's contraindicated to both. So this is um a very easy question to ask any exam to be on any of this is is very fair. Um I think last time I had put the past medical history and verapamil that could easily be slipped in patient's known hypertensive on verapamil. Which of the following would you like to prescribe? And you shouldn't give beta blockers in someone who's got who's on verapamil because the combination of the calcium, this type of calcium channel blocker with beta blockers will result in an asystolic uh profound BP drop. So I just recommend just sitting 10 minutes, 15 minutes looking at the contraindications to both because this could easily come up. I'm not going to bore you and go through each single one because this is just a table that you can find anywhere. You can also pause it, take a picture, learn it yourself and it's probably worth learning the indications. Um So that's the common indications on the left. So these are the reasons why we do see TCS, either chest pain for typical or atypical grafting, cabbage, unexplained, breathlessness or a non diagnostic invasive angio to look at anatomy. So next question, 81 year old patient is admitted to the emergency department with acute chest pain and a raised troponin. He's taken to the cath lab which shows severe triple vessel disease with no convincing target for angioplasty. He's referred for a cardiac MRI to assess viability. LG. Imaging shows 75% subendocardial infarct in the basal to mid anterior wall, 25 to 50% in fat in the basil to mid inferolateral and a transmural in fat in a basil to mid inferior wall, which of the following quandary territories would be most likely to benefit from revascularization. Just give it a go and see what you think. So your split between B and D, it would be good to know why. What makes you think that? So it's a bit mixed, bit of a mixed one. So I'm going to disappoint everyone and the answer is actually a so just, but that's fine. That's the whole point of you being here. So now why is the answer ray? So, so this is how you split the heart. And again, just as a simple question, you could easily be asked, what is the coronary artery model that's used? And it's called the aha 17 segment model for distributing the heart into 17 segments or cutting the heart into 17 segments. And the reason why is you go anti clockwise. So you split the heart into three. So you've got the base, which is this bit at the top next to the valve. Then you've got a midsection and you've got an apical segment. And you basically, what you need to learn is that the base for ease the anterior wall and the anteroseptum and the majority of the apex is supplied by the lady, the infra septum and the inferior wall is supplied by the RCA. And the lateral wall is supplied by the circumflex. Okay. So we'll just reiterate anterior wall and anteroseptum and the majority of apex is L A D inferior wall and inferoseptum is R C A lateral wall is circumflex. So if you can go back to the question, so that's 0.1 point two is viability is defined as anything less than 50%. So anything that is greater than 50%. So 50 to 75 or 75 to 100 is non viable. And therefore, that means that the in fact, this is, is so high or so significant that even putting a stent in is not going to improve the function of that muscle. So the muscle is over 50% dead. And therefore, no, there's no benefit in trying to revascularize it. If there is an infarct that is 0 to 25% or 25 to 50% then the data shows that there is a good chance that, that if you revascularize or stent that vessel or do a cabbage, that, that muscle when it gets more blood um through a stent will recover and function. So that's said to be viable. So the key number here is 50 less than 50% viable, worth revascularizing, anything over 50% is classed as non viable and therefore there is no benefit to revascularizing. So now why is the answer? A the answer is a because let's go through why LG shows 75% in the basil to mid anterior war. Remember what we said, anterior wall is led and it's 75%. So we know that now L A D is not viable. So whatever says L A D in it cannot be correct. So B and er eliminated. So we're left with A C and D then it says 25 to 50%. In fact, in the basal to mid infra lateral wall. Okay. So we've got a viable infarct in the lateral wall and we know that lateral wall is circumflex. Okay. So we know that circumflex as is good. So now we're left with only D or A as the possible answers. And then the last sentences and a transmural infarct in the basil to mid inferior wall. Remember we said inferior wall equals R C A and it's transmural. So that means it's non viable transmural basically means of 100%. That's the equivalent nomenclature. So now you're only left with a, so A is the only one that's viable. I hope that's clear because this is comes up year on year. This is really classic exam type questions. So this specific question you need to know and you need to know the coronary territories and you need to know, remember that 50% is the magic number, anything below 50% worth revascularizing, anything above not worth it as a side point. And just so you don't get tricked. Remember that this is assuming that the patient is right dominant. So right, coronary dominant would be inferior wall is R C A. If the question said left circumflex dominant, then that means the majority of the inferior wall and lateral wall will be is supplied by the circumflex. That's the only difference. The chance I find it really hard to believe that they're going to ask you a question with this type of my card in fight and say that the patient has left dominant. So it's worth knowing that the majority are right dominant. And if they haven't said, then it means that they are assuming that the patient is right dominant, okay, just just in case. So some of you whoever was here last time might remember this question, but I'm going to go through it again because it's really important and comes up a lot. So 21 year old patient was referred to cardiology with a pansystolic murmur heard at the left lower sternal edge. Echocardiogram shows the presence of a perimembranous VSD which cardiac chamber will enlarge first. Okay. So it's a split between A N C which is fair, give you another 30 seconds. Just this is currently seven responses 13. Okay. So it's between a bit of B and maybe see. So the answer is a, so whoever wasn't here last week, the reason is the most common VST is a membrane, this fiesty. And what that means is it's A VST that basically goes from the left ventricular outflow tract directly through the membrane. It's part of the septum into the right ventricle outflow tract. So you can see the shunt is going directly into the right ventricle outflow tract. It's actually bypassing the right ventricle. So the first um jets of blood goes from left venture and outflow tract into the palm tree trunk. So therefore, because it bypasses the right ventricle, then it can't, the right ventricle can't be the chamber that receives the most blood first. So think about it now that it's gone into the right ventricle outflow tract into the palm tree trunk. It's gone from the pommery trunk into the palm, the arteries and then it's gone from the palm your arteries into the pommery veins and it's gone from the pommery veins into the left atrium. So the first chamber to receive the most amount of extra blood is actually the left atrium because remember the membranous septum, the defect goes from the left ventricular outflow tract directly into the right ventricle outflow tract. So it bypasses the right ventricle. So that's the reason why the right ventricle isn't the correct answer because it doesn't receive the blood first. It's the pommery trunk that receives the blood first and then that takes the blood all the way around to the left atrium. So first chamber to receive the most amount of blood is the left atrium. I hope you understand like that's very important concept. If it said there is a muscular VSD, then that means that the blood goes directly from the left ventricle into the right ventricle. And therefore the answer would be correct that it would be the right ventricle that chamber that enlarges first because the blood is going to be going directly from L V two R V. But this specifically says member and accepted. Remember member, this is the most common vst. Um Remember remember this fiesty Ella enlarges first muscular VST RV, enlarges first PD. A some of the pedia is a abnormal connection or a remnant connection from the aorta to the pommery artery. So again, the first chamber that's going to receive more blood is what it's going to be the left atrium, right, because it's gonna go aorta pommery artery, palm vein, left atrium is the first chamber in a pedia is left atrium asd goes directly from left atrium too, right atrium to the first chamber that will be enlarged. It fits what you'd expect. Is this the right atrium? Oh, that's clear. So next question, 34 year old female is referred for a CT PA for investigation of pommery hypertension. The palm tree trunk is dilated, measuring 36 millimeters but there is no evidence of acute or chronic pommery emboli. There are three pommery veins draining into the left atrium under the right upper lope of pommery vein drains into the S V C. The right side of cardiac chambers are enlarged. There is no pommery fibrosis or most status is um in the lungs. What is the most common association with the abnormality described? Okay. Okay. I'll just give you a moment. So the majority of you're going between A N C and I understand why. So, first of all, what's the diagnosis? So she's got hungry hypertension because her trunk is dilated, but there's no p so there's meant to be four palm re veins to on the left, two on the right. And they're all meant to drain into the right lead to the left atrium, but we've got to write up low one that drains into the SPC. So that's partial anomalous pommery venous return. And as crack, the court would say, when you say Pat VR, the answer is sinus fimosis, okay. Um So the common association with a Pa Marion ominous venous return is a sinus. Vanessa's asd for those of you who have said, see, I suspect that's because you're aware that the most common um A S D is the second um type which is accurate. But in the context of an anomalous pommery venous return, the most commonly seen association is the sinus vinosa say ST So that's why A is correct Austrian prime um is usually associated with things like a mitral cleft. Um and it's called an atrial ventricular septal defect. And is the one that you would expect to see a history of Down syndrome or an endo cardio cushion defect in the history to expect you to diagnose that without any of that history, I think is unfair and therefore unlikely. Um The reason why it's not d is because it just isn't. Um And remember what we said about what chambers tend to enlarge first. If we're talking common things being common, then the left sided cardio chambers would enlarge first if it was A VSD. Uh and same with the PD A. So this is just a recall question. If you remember the association, you'll get it right. But for those, you didn't get it right now, you know, if you see anomalous pommery venous return, the answer is sinus stenosis. What is the most common site for anomalous pommery venous drainage in Scimitar syndrome? Again, this is a recall question. So you're really going to know it well, you were and either is fine because then you will know it from today. Just give you 30 seconds okay. So the majority of you said a which is correct. So, remember, Scimitar syndrome is basically a hyperplastic lung that's drained by an anomalous pommery vein into the systemic venous system. So you're going to have a small lung with anomalous drainage that's most commonly um into the IVC. It goes IVC, right atrium portal vein bizarre. But that's the way is IVC, right atrium portal vein. Um Remember if you see hyperplastic lung and a normalised primary venous return, the answer is scimitars and dream. So these are just your common associations that could easily come up. So, sinus fimosis with a pat VR or partial anomalous primary venous return. Austrian primum with Down syndrome will be associated with mitral clift and mitral regurg. Do they have to give you something like that? Aussie? Um Secundum, most common. So, next question, 34 years, I can't speak. 34 year old Bell was admitted to cardiology award with chest pain and a raised troponin. He underwent an inpatient cardiac angiogram which demonstrates unobstructed coronary arteries. However, the cardiologist could not engage the RCA and his concerned about an anomalous coronary artery, which of the following is a gold standard test to confirm the diagnosis. Just give you a moment. So majority of you have said a just good. So is the correct answer. Um And we'll go through a bit more about that in a second. Let's just do the follow up part. So, ct cardiac angiogram confirms the presence of an anomalous right coronary artery arising from the left main stem with a short into arterial course. Which of the following would be most useful to confirm whether this represents a hemodynamically significant anomaly. This is a hard question, hard question, but relevant, I'd call it a differentiated question. We'll just give you a moment to answer. So, split between A B and D and a bit of E. So basically split majority of said D, the correct answer is B. So remember the mechanism of Axion of adenosine is to vezo dilates. Basically, the end effect is to vasodilator, the quarry arteries. When we say anomalous, of course, what we're trying and we're saying into arterial were saying that there's a slit saying that there's an artery that's basically passing between the aorta and the pommery trunk. And what we're worried about is that during exercise that as the stroke volume increases and the aorta expand, it's gonna then occlude that vessel. So if we just vasodilator, everything, we're not really proving whether that anomalous coronary artery territory, anomalous coronary artery is actually doing anything pathological. What we need to do is basically mimic exercise. And the way we mimic exercises by using a drug that's iron, positively ionotropic and inotrope, it basically means increasing the contractivity two with the name of increasing the stroke volume. Um And if we increase the stroke volume, where there for mimicking the true physiological changes of exercise and the the aorta will expand and the stroke volume increases. And then we can see whether that anomalous right quandary is being occluded um during exercise because then that represents a true risk for sudden cardiac ter okay. So anything that says dobutamine is the correct answer except e because they don't do that, that's nothing. So the answer would be debut to be in a stress echo or dobutamine MRI would be the correct answers. Adenosine isn't useful to assess hemodynamics significant in anomalous coronaries because of what we just said it just vasodilator. We need a true mimicker of exercise. So hard question but makes sense. And now you know it. So what are the high risk features? Um Again, it could easily come up as which of the following is a high risk feature for an anomalous quarry. So you've either got slit like ostium, an acute take off angle and inter arterial course. And you can easily play on words here and call it an inter atrial course. Remember it's inter arterial. So it's in between the two arteries, right? Ventricular outflow tracks and aorta. So it's an inter arterial course, not an inter atrial course and an intramural course. And intramural course basically means that the proposed theory is that these slit like origins are running within the wall of the aorta. And if they're running within the wall of the aorta to a mural, and then that means that as the patient exercises and the aorta expands. Then that basically hits the blood flow expansion will then compress the anomalous Connery against them, the inner lining and cause occlusion. The most common cause of sudden cardiac death is with an anomalous left coronary artery arising from the RCA. Remember it's that way around anomalous left main stem arising from the RCA is much worse than the anomalous right coronary arising from the left. Okay. Good high yield exam question that remember there are two types of anomalies. You can either have an anomaly of origin or an anomaly. Of course. So for example, anomalies of origin are ones that arise directly from the pommery artery. They're always malignant, okay. Any anomalous coronary that arises from the primary art is always malignant. And why is that because of coronary steel? So, Corey artery steal basically means that because the pressure in their primary artery is less than the coronary because the coronary artery is a systemic circulation, the primary artery is at a lower pressure. That means that the blood flow will move from the coronary artery, which is higher pressure into the pommery artery, which is lower pressure. So, therefore, you get a coronary steal phenomenon. And then that means that that core er she will not be perfused and that myocardium will therefore die. Okay. So that one is always malignant with regards to courses. Then you've got an inter arterial course is the concerning feature because it increases the risk of sudden cardiac death. The three phrases below are could easily put in a question to confuse you. But these are all benign. So retro aortic pre pulmonic and septal, these are all benign features and you wouldn't worry, remember it's the inter arterial, of course, the slit like origin the acute angle. Okay. They're the ones that you worry about. So these are some examples. So this is an anomalous right coronary arising from the left. So you can see acute angles. If you were to do an angle like this, it's about 10 degrees. And you can see that it's got a slit like origin to look at the origin on this one. Nice and big, tiny here. So that's a slit like origin and it's running between the aorta and right ventricle, right ventricle outflow tracks. So it's inter arterial. So when we're doing the dobutamine, we're trying to do is expand this vessel so that it compresses against the right ventricle outflow tract. And then includes that. Then we can tell whether this is a true uh malignant cory artery. This is an example of a septal cory artery because it's going in between the right ventricle and left actual through the interventricular septum. You can see it's nice and big and is benign and doesn't really cause any problems. And this is an example of a retro aortic circumflex. So you can see that that it is going behind the a water. This is another benign one, okay. 42 year old patient is referred for a cardiac CT for 80 Porteous pay in her resting heart rate is 52 BP is 1 10/60. She has no previous medical history. What would be the optimal time for data collection? You should get a question coming up any second if you haven't already make it. All right. All right. So majority of you have said mid sisterly, mid I ST just give you 30 more seconds. Okay. So the answer is b so Corey artery motion is typically minimal during diastasis, which occurs after rapid ventricular filling, which is usually at mid to end diastology. N sisterly is usually another phase of relatively little cardiac motion that can be used in patients who have uh tachycardic um uncontrolled tachycardia. And the reason for that is because in tachycardia, it is the diastolic period which shortens the end systolic time remains the same. So if the patient's really tacky, a question could easily say the patient's persistently tachycardic despite um adequate um IV beta blockers, what would you, how would you image? And the answer is most likely going to be um and systolic imaging. But in this patient, you've got a heart rate of less than 60. She looks good, looks like gonna be a good scan. So you go with prospective imaging in the midst to end diastole. So this is your normal are are interval. This segment here is about 250 to 300 milliseconds. And then you can see diastole and normal patient is much longer than sisterly. So you want to try and target roughly around here, you've got much more time to play with in diastole. So that's why diocese usually the optimal. But in Tachycardia, you can see the what shortens is the diastolic periods, the diastolic period is like more than half. But the systolic period says to say so you're more likely to get an accurate stable coronary motion in end systolic imaging when the patient's really tacky because it's more reliable. Remember that's in tachycardia, don't get confused. Um Prospective gating just means that your only imaging at a specific time in the cardiac cycle. So you basically because remember in cardiac CT, they're all SCG gated. So the patient's attached to a scan, er constant E C G monitoring. It knows it basically looks at the last 10 heartbeats and says okay, it's your rough are orange full as 1000 many seconds, your heart rate's 50. So we're gonna if you and then you select as a user, you say okay, we want mid to end of yesterday. So then the scan was okay. I'm only gonna scan for this short segment only and then that minimizes the dose because then you're not constantly acquiring data throughout the cardiac cycle. And that's why cardiac CT is massive now because you can get really small doses for very accurate imaging. So next question. 72 year old patient is referred for cardiac MRI. After an out of hospital cardiac arrest, the cardiac MRI demonstrates a dilated LV with akinesia in the mid to a prickle anterior wall anteroseptum and all apical segments. There is a focal outpouching noted in the L V apex based on the history provided. What is the most likely etiology for the outpouching? This is probably a bit out of order in terms of a question, but there's a rationale which I'll teach you afterwards, which is why I want you to be able to answer the question even if the history is a bit limited. So it doesn't matter if you get it wrong. Okay. So it's a split between A and B which is entirely expected. Um The answer is actually a and the reason is, is because true aneurysms most commonly occur as after occlusion of the L A D. And remember what do we have? We've got a con easy in the mid to April anterior wall and the anteroseptum. And we said on the last question, few questions ago that anything that's anti rule anteroseptum is a lady. So a true aneurysm occurs with occlusions of the L A D tends to occur in the anterolateral wall or apex can calcify, rarely, ruptures, false aneurysms usually occur with occlusions of the RCA war circumflex. Remember basil to mid inferior wall, basil to mid lateral wall classically involving the inferior wall, unusual to classify high risk for rupture. And I know a lot of you would have said false aneurysm because it's a cute and that's very fair, which is why I said it's an unfair question. But the rest of the imaging features, the fact that it's an L A D occlusion, the fact that it's involving the LV apex points you more towards a true LV aneurysm. Now, the question would never be like that in the exam, but I just want to hone in on the fact that there are other differentiators other than the narrow neck and the wide neck, which is kind of what you read in the book. And they hate to use things that they the textbook but aren't really realistic. It's actually quite hard to tell the difference sometimes. Um So these are the more these are other secondary signs to look for, to differentiate true versus false. Okay. Next question, you're reporting a chest X ray on A and E and notice a chest X ray showing the heart displaced to the left with abnormal interposition of lung between the left pommery artery and the aortic arch. There is a focal lucency between the left vegetable and the left hemidiaphragm. What is the most likely abnormality? I don't know if anyone's answers yet, but if I made you all fall asleep, okay. So the majority is a bit of a split, but the majority of said to see which is great. So that's the correct answer. And this is a question that either you know or you don't. And now, you know, so the most common form of pericardial a genesis or absence is usually around the left atrial appendage or left palm a tree. The clue on imaging on the description will be that there is a lucent notch between the aorta and pommery artery, which basically represents inter posed lung between those two structures. So here you can see this is an example of pericardial a Genesis. You can see that there is interposition of lung between the aorta and the left primary artery on a normal patient, which is on the left. You can see that there is no interposition of lung between the aorta and the pulmonary artery. So if they ever mentioned abnormal interposition of lung between the left primary artery and aortic arch, they're trying to tell you that the patient has pericardial A Genesis. Okay. You're reviewing a routine CTCA for a patient who presents with atypical chest pain. The reporting radiologist notices that all pommery veins draining into the posterior aspect of the left atrium with an apparent membrane separating the left atrium into two compartments. What's the likely diagnosis? No. So, six responses split between A and C majority of seeing A and you would be absolutely correct. Um This is an example of Courtrai try eight for those of you said C C is actually spelt wrongly and it's actually bland white Garland syndrome which is an anomalous left coronary from the primary artery, um mitral valve, stenosis. They would have to tell you that the mitral valve is abnormal, thickened, aberrant might revive leaf that doesn't really exist, kind of made it up. But you can see how it sounds legit and they will do that. If they don't know an option, they will make something up to fit into the options and it will sound realistic. Um H a ventricular septal defect. Again, they have to mention that the mitral valve is abnormal where you can see that there's no mention of a valve is just saying the left atrium is abnormal. And the only thing that's abnormal that's involved. The left atrium is Cortright trait and that's basically an artificial membrane that splits the left atrium into basically two chambers and it acts like a fixed mitral stenosis. So now the blood that comes in through the pommery veins is gonna struggle to get through the posterior chamber into the anterior chamber. And the anterior chamber is where the mitral valve is and where the left atrial appendage is that could easily come up as a question as well. So remember in court, try to write um all pommery veins drain posteriorly and the left mhm is split into two chambers and anterior and posterior chamber, the anterior chamber consists of the left atrial appendage and the mitral valve. And the posterior chamber consists of for the pommery veins and it basically acts like a fixed severe mitral stenosis because no blood can get through the cleft. Easily 72 year old patient has an outpatient cardiac CT for investigation of Angina which demonstrates a low density abnormality. And the well, the apex this investigated with CMR which shows that the lesion is low on T one, low on T T would know post contrast enhancement. What is the most likely diagnosis? Give you one minute. So split between A and D. So the answer is a, so this is important table, take a picture and learn it. So thrombus can vary it signal characteristics depending on its age. So in the chronic stage, it is low and low. In the acute stage, it can be high and high and in the sub acute can be high and low. So it really varies depending on the age. Remember that thrombus is really common and is the thing that they would want you to not miss in the exam. So the chance of them asking a question about a random tumor is less likely than they are to ask about thrombus. Now, you can't obviously answer the exam with that theory. But if you're not sure and your split between a really common pathology and a really rare one, then on balance, it's probably the common one. Um The reason why D is not correct is because whilst there is no first pass enhancement in fibromas, there is homogeneous late enhancement in a fibroma. So remember, fibrous things retain contrast on delayed imaging. So that's why D is not correct. Myxoma is not correct because it gets heterogeneous enhancement post contrast and this one didn't enhance. So the only correct answer can be thrombus, there will tend to be other keys in the history. So for example, they might say there's a previous infarct and there's, or they might say there's regional wall motion abnormality in the L V apex adjacent to this little lump. And therefore, that's more likely to be a thrombus or if it's in the left atrial appendage, then it's a thrombus. 72 year old patient is referred for a cardiac MRI after an echo shows a hyper echogenic lesion in one of the cardiac chambers on cardiac MRI. There is a 25 millimeter lesion with a broad store which is intermediate signal on T one and mixed signal on T to post contrast. There is heterogeneous enhancement. What is the most likely location for the intracardiac mass that has been described? Yes. So I'm gonna rush through because we've got a couple more questions and time is running out. Um So the answer is left atrium, which is what the majority of you have said. Um So this is a cardiac myxoma which I suspect most of you deduced from the history. So it can, it has a really weird signal characteristics. It's kind of intermediate on T Juan it can be the myxomatous segments can be high on t to. Um, so they, but because the myxoma by definition has like lots of different parts, a bit, bit fibrous, bit calcified bit of hemorrhage. That's why it's so heterogeneous, which is why you can't reliably diagnose it based on T one and T two, you're looking for the other thing. So the fact that it's a round, oval shaped has a stalk is usually smooth, doesn't have any local aggressive features. Um And it has a heterogeneous announcement, that's kind of what will point you towards a mix over. And it's common, it's benign. The production later stalk is what they like to look for um to push them towards it being a myxoma most commonly, it's in the left atrium. And again, if they were to ask you, you, the most common location is butting the fossil over wireless and the order of frequency is left atrium, right atrium and then ventricles. The complications depend on which side of symptoms. So on the left, what can happen is that during H or contraction in the mix? So, because it's productive, waited on a stalk will punch like go through the mitral valve and basically obstructs the mitral valve and that will cause acute heart failure. Um and it can also pinch through the mitral valve and cause embolic complications. And then conversely on the right. If it's going through the tricuspid valve, it's going to cause p these are malignant morphology, ease. So if it says that something is large, greater than five centimeters, it's irregular, it's not smooth. There's evidence of direct invasion of the septum or the myocardium, then it's more likely to be malignant. Things that involve the pericardium or the pleura are really unlikely to be benign and they're much more likely to be malignant and the right heart tends to be harbor the more malignant lesion. So, so angiosarcoma are much more common in the right atrium than they are on the left. So key points, the most frequent intracardiac matters of thrombus. So that's what I'm saying, if you're not sure and it kind of sounds like a it's like a thrombus. It probably is a thrombus. Most projects, primary tumor's are benign and myxoma are the most frequent tumor motasisis are the most common indignance. See, and angiosarcoma is the most common primary tour also just be aware of this Carney complex, which is rare, but it's an easy exam question. So if they ever mentioned multiple cardiac myxoma, as they think of Kearney complex, which is tends to be associated with these weird skin pigmentations um and pituitary adenomas and sat totally cell tumors of the testicle. So Carney complex, multiple cardiac mix, Omagh's after their multiple maxima's Carney complex, multiple cardiac fibromas, think of Gaulin syndrome, rhabdomyoma, think of T S tuber sclerosis. The other thing to mention is if they ask to differentiate a high tea one lesion in the interatrial septum, remember high tea, one is fat or high tea one and high tt is fat. Then you're differentials are either a lipoma of the hr septum or lipomatous hypertrophy. And the way to differentiate is that the intracardiac lipoma doesn't respect the boundaries of the fossil violists. It will be overall shaped whereas an intracardiac, whereas the lipomatous hypertrophy will respect the fossil a virus and tends to be dumb bell shaped. Remember both will not enhance postcontrast. Last question, I think 26 year old man undergoes A C M R as part of a work up for palpitations. There is a four centimeter structure in the right cardio phrenic angle. It has a smooth contour with high signal on both T one and T two. No contrast enhancement on first past perfusion or late gadolinium imaging. The cardiac chambers are unremarkable. What is the most appropriate next step in the management? So five responses majority are saying d some see some e the answer is the. So this is a pericardial cyst. Um and Roma pericardial cysts can either be simple fluid and be low on T one and high on T T or they can be pro tenacious fluid and be high on T one and high on T two. Okay. There's nothing no contrast enhancement on first pass or late God. So it's not going to be pet CT like it's not malignant. So there's no point looking at pet CT post contrast CT if it's not enhancing on first passable late gown transfer, enhancing a post iodine contrast is also unlikely. And also it's smooth everything the history is telling you this is benign. It's less than five centimeters, it's got smooth contour, there's no enhancing. So you're thinking something benign. History is telling you something benign. And one of there's only one option which tells you that it's benign. And the only answer that fits with the question is d it would be very unusual to describe a benign sounding lesion. And then expect you to need an urgent referral to cardiothoracic or to expect you to say that it needs to be followed up. Yeah. Um And that is okay. Now, actually, there's one more question last question. So 72 year old patient presents with progressive shortness of breath and symptoms of right side cardiac failure A CM. Our study shows thickening and restriction of the tricuspid valve leaflets and evidence of pommery valve stenosis. The LV is normal in size and function in the party image, liver. There is an ill defined amounts. What's the most likely diagnosis? Good? Uh huh. Okay. The majority of your getting this right, which is great. And the answer is the cost mode heart disease, um abnormal track hospital pommery valves in the context of a liver lesion. The answer is casting with heart disease. Okay. There's no, don't even if you see that in the question. And then the answer is constantly, I wouldn't even don't confuse yourself and look at any other options in terms of valves. In general, aortic stenosis, high yield staff, degenerative or arthroscopic is more common than bicuspid mitral stenosis. The most common causes dramatic fever, mitral regurgitations to be degenerative prolapse, tricuspid stenosis most commonly seen in the form of rheumatic fever. But if they ask you about rheumatic fever, specifically, the most commonly affects the mitral valve. Tricuspid regurge is most commonly seen by right ventricular dilatation because it basically stretches the tricusp ID Angeles and it therefore can't close properly because it's been so stretched. And that is, it's so I will hand over to Jordan, I think who's gonna if you don't? Great. Thank you so much. And that's great talk. It's quite difficult topic you broke down, made understandable even to me. So, thank you for. That was really helpful. I'm just going to send the feedback link out to everyone. Now, in case anyone has to leave, I know it's half seven and these talks normally finish after and a half. People do have questions. Um, then, then please do now will, um, make five or so minutes for, for any questions people have, I'll read them out from the chat to people, um, that people send to send in the feedback, also be emailed out after the session will be recorded and we'll make the recording available to everyone. Let's give it a couple. I didn't have one question, Simon. Um, it was of pericarditis. Uh What are their typical imaging features of that or is it so, perry paralyzes diagnosis is difficult for radiology to diagnose. Um It was more a clinical history with, you know, like sitting forward and clinical presentation. The only imaging manifestations that we get on CT is that the presence of a pericardial effusion is a secondary sign but not a sensitive sign. And if you're lucky, you'll get pericardial thickening of greater than four millimeters. So those two things in the context of acute chest pain, you would then raise as pericarditis, but it's not a definitive diagnosis that we can make as radiology. Okay. Thanks a lot. Yes. But imagine it'll be quite mean for them to ask a question. Um Well, Procar doctors is the answer. Yeah, exactly. So you got one question to chat for the COVID vaccine, myocarditis. Are there any particular distributions of the L G? I suspect it's exactly the same. So Michael is, is generally can affect anywhere. So you can have Michael eyes of the lateral wall. You can have Michael is over the interior wall. You can have it anywhere. The most common location for Michael is, is the just the basal to mid lateral. Um I I suspect that COVID related Michael items wouldn't have made it into the question bank just yet. Um So I suspect it will still be the common locations. I think it would be unfair for them to say myocarditis in the anterior wall. It's much more likely that they're going to give you a if it's a myocarditis question is gonna be subepicardial enhancement in the basal to mid lateral. Okay, thanks Senen. Um No more questions at the moment. Um So I think there's no more questions we can finish it there. Um So thank you everyone for attending. Um Again, please fill out the feedback. Um It's in the chats we go to.