Christopher Kramer, MD was a keynote speaker at the first inaugural Heart & Vascular Symposium hosted by Georgia Heart Institute at Chateau Elan Resort & Winery in Braselton, Georgia. Dr. Kramer discusses state of the art cardiovascular imaging primarily focused on CMR and echo.
Good morning um Welcome to everyone on our second day the Georgia, heart and vascular symposium. It's great to uh greet you all. Can I have a quick show of hands I assume most folks were in the hotel last night. Right Well um this was not an accident. Right? So the alarm was set at 447 for there's apparently a planetary alignment that you can only see at 447 is what Dr hall tells me. Um But no thank you and obviously um good to see you here. Hopefully some folks will continue to come on in. But I think today we have a absolute fantastic lineup that will be kicked off by our keynote speaker, Dr Chris Kramer who I'll introduce in a minute. Um I do want to say a couple of words about yesterday because yesterday was the first day of our Georgia. Heart investors symposium. We did two fantastic live cases from the Cath lab and had an excellent um interventional E. P. Session and stemming and shock sessions with, we talked about this last night about what we're about. Right? Um I don't know how many of you heard the really moving presentation by dr uh Appeal Peric who himself is a cardiac arrest survivor. Um the urologist who was down for 30 minutes and received CPR by his wife and eventually now is practicing. So um you know what we're about is not only learning and sort of focusing on holistic cardiovascular medicine but the delivery of health care through the patient's eyes and the patient experience. So um I think today you'll you'll see that our our agenda is gonna focus on cardiovascular imaging on cardiovascular prevention, metabolism, lipids, women's heart disease, congestive heart failure therapies that are just really expanding and then the peripheral arterial disease and pulmonary disease. So without further ado um I think the kick off is gonna be fantastic. We're gonna have uh dr Christopher Kramer um who's the George Bell er uh Professor Distinguished professor of cardiovascular medicine and chief of the cardiovascular division at the University of Virginia Chris is um you know one of the top leaders in the world and cardiovascular imaging, cardiovascular M. R. I. As well as C. T. Um And Chris. Um and his lovely wife, Cathy. Um and my wife and I are really good friends from when I was at U. V. A. When I when I was a young faculty we uh we played tennis together and we also wrote papers together. Had a lot of good times. But I think Chris has talked today is I think he's gonna focus on CMR and echo cardiac M. R. I. And Eco. Um And so Chris thank you for joining us. Habib thanks for the invitation to come to speak to you today and I will focus on CMR and Eco mainly because Leslie Shaw who I'm sure will give an outstanding talk in a few minutes on uh nuclear and C. T. So we didn't want to uh overlap our our talks and it's great to be to be here. And uh to have to be bring bring back those memories of a couple of decades ago when we were a little more spry around the tennis court. These are my disclosures none of which have related to the topic of today's talk. So we'll start with a case. Uh It's uh the case is a 54 year old female with long standing hypertension diagnosed over two decades before bilateral carpal tunnel syndrome type two diabetes. And a cardiac arrest with an I. C. D. Who presents to our HCM clinic for initial evaluation to exclude hypertrophic cardiomyopathy. Her cardiac arrest was due to ventricular tachycardia and she achieved ross after cpr and four defib relations. She actually has a family history of multiple family members with heart failure and a sister who died suddenly in her fifties. Her E. C. G. Showed poor R. Wave progression but was fairly non specific. Here's her eco um second movie isn't playing for some reason shows severe concentric LV. H. With hyper dynamic function. There was no sam and no L. V. Outflow tract obstruction. So the question is you know is this hypertrophic cardiomyopathy or is this something else? So we went along there is the second movie you can see uh hyper dynamic function. Severe L. V. H. And also thickened atrial septum. Her. This these are her late gadolinium enhanced images uh by CMR on the three chamber long axis on the left. You can see uh sort of mid wall right late gadolinium enhancement and on the short axis you see this uh patchy lateral wall and sub epic are ideal LG. Now she also had a pericardial effusion at the time of the uh the CMR. With this pattern of late gadolinium enhancement. The question of amyloid was raised. As along with the other findings. The concentric concentric city of the L. V. H. The pericardial effusion, the thickened atrial septum history of carpal tunnel syndrome. So amyloid was was raised and this pattern of LG was certainly consistent with a L. Amyloid not A. T. TR. Which tends to be more diffuse. She had a pyro phosphate spec scan which was negative for T. T. R. Which we could have predicted from the CMR. She had abnormal serum free light chains with restricted lambda monoclonal itty. She had a bone marrow biopsy was actually negative for amyloid. So she had to go on to uh tomorrow cardio biopsy which did show uh positive staining for congo red. She's been started on chemotherapy for a while amyloid and is discussing a stem cell transplant. While this is all going on, she has persistent non sustained V. T. And occasional anti toxic cardiac pacing from her device. It's hoped that her therapy will reduce her burden of N. S. V. T. So this is a case that shows the power of cardiovascular imaging to focus the diagnosis of unrecognized uh cause of left ventricular hypertrophy and differentiate the underlying ideology. So I'm gonna talk about CMR uh as as applied to ischemic heart disease and cardiomyopathy. These and then discuss what is newest in echo. So these are our typical uh steady state free procession images. Get seen movies of the of the beating heart, very high resolution. This is in a in a patient with a recent uh a pickle em I you see the small wall motion abnormality in the apex on the two chamber on the left and the four chamber on the right and a small L. V. A. Pickle rhombus. This technique gives us very high contrast to noise between the myocardial and the blood pool and we can see the valve leaflets well as well. The other technique we use all the time that I showed earlier is late gadolinium enhancement. Which is a technique that detects not only infarct but any cause of fibrosis or increased interstitial space such as shown in the amyloid case I shared earlier. It's a technique that was developed around 1999 which Noel's the signal and normal myocardial. Um And for two reasons gadolinium gets caught up in areas of scar or fibrosis and that is one because of uh increased volume of distribution for gadolinium within that scar. And secondly delayed washout. So we image 10-20 minutes after giving standard doses of gadolinium and uh you see an image such as you see on this slide in a patient with a 50% trans mural infra lateral myocardial infarction. We also do stress testing with CMR. It's really uh starting to achieve its proper place in the stress armamentarium. We get three slices during a dennison and dennison infusion. You see stress on the top, rest at the bottom during rest imaging. There's homogeneous uh uptake of gadolinium in the myocardial. You see that myocardial is homogeneous lee gray during stress in this patient. You see the dark zones especially in the mid slice and the a pickle slice on the right in the anterior lateral and infra uh lateral walls consistent with two vessel disease which was subsequently demonstrated at Cath CMR stress CMR used to be criticized. So there weren't a large outcome studies using it. But here is one published in the new England Journal a couple of years ago led by a. K. Nagle. The M. R. Inform study uh nine over 900 patients randomized to either a CMR guided uh study of for chest pain or straight to the Cath lab and FFR guided therapy and what you see at a year and the outcomes are longer now and are similar at a year. There was no difference in outcomes between the CMR approach and the FFR approach, fewer patients in the CMR uh approach. Obviously got Cath fewer got interventions yet the same outcome was obtained so you can take the non invasive approach and get the same outcome as you would, sending the patient to the Cath lab and getting FFR. And this is a registry of over 3000 patients from multiple centers around the US showing that outcomes can be stratified by the findings on stress CMR. The top graphs uh go from no ischemia, no late gadolinium enhancement to the middle groups which are either ischemia or late gadolinium enhancement meaning infarction. And then the worst outcome is in the top group which are patients who have both ischemia and prior scar. Late gadolinium enhancement. So outcomes are stratified by that as well as by the extent of ischemia. On the bottom two panels going from no mild moderate to severe ischemia outcomes. Uh And these are hard outcomes, not revascularization. Uh I want to turn now to the role of CMR and cardiomyopathy. These, it's an important technique to assess for myocarditis has been used a lot recently to look for both. Covid and vaccine related myocarditis. So it's part of the writing group of the rewrite of the lake louise criteria which identified what we need to make the diagnosis of of myocarditis. The first is evidence of myocardial edema by either T. Two weighted imaging or T. Two mapping evidence of increased interstitial space. Either by showing late gadolinium enhancement or an increase in what we call the native T. One of the myocardial which we can measure easily at the scanner and lastly supportive criteria, regional or global dysfunction and a pericardial effusion. HCM. Is a diagnosis that should prompt uh sending your patient to CMR. Not only for assessment of the morphology of the type of HCM. As shown in the patient on the left on scene who has both reverse septal curvature and a pickle subtype. But also to demonstrate late gadolinium enhancement or scar which is president about 50% of any all comers with eight cm. But what has been shown in the last few years is that the extent of LG is predictive of sudden cardiac death. Once you have more than over 15% LG your likelihood of sudden cardiac death doubles from uh typical patient with 8cm who have the risk of less than 1% per year. It increases to about 2% per year if you have more than 15%. Uh uh L. G. And that is now in the latest guidelines a to be indication for an I. C. D. So very important to get CMR and your patients with HCM to risk stratify them sarcoidosis. Again CMR is a hallmark of making the diagnosis. Pet is an adjunct for a diagnosis inflammatory infiltration of inflammatory granuloma. Here's a patient with incessant V. T. And R. C. C. U. You can see severe bio ventricular dysfunction with a unusual wall motion pattern not typical of ischemic cardiomyopathy. You can see that uh the pattern of L. G. E. Is quite specific for sarcoidosis. The L. G. E. Is mid wall and sub epic are ideal with sparing of the sub and cardi. Um And there's classic finding of basil anterior Antero septal LG. E against Sub epic are ideal and that's why it often causes A. V. Blocks are coy because it's right up against the A. V. Node there in the basal septum. Our group is shown in this meta analysis that the presence of any LG is associated with a six fold increase of the combined outcome uh of death and VT and a trend towards an increase in all cause mortality and subsequent meta analysis with larger number of patients have confirmed this. So uh the L. G. And extensive LG is an indication for I. C. D. And sarcoidosis amyloid. This is a case of T. T. R. With more diffuse late gadolinium enhancement as opposed to the A. L. Case I shared earlier. And uh Mike Salerno formerly with our group performed this meta analysis published in Jack imaging showing that measurement of extra cellular volume and the T. One of the myocardial are the most which we can do uh in a straightforward manner on CMR is the most potent predictor of outcome. L. G. E. Is does predict outcome but not as potently as extra cellular volume. So in the last few minutes I want to turn to what's newest in echocardiography. Well first Ai Ai is not going to replace us Echocardiography furs anytime soon but it certainly is good at measuring left ventricular ejection fraction shown in this large study of several 1000 patients from the Stanford group where they trained just on LV function and were able to show diagnose an ejection fraction less than 50% with an area under the receiver operating curve of 97.0.97. So if all you want to know is E. F. Uh artificial intelligence may be the way to go. Obviously there's a lot more to get from an echo valvular disease, diastolic function etcetera. So we're not gonna be replaced anytime soon. Maybe for measuring the F. Though for measuring mitral regurgitation. What's the best test? Well, three D valve quantitative in is really coming to the fore measuring three di Pisa and three D. V. Nand contractor uh in this meta analysis comparing the uh to the gold standard which is quantitative CMR. The best agreement was with three D. Pisa. So measuring the extent of the jet on uh three D. Imaging, There's exciting new information about measuring myocardial work by measuring strain and blood pressure. You can map out uh the work of the myocardial um and in this study in hef ref of 105 patients with a mean e. of 28%. They measured global constructive work. So the positive strain or uh and uh relationship to uh to pressure. And they found a cut point of 530 that the outcome was much better in the patients who were able to show that level of global constructive work. Compared to those with below 530 had much poorer outcomes over a year and a half. Follow up atrial strain is also showing its importance in Hef pef especially uh slides on the left are from studies at the Mayo and Barry bar Borlaug's group showing that you can measure uh conduit atrial strain which is early diagnosis early. But the most important marker is reservoir strain which is strained throughout the entire uh period of dia silly. And then the A. U. C. Curves on the bottom uh left. It's the reservoir strain and its relationship to E. Over E. Prime. That was the most potent predictor of heart failure. When you're differentiating dysosmia if uh due to heart failure preserved ef from other causes such as lung causes. So measuring atrial strain can really pinpoint the diagnosis of heft and it's useful in atrial sarcoidosis as well to show atrial involvement with reduced strain. Just briefly. This is a slide lent to me by Jonathan linder who's joining our faculty uh in a month or so. He's an expert in contrast Echo. Uh He's done a number of studies using Vaso dilator contrast echo to demonstrate micro vascular dysfunction in patients with primary microvascular dysfunction as well as transplant. Plant vascular empathy by quantitative profusion at stress and rest and demonstrating reduced perfusion reserve. As shown on the the curves at the bottom. Right. So in summary CMR is an outstanding technique to diagnose and prognosticating ischemic heart disease. It's the single most important technique to differentiate cardiomyopathy. Oven non ischemic cardiomyopathy is of unknown cause. And there are a lot of exciting new uh advances in X that are gonna help us identify patients with HeF hef with abnormal prognosis. Hef, excuse me, Hef ref with uh adverse prognosis, identify patients with HEF HEF appropriately and diagnose the severity of valve disease. And with that I'll end and thank you for your attention. What?
