In this Cardiovascular Medicine webinar, Mayo Clinic cardiology experts Bernard J. Gersh, M.B., Ch.B., D.Phil. , and Mandeep Singh, M.D. , moderate a discussion of the pathophysiology of acute COVID-19 cardiac injury and the spectrum of late cardiovascular sequelae. A key part of the discussion is the extent of resolution of acute cardiac injury and its impact on late cardiovascular symptomatology.
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Hi everyone. My name is Mandy Singh and I'm a professor and director of the acute coronary syndrome at Mayo Clinic in Rochester and it's my distinct pleasure to invite. But he doesn't need introduction anymore. He's been aligning force for for our acute coronary syndrome webinars. And today Dr Gersh is going to speak on long term Cardiovascular complications of COVID-19. Um This topic has made headlines since the onset of the pandemic, but little is known on what happens after the acute events have passed. We know from from the literature that ah people who present with acute coronary syndrome present less present late. Um We also know that most people are mildly symptomatic or asymptomatic. And then there's a gradation of severity from mild to moderately severe which needs hospital stay to an ICU like care. But we don't know what happens to these individuals after they are discharged or when they have this covid. And then what happens to them afterwards. Dr Gersh has highlighted in his recent paper and has done a lot of research not only on the cute events, but also what happens long term. What are the complications? What are the cardiovascular complications we need to look at at these patients what kind of additional research we need to do in order to better understand and then focus on where our research strategies should be on these patients. Long term dr gersh. It is my distinct pleasure to invite you again in this forum and I would like to uh I mean it's a it's a it's a it's not a pleasure it's an honor to have teachers like you who then illuminate all of us on the on the themes that nobody thinks about. You know and and this is one of them that long term complications. Nobody thinks about what happens after the acute. Um It is over so dr gersh help us understand what are the long term complications of covid 19. Thank you. Thank you men deep and as always, it's a pleasure to be here long term cardiovascular complications of covid. Now, the path of physiology and manifestations of what are called cardiac injury in COVID-19 is a bidirectional interaction and I'll explain that as I get towards the end of the slide, the path of physiology is really very complex. Severe sepsis, hypoglycemia, cytokine storm the Brandy keenan hypothesis. Auto antibodies, regular empathy in diphtheria and microvascular information dysfunction. All of these path a physiologic entities probably take place to a greater or lesser extent In our patients with COVID-19 who have cardiac injury, cardiac injury. Other manifestations of it. Type one. Myocardial infarction due to sympathetic nervous system activation, inflammation in itself can cause plaque rupture hypoxia, hypoxia mia and increased myocardial oxygen demands due to tachycardia and sepsis Can lead to a Type two Emmy Takasu bo has been clearly reported in increased numbers during the pandemic. Not surprising given the stress of the pandemic. Myocarditis is the usual suspect but it's actually an infrequent culprit. And I'm going to come back to this because there was a huge amount of publicity about myocarditis early on and late thrombosis. Arterial and venus probably plays a critical role in the cardiovascular manifestations of covid. It tends to be more plated dependent. It may be viral mediated plated inflammation. There is also evidence for hyper coagulation, hypercar regular ability of red cells. But the end result is an increased rate of thrombosis, arterial and venus. In terms of the clinical outcomes, The communist manifestation of cardiac injury. It's just a troponin rise, chest pain. Am I heart failure, shock RV dysfunction. Arrhythmias, pulmonary embolism, frequently reported stroke and microvascular dysfunction and pericardial involvement. Now, why I say it's a bidirectional interaction by these modifying factors. Because what has been associated with the epidemic has been a delayed presentation to the emergency department, delayed diagnosis. Late treatment which in fact can contribute to exacerbating cardiac injury, preexisting comorbidities, fever drugs including antiviral drugs, some of which may have some cardio toxicity, electrolyte abnormalities and simply logistical constraints in health systems that are overwhelmed by the magnitude of the pandemic. So this is from a recent review by Dr Satterfield, one of our fellows at Mayo myself and Dr Deepak. But from the Brigham ah the acute cv complications. Arrhythmias Myocardial infarction, pericarditis, left and right ventricular systolic dysfunction, stroke and deeply in thrombosis. And the question is, what is their long term impact. We know a fair amount about what happens acutely but what is the long term impact now myocarditis does occur. And this is one report um from New Jersey two cases no prior CB History shop presentation. A week after covid diagnosis, treatment with steroids and iron. Our troops LV function on echo. Look at the pro BMP 50 53 2000 and five Pg per ml. And then four days after admission. A significant improvement in ejection fraction In case number to the same kind of presentation, 45- 55% after discharge. And this is very consistent with acute myocarditis. What is interesting is this entity have delayed onset myocarditis following covid 19. This is a study from the U. K. Nine patients Um black African ancestry and seven mean age 36 years. And they all had acute cardiac decompensation with the clinical features of recent covid infection. Follow up at least in follow up, complete recovery was noted in four patients. But this is what is interesting the cutie. They had multiple negative SARS Kobe covid to rapid real time pcR testing. But subsequently the car's COVID two antibody levels were extremely high in all patients. So this is an example of delayed onset myocarditis. One of the early histological autopsy studies on 21 patients who died of covid using microscopy and looking at the composition of the inflammatory cells. What they saw in terms of cardiac pathological changes was RV strain in 19% Vocal pericarditis, 19 And a cordial from versus in 14 diffuse macrophage infiltration in the majority small vessel thrown by which I believe are an important catholic physiological feature In 19%, but only 14% had lymphocytic myocarditis. In this study from the Mass General Hospital, another autopsy study of 41 patients with fatal COVID-19 virus was noted in the heart with the histological features of myocarditis In for patients virus in the heart without myocarditis noted in 26 patients And no virus, no myocarditis in 11 patients. And their conclusion was that cardiac infection with SARS Covid two Is common among patients dying from COVID-19 but often with only rare infected soul, even though uh cardiac infection and virus is present. But cellular infection with myocarditis is uncommon. And at the time of the start of the epidemic, I think we all felt that we would see a huge number of patients with myocarditis and then this rather definitive autopsy study from Johns Hopkins 227 autopsies from nine countries. And the conclusion was that the initial review of the data indicated That myocarditis was present in 20 hearts 6.2%. The closer examination of additional reported information revealed that most cases were likely not functionally significant and the true prevalence of myocarditis is likely much lower In conclusion across 277 cases. Covid related historic pathological findings were common, but myocarditis was rare and these are the various autopsies and what you see is the impression of myocarditis really came out of one only one or two autopsies shown in orange here. The rest demonstrated no evidence of myocarditis. So what I really want to talk about in terms of the spectrum of the cardiovascular sequelae of COVID, 19 survivors is described on this slide. There are two large groups of patients, one of patients who had an acute illness mild or asymptomatic, our patient case. And what is the incidence of long covid in these patients? The other group are those who had an acute illness. It was severe, they were hospitalized and they had evidence of cardiac injury. And the question is in these people who had an acute illness, what proportion of these patients And these patients we'll have long haul coke with basically non specific symptoms. And the other key question is in those with acute cardiac injury with structural involvement acutely. Do they continue to have structural cardiac involvement and late cardiovascular complications? Or does this result? And there are some reports now of some patients who had a mild acute illness. They don't just have long haul covid, but there is some evidence of structural, late structural cardiac involvement. And we need to realize and I need to emphasize that we're in a changing world. This is all new and there's a great deal we have to learn. And I'm trying to summarize, at least to some extent, what we know at this point in time. This is a recent report from the National Center for Health Statistics and what you see our weekly death rates in the United States by cardiovascular cause For 100,000 of the population. Yellow is 2019. Oranges 2020 encompassing the the epidemic. And what you see is a striking increase in a late mortality due to ischemic heart disease. Heart failure. No different hypertensive disease is another increase, cerebrovascular and other circulatory diseases. No increase. Now, that doesn't mean that in a year or two's time we may not see an increase in heart failure, but at least these are cardiovascular deaths. In the first a few months of the pandemic conclusions causes a multifactorial, including the avoidance of hospitals, delays in seeking and deferral of outpatient and procedural care plus the cardiovascular so cleaning perhaps of undiagnosed covid 19. Now, um I want to focus on an entity called collateral damage. And this is a paper from the United Kingdom that I was proud of. It was published by DR Kyte who was a fellow of dr Anthony ger slick dr goose neck. Um It was a real pioneer of interventional cardiology in the UK. I think the first implant, a stent has done wonderful trial work. It was a very good friend. And what he did. He set up This registry of 55 interventional centers in europe, the UK and around the world. To look at what happened during the covid pandemic to patients with an acute coronary syndrome. The sad and the personal part of this is the last conversation I had with dr gersh click. He was in the icu that he set up 25 years ago. We were discussing uh the review of this paper and how we should respond to the reviewers and Tony died of of Covid in Leicester England. This was pre pre vaccine. Now, what we were able to do in this study was compare the results uh in during the covid epidemic with two large databases, pre covid in the UK and these were databases of everyone in the United Kingdom that had an acute colony syndrome. Covid in orange pre covid and yellow. If you look at symptoms to admission time, It went from 179 to 339 minutes. So it doubled partly, I think understandably due to a perceived perception by patients that hospitals are a dangerous place to be and they delayed presentation. If you look at the door to balloon time, it went from 37 to 83 minutes more than doubled. And this was striking in hospital mortality pre covid for all comers with acute. This is just the stem e data In hospital mortality 5.7% increasing to 23 And cardiogenic shock 8.7 to 20.1%. So this is what I call collateral damage. And one of the unresolved questions here is in those patients that survive. Are we going to see a late epidemic of heart failure and arrhythmias and that remains to be determined. So this was the experience during the early phases of the pandemic. And what is important I think to emphasize this paper by great stone of 10 randomized trials of patients undergoing re perfusion therapy stratified them into court trials of infarct size. And if you look at the one year mortality in those in the highest quartile greater than 29.8% of the left ventricle involved, Almost 9% mortality in those in the lowest quartile, less than one mortality. And again, I want to go back to the study, I've just shown you with a tripling and the the incidents of cardiogenic shock. I think we will see amongst the survivors a significant number with very large impacts and late complications. Another list perhaps dramatic but equally important aspect of collateral damage is written in this paper by one of our fellows, Dr oren and myself and others. And that is the cardio metabolic toxicity of social isolation and emotional stress and particularly amongst the elderly. And we state in the conclusion, understanding social isolation and it's public health consequences is the key to minimizing the late Cardio metabolic burden of COVID-19. But it's also fundamental to optimizing Cardio Vascular health outside the context of COVID-19 going into the future. And what we really meant was in during the periods of isolation, blood pressure was not well controlled. People did not come for regular outpatient evaluations and in many cases hospitals were ill equipped to undertake those outpatients evaluations. People exercise less smoke, more gained weight and these are the cardiac metabolic consequences which may translate into adverse cardiovascular health outcomes. Go back to this slide again, I've dealt with collateral damage. And really what I want to focus on is the post acute illness manifestations, cardiovascular manifestations namely Long Covid. And what happens to the patients who have acute cardiac injury? Do they get better? Do they get worse? This is a quote about influenza. If if influenza is a riddle wrapped in a mystery inside an enigma in the viral genes of the riddle, the variable surface antigens for which they code are the mystery and the course and the cause of epidemics. The ultimate enigma. Well, isn't there? Shorty and skepticism. one of the clinical characteristics of the multifactorial path of physiology and etiology of Long Covid, I might add this quote about a riddle wrapped in a mystery inside an enigma was first major, or the initial quote was by Sir Winston Churchill In the 1930s when he was asked to explain what he felt about Russia. But I think it's a very apt quotation for re dealing with today. So, if you look at post acute and particularly long haul Covid, they have cardiovascular symptoms, pain palpitations, breathlessness, Ortho static intolerance. Some of these patients may have myocarditis will come back to that. Arrhythmias LV and RV dysfunction leading to heart failure. But the majority we have basically we see non specific findings on imaging and no heart failure. What are the causes? Question marks, long term tissue damage. Perhaps unresolved information. I think very possibly an autoimmune phenomenon and clearly autonomic dysfunction. But I might add despite the severity and then LTD and severity of the symptoms that really limit the quality of life of these individuals. The findings in most cases, from a cardiovascular standpoint are relatively non specific but we really need to study in these patients, the autonomic nervous system in more detail postural Ortho static tachycardia syndrome pots. I call it the electrophysiology, electrophysiology ist nightmare because pots is a very difficult disease to treat. And it again has a major limitation upon quality of life. But it's not an electro physiologic disease. It's not an arrhythmic disease. It's autonomic dysfunction and a neurological disease and overlaps with chronic fatigue syndrome and post covid 19 and we are clearly seeing increased numbers of these patients with the long haul syndrome. Now this study gained a huge amount of attention. 100 patients came from Germany Frankfurt dr zaius group, 100 patients, 33% were hospitalized, mild or no symptoms. In the majority Mean Age, 49 years, frequent comorbidities and then they had seem memory, cardiac magnetic resonance imaging At 71 days median after the acute episode. Um at the time of CMR 76% at an elevated high sensitivity troponin And the findings were in 78%. There were abnormal CMR finding Increased native T one Mapping, increased native T two mapping And late gadolinium enhancement which is not really non specific in 32 patients. And this literally frightened the daylights out of all of us because suddenly we now look at the spectrum and particularly the fact that a number were relatively mildly symptomatic. I had mild disease. And we're now looking at the specter Of 78% with long term cardiovascular manifestations. Now there's been some other more recent studies and I do think that that first that study had its limitations in terms of there was a lack of control. But now there are more recent studies, this one from Norway 204 patients, 20% in the Ido 12% integrated. And at three months, these are the findings. LV systolic dysfunction was uncommon. RV systolic dysfunction. An LV diastolic dysfunction was present in 50 probably associated with pulmonary pathology and RV strain and debilitation which could also interact with the L. B. Cardiac arrhythmias of uncertain clinical significance were common PVcs and non sustained VT Persistent disks near and 50 Fatigue in 2/3. And I might add that these were not associated with eco features of cardiac dysfunction. So we have a large number of patients with persistent symptoms, dysentery and fatigue and a significant number of patients with non specific um findings in the left ventricle and the right ventricle that are really not correlated or associated with the symptoms of shortness of breath. This has just been published. It's a pre print from Oregon health sciences. 1355 patients and controls covid positive In 24%. And they were a mixture of symptomatic and asymptomatic. The primary outcome was CV morbidity and mortality And it's six months covid positive. The primary outcome of CB morbidity with less mortality but significant morbidity and those who were covid positive. It was 12% and those who was covid negative 6%. And the adjusted hazard ratio Was 1.71. So for COVID positive patients there was a 71 Increase in morbidity and mortality at six months. Well cardiovascular morbidity and mortality all cause mortality after adjustment. They showed that the time to all cause death was 65 days list in covid positive patients And this is in people followed beyond six months worrying. And then this huge study published about a week ago in nature from the V. A. Health system, 154,000 patients With approximately 5.5 million controls who did not get covid And approximately six million historical controls from 2019. The majority were not hospitalized and that's important and only a minority were in the ICU. And one year. They say there's a 2-fold increase in incident cardiovascular events listed as cerebrovascular disease. Dis arrhythmias. The scheme is heart disease, pericarditis, myocarditis, heart failure and throw metabolic disease. But we don't really have any details of these specific cardiovascular morbidity. They say it was present in non hospitalized patients but increased in a graded fashion with increasing severity of the initial disease, which you would expect present in all age groups and in younger patients without risk factors such as obesity and diabetes. So concerned 23 papers that really are of concern and obviously we need more information. So I would summarize some of the studies to date by saying abnormal imaging findings in recovered patients are frequent, whether it be emery or echo other imaging uh two, what is the clinical significance and lack of and and the fact is many of them had a lack of controls. And this applies specifically the athletes who do have highly high grade, highly competitive athletes do have abnormalities on MRI's and echoes if you look for them, what is the correlation of these findings with symptoms and the severity of the initial illness? And what is the natural history did they resolve? Do they persist? I've seen several reports now of late gadolinium enhancement in a non ischemic distribution, something we see with dilated cardiomyopathy and it's an adverse predictor and it may predict later arrhythmias question showing here do they lead to late heart failure? Don't think so. In the majority, the arrhythmias if it's just pvcs and atrial extra system is of no concern. What's the impact on full activity in regard to athletes? This was a large study from professional athletes in the US professional sports leagues. Covid positive. This is a misprint prior acute illness. 58% of these athletes were symptomatic. Almost half were asymptomatic. They had cardiovascular testing at 19 days And it was completely normal. In the vast majority. 759 Out of seven, 30 athletes had one or more abnormal test results. That's 3.8 either on trans thoracic echo. Five had proponents three. The combination of an abnormal EKG and a trans thoracic echo And 12 trans thoracic echo and troponin elevation and using standard H. A. C. C. Guidelines. There were two out of 789 with myocarditis And two with pericarditis. Pretty reassuring Bond lock and we really don't know what most of these non specific findings on echo and BCG. Me and then dr jim you'd Elson from Tufts wrote this very, I think good summary returned to play for athletes after covid 19 infection. The fog begins to clear uh Studies on total 6753 athletes and this is the prevalence of myocarditis on CMR imaging and what I want to point out There are two outlines the vast majority of these studies showed evidence of myocarditis, basically Not to four And several with zero a couple of 1.43%. These two studies seem to be outlines Uh total myocarditis 2.8%. And of those patients, 31.9% were asymptomatic 2.8% on on CMR Studies which is this graph. But if you look at myocarditis in the full cohort Including those who did not have emery only 0 .94%. I thought this was a very good editorial which basically emphasized The significance of COVID-19 associated myocardial injury power over interpretation of scientific findings. Can few media sensationalism and spread information when the first data came out on MRI findings and particularly in athletes there was a huge media and public response and one of great concern which I think is to a large extent um now being delayed not completely but at least reassured this is from a widely read blog setting the record straight. There is no covid heart from john man drollas. After a year of frightening headlines, widespread concern and countless retweets that the virus causes Covid that causes covid 19 may attack the heart more aggressively than any other viral illness. The verdict is in it doesn't well I don't agree with that totally. I think it does affect the heart. The question is how frequently and I'll come back to that but it's not to be ignored. So if you look at the late CV complications of COVID-19 I think in all likelihood we will see Serious late cardiovascular complications of COVID-19 infection. The question is, will it be frequent, uncommon or rare? And that remains a question mark. I yeah, figuratively feel it will be uncommon or rare, but it's a question mark. And so to summarize, what do we know? Cardiac injury during the acute phase of COVID-19 is common and an adverse prognostic factor. The etiology is multifactorial in covid survivors, cardiac abnormalities and imaging and frequent irrespective of the severity of the acute illness. What don't we know? We really don't know the natural history and clinical significance of the abnormal findings in acute survivors. We do not know the late natural history of survivors of acute coronary syndromes who had delayed therapy has shown in that UK study. And I might add that study of Dr gersh Alex has also been repeated by DR TIM Henry in this country. The mechanisms and etiology of the different manifestations of virus presence in the heart are really unknown and the approach to competitive athletes and whether prior guidelines on myocarditis are applicable to the covid population. I think they are. I think we do have guidelines about the return to play for athletes after flu and other viral illnesses. And I think those guidelines are probably going to be applicable to the COVID-19 Athletes with COVID-19 infection, Mark Twain made this tremendous prescient quote, what gets us into trouble is not what we don't know, it's what we know for sure. That just ain't so and I think what we can conclude with is this profound thoughts. What we do know for sure is that there is a great deal more that we do not know. And so my final slide makes the plea for more data. We need perspective large specifically phenotype longitudinal follow up studies including athletes and different and different ethnic groups. This is a really important entity to emphasis and the question of the questions, symptoms, functional limitation, morbidity and survival. And these are the imaging endpoints that have to be collected CMR event monitoring and stress testing. The duration of follow up needs to be not just months but years. And I'm pleased to um note and that these kinds of very large studies are now ongoing. N. H. L. B. I. Is a very large study in this country but there are several ongoing studies such as this in different parts of the world and we will get the answers in the not too distant future. But I think it's really important that these studies are not just short term. Thank you for your attention. Thank you dr gersh it was very illuminating and fascinating talk as as always, I think for the audience. I think it's very important to differentiate the risk from the burden of disease. So risk being like for example, you said Maya cordite is the hazard ratio for Maya cordite is in this recent via paper has been five as compared to arrhythmias or for example ischemic heart disease Where the hazard ratio is aboard 1.7, but the burden of disease is very low for myocarditis long term. Whereas the burden of disease for more common problems like arrhythmias and ischemic heart disease is much more than than less common problems like myocarditis. We did report last month on 32% reduction in patients presenting with a CS, but then there was a relationship of the decline in their presentation with the lockdowns that happened statewide. Um there are several questions from the audience and I'll go over one x 1. The first question is by dr straws and she says now in the MGH study you said there is no virus, the zoom, my quad itis. And then how are they attributing did death to cardiovascular complications effectively, the MGH study was 41 patients, four of them had clear viral myocarditis. A significant majority had evidence of virus in the heart, but without myocarditis and that means that there was virus in the heart without the histological appearance of viral myocarditis. And then there were about, I think 11 patients that had no virus and no myocarditis. So I think it it is um it is certainly possible to die from an acute viral infection of the heart or even from a late violence or the late complications without having myocarditis and it may be that and it may be now I emphasize them maybe because these are the unknowns. Um it may be that virus in the heart causes microvascular dysfunction and ethereal dysfunction or end ethereal dysfunction leading to thrombosis, both in a macro vascular and microvascular level. So yes, you are dying of, you're dying of thank you very much. Let me just I'll go to that slide. Yes, you are dying of a covid infection of the heart. But it may be that it's not myocarditis at all. It is. And this is the study you're talking about here in the heart for patients Viral in the heart without myocarditis. 26 patients for patients with myocarditis and 11 patients without. And I actually think if I go back to this very complex first slide, I do think that, let me just bring it up here. I think this is not just I think, I mean many people think this is a very important entity thrombosis, arterial and venus. And it may be viral mediated plated information, inflammation. And then I think this is really important as well. End epithelial and micro vascular inflammation and dysfunction and that maybe in the long term an important, a really important cause of long term morbidity. And we have seen reports of patients. Um and I've heard of this on a personal level of patients who are perfectly healthy before Covid who developed classic microvascular engine who at caF have astral choline Visa construction, which is how we define Visa spasm. So I think that and myocarditis is the usual suspects the obvious suspect, but it's relatively infrequently. So, just getting this forward. DR bowl asked how does this covid 19, cardiovascular complications compared to other covid variants and also more recent omicron. Have we learned from or are there studies published on different variants of even COVID-19? How does that affect the cardiovascular or we don't have? I don't really know the answer. I mean, I think I know about his much as you do about the biology, but and and and obviously none of us have virologists. I mean, what I do know is the prevailing viewpoint is that omicron is a much more benign variant, It's much more infectious, but it's more benign. Ah Having said that in older patients with comorbidities, it may still be, it may still be lead to a very severe illness. What I don't know is any study that has looked at cardiac injury is defined by proponents and drawn the conclusion that it is less, there's less cardiac involvement with one variant versus another. What we do know, I think generally now is that, oh, Macron is associated with less hospitalization, a lower duration of hospital stay. It is a more benign condition or benign variant doesn't mean that some people won't have severe injury. But I don't know of any, I mean severe disease. I do not know of any direct comparison of at least published of cardiac injury in Delta versus oh, Macron. My own impression would be that it's more severe and more frequent with Delta. Now, dr kumari asked, is there a difference between when you get viral myocarditis versus those in frequent cases of vaccine related myocarditis? Yeah, I think there is. It's a very good question. I think vaccine related myocarditis is really probably an autoimmune related inflammatory condition of the heart. No question. It's not you. It's been seen. It was described with chickenpox vaccine years ago. So it's not new. It tends to affect young males and teenagers and it's very self limiting. At least. I think in all the cases I've seen published, I think that myocarditis when it occurs with covid is a a marker of more severe inflammation plus perhaps inflammation and maybe other cardiovascular manifestations. But we do know is from the center for I think it's from and center for National Center for Health Statistics. Um, that the likelihood of myocarditis with the vaccine, which does occur in young people tends to be males, tends to be teenagers. It is still less then the incidence of myocarditis acutely in covid 19. So even with the vaccine it's still less frequent Than in patients that get severe COVID-19 infection. So I think that the I think that the documentation of um mm hmm myocarditis and pericarditis with the vaccine should not be used as an excuse not to have the vaccine. Very good. Um Dr Marx asked about pots and he mentions that shall we do cardiac M. R. In those patients? And then also what is the role of inflammatory markers for a routine surveillance in these patients? I I absolutely don't know. It's a very good question. And this is being looked at right now in these long term prospective studies that all collecting evidence for acute cardiac injury acutely namely troponin elevations and seeing what happens to them over time and how they correlate with persistent symptoms. Because it is possible that some people with persistent symptoms may have ongoing information. Well I think I think it's probably auto immunity. So we don't know at this stage what the role is of the cardiac biomarker is late personally, I would get a measurement of troponin and perhaps crp in these patients. Would I do M. R. I. In people with pots routinely? No. I think God if if they had an abnormal electrocardiogram and detective the echo is abnormal, then I think it's reasonable to get an M. R. I. I wouldn't do it routinely. I think that I've seen parts working as an electro physiologist. I've seen plots frequently. Um after undisclosed viral illnesses whether they be flu coxsackie, who knows. But typically all right. Women in their 30 educated many of them active athletes, quite serious athletes and it's a debilitating condition. And the reason I say the electric physiologist nightmare there's not much we can do for them. They have these postural tachycardia obliterating these patients would be a disaster. And what they need is really, you know, Potts was first described at the Mayo clinic in detail by dr Philip Lowe, a neurologist and it's a disease of the autonomic nervous system and uh neurologists take care of them. But one critical aspect of pots is a very a comprehensive multidisciplinary, a rehab program with graded exercise, sometimes aerobic exercise in water in a pool, but it needs a comprehensive multidisciplinary group. Do you think the one predilections of this virus for the autonomic nervous system? That's why I think I've seen it after other viral infections and what I think really is important when these patients come and they're pretty debilitated. A significant number. Told, look, you don't have an infection anymore. It's all in your head. It is not. It's real. And it's how about how about changing the topic a little bit uh dr boats asked about hyper quality ability. What is the difference or what are the differences you think are if you want to compare acute covid infection versus a long term or chronic covid infection? I don't think we know that. So it has implications on the anti coagulation and such because the pe and And arterial thrombosis is much more common after COVID-19. Absolutely no question. And you know, there's a lot written and they're all good, good consensus guidelines on who should be discharged on oral anticoagulants and a substantial number of people. And obviously if they've had a DVT or a p a a pE during hospitalization, I think the discussion is, how long do you anti coagulate them for? Is it three months or six months or whatever? But I don't know of any studies on coagulation factors in patients presenting At 3 to 6 months with with, you know, non specific symptoms. I just don't think we have that data. So there was 1 to 10 dus now you mentioned this collateral damage issue. Right? So the symptom onset to um presentation time door to balloon times, they're all prolonged. And he mentions that, is it because of lack of healthcare workers being present or while they're waiting for the covid test. So that's one part of the question. And the second part is that, knowing that underserved minority patients and higher rates of covid infection and traditionally have poor CVD clinical outcomes. How can we effectively determine future incidents of CVD within that population and possibly aggressively address the risk factors at the same time? Well, I think that's a very good. It's not even a question. It's a statement and it's a very important statement. I think that the collateral damage that we've seen, it's not universal. I know I presented some of these data in europe and in some centers in europe, they didn't see that it really didn't. So it may be region specific. It may be in part due to the logistics and the logistical constraints and the availability of resources in that particular region? It may also be patient specific. Some patients may be more reluctant to go to hospital than others and it may depend upon the quality of the hospital in the, in the area. So there are multiple multiple factors. Um, the second part of your statement, I I echo that Covid has brought out disparity. So brought has magnified the disparity is already present in our society in the delivery of cardiovascular camp. And they've been magnified by Covid. And of course, um, these minorities are at a greater risk in terms of cardiovascular risk factors with or without Covid. And so I think that the impact of isolation on cardiovascular risk factor management and it's late implications is profound. It's going to be very difficult to study, but it it it is really an issue. And that may be one of the things that is responsible in the one slide I showed for the late incidents of hypertensive deaths during the first year of the pandemic. Yeah. Um, if we have to focus on groups, you you mentioned athletes is one right, which where even though The overall myocarditis incidents is less than 1%, but can have profound implications for that high intensity exercise group and can be fatal even though they may not have symptoms and then you brought out the the race and ethnicity issue. Do you think the other susceptible susceptible group that we may need to have special focus on will be older individuals where there are tons of co morbid conditions that make them more susceptible to a long term covid infection sequel. Yes, I think so. I mean, I think that in terms of competitive athletes, there are good guidelines in in focus. I mean in print that are not just covid related related to any athlete with the viral myocarditis and they're good and I think they ensure safety. There's a role for stress testing, there's a role for imaging. It may be a role for all to monitoring and some what I think we haven't he had seen and there are a number of sports medicine, individuals who are looking at this and that is if you're a top class professional athlete And you lose 5% of your performance, that could have a huge effect on their livelihoods and their successes and athletes, hopefully that's not going to be an issue and not a long term issue. But it's something to think about. You talk about older older individuals with comorbidities who have higher morbidity from acute covid. And I think it's reasonable to suppose, I suppose hypothesis that they may be at a greater risk of long covid, but we don't know that that's what the studies again are looking at And dr kumari has asked again about, do you have any ah imaging or any markers, for example, you said post vaccination. Myocarditis is mainly autoimmune any inflammation or any other markers that will help the audience differentiate Because you have patients who received a booster or a vaccine and then got into a presentation with myocarditis. Now they are unsure whether this is a covid infection or this is a my vaccine related myocarditis. So are there any, no, there's no way you're really going to know. I mean, it's a clinical scenario. Someone in really good health, 17 year old year old, Excellent Health. They get a vaccination and four days later they got chest pain with market artists and more frequently pericarditis that that that's all I need to know. And the likelihood that they will resolve is very very high. I think probably almost universally it will resolve within a few days. And that actually we did see with varicella chickenpox vaccination years ago. In fact, in up to date, we've got a paragraph in up to date on varicella myocarditis. And I actually raised the question of whether it was redundant and just of historical value and we should take it out of up to date but not of course it's not because of the Covid vaccine. Now, what is difficult. I have seen some slides of an M. R. I with quite extensive late gadolinium enhancement in a young individual that individual had covid and subsequently was vaccinated without an acute vaccination um syndrome? No, there it gets difficult. I don't know whether what we're seeing related to scarring from the original infection or whether it was related to the vaccine. But I don't think the vaccine, my understanding is it's very short lived, Severe and painful for 2, 3 days, as pericarditis always is and then it goes away. So I have a few minutes left and it's quite unusual. But I think something that I wish to ask you for a long time as my mentor, as my teacher and I think it will help people who are viewing and listening to your talk is how they can become burning gersh, you know, so just let us know in a few minutes. I know you've had a carrier of or in cardiology, I just want to know and if you can let all the audience know, where did you start and how did you become Bernie Gersh and how can they become lethargic? And Nishimura and Bernie Gosh, if they wish to, what do they need to do? Maybe maybe most of them are too sane to want to become. Do you go through all of that? I think my Children would have a different answer that question. Well, I think, you know, I think the key is you have to love what you do, You have to be fascinated by by what one does. And aside from being a clinical cardiologist who spent most of my time in the CCU I just found a lot of very interesting questions to ask that come up in your day to day clinical practice and then when you work in an institution like ours, one has the resources to sit down and say well we you know, we don't really know, let's look at it. And one of my mentors bob fry who always said to me, don't just quote everybody else's data. What about our data? What what what are our data show us? So I think you have to have the curiosity and the interest and there's no shortage of interesting questions. And I had a meeting last week with some of my colleagues in the artificial intelligence group and we've just come up with three or four really interesting questions that need to be answered and we will answer them. And then I suppose the other aspect of it is We're all very busy and no one's going to do it between nine and 5, you have to you have to work longer hours. And for that I'm very grateful that I've had an incredibly supportive wife and family, Incredibly supportive. They've supported me and my career for 30, 40 years. I didn't I don't really know how to answer that. I mean it just happens or it doesn't but you have to work and ask the questions because um I frequently get off some really good questions from non academic cardiologists who say look I've got a patient with a B and C. What do you think? Can you say? You know, I'm not sure I've seen that before. Maybe we should try and study that. You have to love what you do because it is time consuming. So so three things I love what you do right curiosity and a loving wife. Not in that order, not in that order now. And loving wife and Children who are supported because they're the ones that you know when we're working nights and weekends sometimes and you know, take the time away from them and then obviously you've got to have a a certain amount of intellect. Yeah. Yeah. No it's been it's been a pleasure and an honor again until we meet with with another fascinating talk by you Till then be well and we'll see you soon. Thank you very much, mandy.
