Cardiovascular Risk in COVID Recovered Patients

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Cardiovascular Risk in COVID Recovered Patients

5 Aug, 2 PM

[Music] so welcome everyone uh sir is here with us for the third time and this is the first session in the heart of the matter so on netflix uh this is the actually a different uh uniqueness of metrics i'll tell you uh we have interesting clubs and every club has its own dna uh which is framed by all the top doctors across the country and heart of the matter is one of those uh so here sir will be discussing some amazing topics in cardiology not just for cardiologists it this will be useful for some other specialities too so likewise today we are discussing cardiovascular risk in covert 19 uh recovered patients so uh this is something actually all physicians for that matter should uh know about today we are back with an amazing session cardiovascular risk in government 19 recovered patients so uh so i as but as i can guess we don't have a lot of evidence here it's all clinical picture and based on that we have come to some conclusions right a lot of it is not available no it's not a lot of it is available surely for acute but what she meant by omitting the word chronic is that yes a lot of things are missing on chronic complications because we don't know what will happen beyond two years nobody knows the virus has not been there for two years now so the biggest concern that we have started getting worried about is what are the long-term sequelae what are the long-term effects of govid19 on heart now people would say why sir are you interested in all that stuff no i'll give you certain reasons why it is in one of the most famous study done in germany where they looked at the cardiac mri of patients who suffered from covid19 these were 100 patients and beyond the recovery they found out late gadolinium enhancement which is the cardiovascular manifestation of you know virus actually interacting with myocardium being picked up on cardiac mri that was found to be present in 75 patients nearly which meant that because of the high preponderance of a s2 receptor which we all know is 2 is the receptor through which the covalent 19 transfects or goes through the cell and because myocardium lung and gi tract apart from to some extent brain and the vasculature has got the highest number of these receptors present that's why you expect these viruses to go and bind at that site now when that has happened once the virus has reached that level and the immune system tries to get rid of it beyond the replication what amount of the dysregulation or cell alteration or genetic modulation or cell degeneration takes place in the long term nobody knows we all know from acutes equally that yes in one of the studies 75 nearly 75 in some some one data was 74 the other one was 76 but you can say roughly three fourth of the patients will have one or the other type of cardiac involvement which may be in majority asymptomatic so you may think many mild kovitz you had a very mild disease nothing was much there to look for but even in such subgroup of patients you may not have overt manifestation but still viral transfection and viral involvement to the myocardium still would have happened now it acute phase it can cause myocarditis uh vascular vascular thrombotic milio arrhythmias it's been in one of the studies been shown that in patients who are more than 70 years of age 61 patients in acute covet came with atrial fibrillation now that's a very high percentage for presentation again another in another example how this virus though we always assumed that it's the lung or the gi but cardiac status is not mentioned so probably be underevaluated under assessed under reported and under treated cardiovascular manifestations only when the patients ended up with a rhythm rhythm abnormality or cardiogenic shock or acute mi or a thrombosis that everybody woke up so maybe maybe it was under evaluated in the sense that we were always chasing the lung because of the desaturation and when you ended up looking for biomarkers you would end up finding a lot of issues in these patients with elevated troponin cpkmed d-dimer bnp and then again we often ended up counting upon these parameters to be uh ascribed to something else you know this is a dic kind of a situation uh troponin will falsely rise because of renal impairment uh d-dimer or thrombosis it's the endothelia that's why it's gone up or maybe there is pulmonary embolism or there is a venous thrombosis etc etc so of course those were the other reasons to cause the elevation but then we probably ended up being more aggressively watchful for finding out how much subtle subacute not a very severe form of cardiovascular infestation had already taken place now as the time goes by once the lungs fibrotic changes regress and disappear once the gi symptom starts healing off the lung tends to have some of the patients tend to have lung showing fibrotic bands uh the presence of fibrotic tissue reduced lung compliance some of them have chronic hypoxia they will require long-term oxygen therapy but this is manifested in lung what about heart heart will not show any symptom unless you assess them in the long term manifestations that can be presenting in as an acute manifestation of a chronic carrier state now that would manifest sometimes in patients coming with an acute mi later on that's why this topic has been brought up here so in last second wave uh post second wave my own practice we have treated almost four to five young guys who had previous coveted last the second wave did not have any other risk factors non-smoker no family history no diabetes hypertension who presented with acute mi so my query and question then goes back again to this thing and a lot of my colleagues have started reporting this that they can come with acute mi beyond two months three months which is like once they've recovered completely does that mean that the kovit continues to have prothrombotic believe despite getting cured from the acute illness phase in these subgroup of patients some of them were either even on aspirin despite that now with that thing in picture maybe this is requires a long-term study whether this is just an anecdotal finding we all need to find out but we have a postulate to suggest that probably these patients can have a long-term impact of covid19 which we are yet to assess which can manifest later on in their life now with this ongoing the next question that arises is how does it impact my practice now how does it imp how it has impacted my practice and how it should probably impact anybody's else's practice is now when a patient comes to me in a stable state when he comes with an acute mi stage of course you do an angioplasty or thrombolysis or treat them for acute mi like the standard protocol and start them on dapt etc that's for the acute presentation of a chronic coverage as you call it you know something beyond once his antibody titus have started emerging and he's rtbc are negative as the lung is healed i'll call that the chronic recovered ko weight presenting with an acute coronary beyond that when a patient comes in a chronic recovered state of covet to you for a chronic symptom not an acute symptom he's come for a routine checkup say for hypertension say for diabetes say for a patient presenting with a typical angina so what would that impact in my practice what we should be doing number one all patients who have recently recovered i tend to send their troponin i cpkmb bnp and d apart from d dimer once they are coming for the first cardiac consultation beyond recovery from covet why it can tell you a smoldering ongoing small myocardial injury ongoing if you can find these high sensitivity biomarkers elevated you know that these are at risk patient number one number two if this patient has been beyond the allotted phase of say once you've done up top cpk it's been done by the previous physician or have done and they have come negative and they've come to you i do ask every patient now for a risk factor to be mentioned as did he have probate why is it important now people would say sir eighty percent zero positivity rate is there but remember eighty percent zero positivity is for uh patients which included vaccinated ones non-vaccinated ones patients who are already uh recovered in the previous wave or who are just asymptomatic previously and they somehow acquired but if you had a frank developed covet due to an immune response remember this is like a immune response kind of an injury not everybody is responding in the same fashion so if somebody comes back to you who had a bad covet in past that means he has a possibility of generating another immune response in the same fashion this should be mentioned as a risk factor for a cv viewpoint so apart from history of diabetes blood pressure family history lipids and sick smoking eye all sedentary lifestyle basically the classical risk factors that we know of cardiovascular disorder i also mentioned whether he had past history of kovid or not because if you know this then you would always be more watchful so this is how my second point of practice has changed so one is look for biomarkers second is identify them as potentially high cb risk and third is if these patients do have positive coverage history my potential of therapeutics is slightly lower what does it mean so suppose there is a 30 40 year old male who comes to your clinic and because he's less than 40 if his ldl level is 130 i would still probably be not giving him statins i would say we'll what we'll wait because as per the guidelines beyond 40 is when you start statins for the dyslipidemia unless you have risk factors or you have established a cvd which means if you are diabetic if you have already undergone angioplasty if you have families etc if you don't have anything you are just primary first time coming patient and you have sent a lipid profile is less than 40 no serious factors no problem just a routine checkup no diabetes no hypertension no angioplasty no anything no crm no family history less than 130 i'll say okay let's wait you start lifestyle we'll review you in three four months we'll see how we limit look but now though this is not from a guideline if patient mentions that he has a history of covad my threshold of putting a monostatin or for a stable cad established on an aspirin would be much lower same would be the case for looking at their heart rate if i find patients a lot of patients these days come back with tachycardia their baseline heart rate is now 100 instead what used to be like they would say i would jam and my heart rate used to be 70. i would put them on a beta blocker because this is again dysautonomia which has been documented now very clearly in literature post overweight so a lot of these patients will come with tachycardia or there will be other extreme coming with bradycardia so there are both kind of manifestations that can be present but once they recover from the acute phase and if they continue to have tachycardia these are again high severe risk patients potentially again that evidence is yet to emerge because what is going to emerge in next five seven or ten years or over a decade in patients who've suffered from covet only time will tell but assuming that the post covet patient with the postulate that most of the patients have preponderance h2 receptors in their myocardium on top of that there is an mri study which shows that a lot of patients do get cardiovascular infestation of the virus in the acute phase which may or may not persist later on but even if it does not persist can have healing with fibrosis which again it's a welfare pro erythemic focus or now that we are finding some patients post covered in young phase without any past history coming with an acute mi is it a pro thrombotic milieu that the kodi leaves behind we need to be cautious i'm not raising an alarm bell i'm not scaring people in general and because i'm talking to a forum of doctors here it is just to tell them that like you take history of diabetes like you take history of hypertension like you trick history of dyslipidemia same way do please take history whether they've suffered from a covet illness or not especially if required hospitalization if they have your threshold for suspicion for development of cad or other risk orders should be much lesser and in such patients maybe not only you should be evaluating them with biomarkers if required an echocardiography you will also probably have to be putting them on the primary preventive therapies at a much lower lower threshold at much earlier stage in such subgroup of patients so to conclude i'll now summarize the math the topics that i've talked about number one there have been studies to show that the cardiac mr has shown that the covate can cause majority of the cardiac patients have some kind of involvement in acute phase a destabilization of the myocardium also can take place in acute phase this can be by mri late gadolinium enhancement number one number two arrhythmias in elderly and number three of course we all know acute mice thrombosis etc once they recover there are three things that one should keep in mind number one send for their biomarkers if they have not been done especially antipropane p be a dropout in i and cp can be high sensitivity preferable to look for what is involved or not number three if once you have done that and that's normal if it's abnormal you have to do echo and for do further work up if it's normal then keep asking history of covered as a risk factor in all opd patients that you see and number four when an acute mi ends up in your clinic make sure that you're asking whether they had a past history of covet this may be the awkward manifestation that may be present so these are the important take homes in the chronic disease these are all postulates and hypothesis because we don't know what are the chronic manifestations of covered in long term but i've given you certain evidences how it may persist in one or the other form with anecdotal case reports now presenting now patients coming and maybe that also explains some pro-thrombotic effects of some of the vaccines that we are seeing in some of the subgroups so i'll not name any vaccine no controversies no population but you all know with subgroups of which vaccine people are coming with pro-thrombotic and acute illnesses so that may be responsible partly can be explained by this sub group so i end my uh i conclude my uh talk here and now we will be open to questions and i think there are a lot of raised hands and they have a lot of messages and chat boxes which you can help me out yes sir there was one question how often do you see uh cardiomyopathy in government fiction so if you can address that is the japanese name for fishermen spot this is how it looks like a pot of a fisherman it's a small tumbler so you have the bases of the heart looking normal and the apexes are blown out this is how it looks like this is a package so this is the neck and this is the container so you have a narrow neck and you have a broad container so the container is broad at the base and it's narrow at the neck the neck is the basis and the apex of the heart is not contracting so non-contracting so this is like non only these stock contracts the apex does not contract so only this is contracting this is how the heart looks like that's what the taco super this is basically stress cardiomyopathy and we reported five papers for our own we have done five publications of takotu which very common stress cardiomyopathy means any stress causing sympathetic release causing myocardium to get stunned and remember that stunning of the myocardium is done done it is primarily at the apex and the bases continue to contract because of disproportionate presence of their receptors so this is usually benign it can happen you know lb dysfunction that develops immediately after acute stress we we found it a lot of times in the bh epidemic of earthquake a lot of stress cardiomyopathy in that time when the earthquake had happened a lot of such people came back with you know dysfunction and then they were reported to develop supercardiomyopathy this is a reversible state which completely improves upon with time but in that suburb its prognosis was worse than those who had did not have kovid and kakotsu this was our first finding that we published now other thing is that the male and female preponderance when you compare usually taco super develops in females but in kovid male and female preponderance was equal that means that males can get as bad a takotsumo as compared to female so the stress of the disease itself the fear of the disease itself and the fear that i lose my family i'll die of kobet was also probably responsible partly for it but now it's believed as was pointed out correctly by dr madeway that this virus itself can stun this is one more example how acutely the heart was getting involved by covet virus can present with taco super cardio so again this was usually transient uh it has an overall good prognosis compared to a patient developing dilated cardiomyopathy overall but again it's got worse prognosis as compared to taco in a patient who does not have chores compared to patients not having covariant aqua super tacos is bad it's worse prognosis with male female equal preconditions so that's the point um that i wanted to brought up uh so there is one question uh the routine cardiac workup in post covered uh yes so yogesh has asked this question um so it's a good question so as i said if the patient is a high cv risk and he's come out from a bad pneumonitis for which he was hospitalized and if his troponin i cpkmb and bnp apart from d-dimer were not done i would surely get it done from the acute phase in this recovery also a lot of times sub-segmental small pulmonary embolism may be missed and that's why you must do an ecg as well as echo also for these patients so ecg echo and blood these three things i believe no patient would you know mind getting it done because a lot of these patients can have small sub-segmental pulmonary embolism which may not be picked up and you know getting them a contrast ct pulmonary anger for everyone is not a good idea so if you find that the pulmonary embolism is uh the pa pressure is high then you can subject them to a ctpa but if the pulmonary pressure is normal then that means it's a sub segment to small pe for which anyway now everybody is giving a novak for quite a while so in that case probably it won't be warranted to do a ct pulmonary angiogram for everyone you can just pcg and the biomarkers that i mentioned in acute phase and then if everything is normal then probably nothing more if these are normal okay so sofia you are on stage can you ask your question unmute your selfies um good evening sir uh so if the patient is recovered from severe core pneumonia uh from last uh nine months and uh in this time period there was no postcode complication is there further chance of developing any postcode cardiovascular risk correct so that's what i'm saying risk factors like diabetes hypertension family history elderly age presence if any of those things were present then you would not stop getting the work up done you would probably then go ahead and at least get a good cardiovascular workout done if the patient was lean and then 20 year old young female unit just had a ct and showed that pneumonia i don't think then probably you need that an extensive workup especially in the long term gone by but then if there were symptoms and which you thought was probably a pneumonitis which led to dyspnea and fall in saturation and if there is a smallest of suspicion that this kind of pneumonia with a ct score offset 12 or 10 out of 25 and patients having saturation of 85 you should rule out pulmonary embolism that's one common mistake i mean the misdiagnosis you know it's under diagnosis in such kind of a subgroup of patients though ct score or a ct value in rt pcr does not always correlate but sometimes it can give you a good idea if the lung is not so badly involved more than 50 lung is still okay and the very bad saturation extremely low saturations or a very bad requirement of oxygen you should always be ruling out pulmonary embolism uh sudden cardiac event in postco with patients as they are asymptomatic mostly yeah so uh asymptomatic patients you somebody is already asked about the question on inappropriate cardia so i'll clap the two together inappropriate sinus tachycardia and sinus bradycardia and long qt interval and loss of respiratory variability are predictors even in non-covate situations of sudden death though they are not strongly associated but they are all predictors heart rate variability is a good predictor of a certain cardiac death in any situation so long qt interval resting heart rate heart rate variability all will be predictors of sudden death but then it's it's very difficult the sudden death itself is a broad term you could have arrhythmic deaths you could have thrombotic threats you can have pulmonary embolism there so again as i was answering the previous question what you're probably looking at is sudden death cause caused by what if you are having a suspicion of sudden death which can be implied upon by pulmonary embolism then it would be interesting and important that you actually get their echo done and for arithmetic of course you can do either a signal average dcg as it is called as but which is very rarely done at least a baseline ecg and if there are rhythm disturbances that are found or a long qt you may actually end up doing a holder monitoring so echo holder are two important things that can help you but at least an ecg echo is good enough to at least screen out all of them i hope this answers your question uh so there is one more question on anticoagulants um which which remains beyond 100 without any reason of hypoxia and this is very common in covet post code recovery which needs to be treated with beta blockers very common i've treated a lot of patients with that and this is again a risk factor per se now you should be very cautious in these subgroup of patients not to be treating them with you know just rehab you'll have to put them on beta blockers and this again reflects the dysautonomia that may ensue as i was mentioning in covet patients so and for those patients who don't have any uh pre-existing cardiac condition uh how long do you recommend anticoagulants and antibodies agents so no risk factors again the guidelines have been talking about again this is a new disease so everybody has every country has got their own practice and their indian guidelines which have emerged if no risk factors then usually a month is good enough 28 days in a hospitalized pneumonia is recommended based on a lot of studies 28 days of novak is good enough aspirin you can actually stop if you're giving nowhere because it increases bleeding risk statin some people argue is preventive in nature so it could could be continued beyond a month usually you would not require a low act aspirin some people give it up to three months and then discontinue but in a patient whose high cv is probably i would stick around you know giving them aspirin and starting though you can discontinue know what if they don't have a thrombotic history like a deep end thrombosis or a pulmonary embolism or arterial thrombosis in which case of course you will be giving them a longer duration of um so i'll clap up two three questions more and ask you together so uh people are asking when or the patient is being discharged uh with her cardiac condition uh what lifestyle changes do you recommend to that patient are there any preventive majors that you have to tell them uh sorry in kovate or in cardiovascular disorder uh a patient who is getting discharged cobit patient with a pre-existing cardiovascular condition good question so i in that condition you will give him all advice that you would give to a patient who is recovered from an acute mi so what is that a graduated rehab uh lifestyle change including dietary change so because this patient is recovering from an acute illness which is if he is hospitalized and i am assuming that he is recovering from a hospitalizing requiring covet which means his pneumonia right it was not just an rtpcr positive and isolated in the hospital so if he is getting discharged from a hospital for which he required hospitalization means that this was a acute enough severe illness in a patient who's into inflammatory milieu because of that kind of a state it would not be a good idea to put them on a quick rehab because then it would increase their cv uh tolerance you know it would be checking on the cardiovascular tolerance and would be substanding substantial risk for uh triggering an acute coronary even so in that case you would always do a graduated rehab ranging over two to four weeks like you do for a cardiac patient uh 15 minutes walk adding 5 10 minutes every ten five five seven days and then going up to 45 minutes to reach the peak exercise at four to six weeks so that's how you should be chasing any cardiovascular patient who's recovered from an acute illness like covered pneumonia so any specific uh things that you want to mention about the nutrition uh or yes so nutrition is per se a very broad topic in cardiovascular disorder we can discuss this in some other session per se but of course it remains pretty much the same you would not do a lot of fats you will not do just pure carbs you'll include surely some amount of proteins again 50 to 60 the classical role that people mention 10 percent less than 10 10 of fat and more than 15 of proteins so something in that range 20 to 30 is what is ideal 50 to 60 of cup but most important of all this is so you must include a lot of fibers which is at least by weight in grams of 300 to 400 make sure that there are at least at least two to three servings of fruit which is roughly to say you have one fruit in the morning and one fruit in the evening and then on top of that you have one plate of salad in the lunch and one plate of salad in the you a reference of 300 to 400 grams that you're anticipating of course vitamins again a lot of people are anyway overtaking so i think once you add a good amount of green leafy vegetables with fruits you're taking care of that as well anti-inflammatory diet yeah uh yes so post-vaccination is there any cardiovascular risk associated with it i know that's a very broad topic too so now a lot of european countries raised that signal for one of the vaccine they got it cleared again they came back so then then that signal was taken off uh they had mentioned a thrombotic risk and then there were again with one of the vaccines in europe and then they removed that tag they did mention so i think with the mrna vaccines they did not raise that much of a signal but with an mrna vaccine it's a new technology i mean if you were to ask me are you comfortable taking a mrna vaccine versus a modified led vaccine or you're comfortable with the killed virus if i was to choose i would go with a killed virus you know that's always a better idea that's the classical way from edward general days you know you kill the virus and then just give it so it's just immunogenic and doesn't create a disease why would you let a live virus enter your body or maybe an mrna enter your body and transfect you and you don't know what happens 50 years down the line this is the first ever developed mrna vaccine that's coming so people can have their head but i mean maybe i'm just an old-fashioned guy about choosing between vaccine and going by relying more on rahul david then going with dashi savage to open up the bat thing because i don't know whether he'll click or he'll not but um i think it's better to be with the wall than be with a slasher outside the offstar so maybe i'll be happy that ways i'll stick with that but then of course no it's any vaccine is better than no vaccine so get vaccinated is of course valvular changes that we have seen uh okay so so can you mute and unmute yourself i'll just go on nude but okay i've muted myself and i'm back i'm not hearing any echo now right okay so yeah so valvular changes uh include some amount of regurgitation uh primarily and these are all derived because of the dilated cardiomyopathies or tacos cardiomyopathy primarily the valves are not so much as to receptor driven valves are getting involved with m protein of the rheumatic fever we will have some session that on that also some other day but not covet co it doesn't have m protein spike proteins to cross factor transfect with so not much of the valvular changes per se but then they are all secondary changes that can happen uh after the dilatation of the ventricle that's all otherwise no not as of now again what happens 10 years down the line you don't know [Music] okay so have a sign in your name is the next session that i'll be having in this club and uh for the other clubs let's see when we come with the meds calls and the debate is the next thing that's happening in my third class so then we'll have another session in the debates uh again we're looking at your suggestions as to what topic you guys want and we'll go again with the audience choice rather than our own choice you will find a form for that on the app if you want to suggest anything to sir or any other club to you can do that your suggestions are always welcome

Description

COVID recovered patients are still at risk of various systemic consequences and, one of those is risk of cardiovascular diseases. We need to watch out for those signs and take appropriate precautions accordingly but how long do we need to keep an eye and what are signs? Let's dive in and understand with an eminent cardiologist Dr. Kamal Sharma.

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