COVID Rehab & Recovery Series: Cardiovascular Implications of COVID-19 with Stephen Andy McCullough, MD: Sunday, 07-26-2020


Ladies and gentlemen, welcome this evening to another edition of the COVID COVID rehabilitation and recovery series, courtesy of the pulmonary wellness foundation. Our guest tonight is dr. Steven Andrew McCullough. Dr. McCullough is an assistant professor of clinical medicine in the department of medicine, division of cardiology at Weill Cornell medical center in New York city and New York Presbyterian hospital. In addition to caring for patients at the wild Greenberg Santa Fe, he interprets and perform stress tests, echocardiograms, and attends on the inpatient services at New York Presbyterian, which means he’s going to have a lot of the answers that you guys are looking for. He was born in Shreveport, Louisiana, and completed his undergraduate education at LSU, and then attended Mount Sinai school of medicine, where he graduated in 2012. Welcome dr. Mccall. And thank you so much for being here this evening. Thank you. So I’m one of the things that we’re seeing is initially when COVID hit us here in New York and really worldwide, which was thought to be a disease of primarily lung injury, respiratory involvement, and acute respiratory distress syndrome as time goes by, we know that nothing could be further from the truth.


Can you talk a little bit about some of the more common cardiac implications that you’re seeing in your work with COVID patients? Yeah, but you know, contextualizing this disease in a context of other pulmonary viral illnesses is important. And if you don’t take what we’ve learned from COVID-19 in the context of these other diseases, then you CA then you have basically no, no blueprint, no groundwork from which to understand that the appropriate care of your patients. And so if we look at all of the HRDs literature, acute respiratory distress syndrome, literature, going back to the late seventies, early eighties, we know that inpatients who have a RDS, there’s a propensity for increased blood clotting. So either in the lungs, themselves or in other parts of the body and alongside that, there’s the potential to develop a syndrome called multi system organ failure.


Multi-System organ failure is driven usually by the immune system. And it’s where several different of the body’s organs can shut down kind of in an unpredictable manner. And it’s one of the reasons that patients who have HRDs die. Now, all of that said, I think that we have to understand that going into treating this virus, the, the likelihood that it was only going to be a pulmonary disease, knowing that we have 40 years of data from other viral ERDs, particularly would have been a bit shortsighted. And so I think that if anybody approached this disease, thinking we’re only gonna treat the lung manifestations of this disease and not look for anything else, then those people were going to be prone to mistreat patients. And so whenever you look at the course of patients, especially in the ICU who have ERDs it can either be mild.


We say mild HRDs, moderate ERDs, or severe RDS. And in the patients who have severe RDS or severe lung injury, the hormones that are released by the immune system while trying to heal that injury do damage to the heart. It happens in almost all of our ICU patients who have had the flu. And it certainly happens in COVID-19 I think in trying to assess the differences of COVID-19 from these other severe viral respiratory illnesses. That’s where we’re, we’re trying to feel what is truth and what is not knowing that if you’re, if you’re a decent doctor, which almost all of the ones that I worked with are you’re looking for these other organ manifestations. And so whenever you have patients who have this immune response to COVID-19, what we see is that in a small subset of those patients, they can develop heart failure where the pump does not squeeze normally that they can develop a heart rhythm abnormalities.


So most commonly being atrial fibrillation, which is a common heart rhythm abnormality of the older patient. But whenever you have young patients who have AFib, the symptoms can be pretty debilitating. You can develop a low blood pressure from those hormones, and that needs to be supported with medications to keep the blood pressure up. And then the longer that patients are ill from the virus you develop pretty profound deconditioning and dysfunction of what we call the autonomic nervous system, which is essentially a part of the nervous system. That’s hormonally driven and dictates basically how we how we deal with our symptoms on a day to day basis. How far can you exercise? How far can you walk? How easily do you get fatigued? And those hormones can get out of whack really easily. And I think that’s where that’s where we see the biggest impact of this virus is, and those type of symptoms, however, severe cardiovascular manifestation of the disease are there, but they’re there in a lot smaller numbers than then I think what we initially expected based off of the data off of Wu Han. So when the Wu Han cohort whenever they started publishing papers on their cardiovascular complications and late November, early December, they said around 7% of patients are seven out of a hundred people would develop heart failure and refractory what we call shock which is basically the body’s inability to


Supply blood flow adequately to the organs because of the failing heart. I would say in our critically ill patients, we certainly saw patients who had shock from heart failure, but the numbers were a lot lower than that we’ll find cohort and what the wound cohort did not comment on was basically everything else. The inability of people to exercise, how long the symptoms lasted afterwards and then the arrhythmias. And so I think that’s, that’s what we’re seeing. If you want to know longterm consequences of what we’re seeing is just debilitating fatigue. And and in at least 10% of our patients that came through Cornell abnormal heart rhythms,


Can we talk just get a few of the terms straight. So we hear a lot of terms kind of thrown around in the, in the media. What specific hormones or chemicals are we talking about when you say what are you referring to? So like, what should we be on the lookout?


So, you know, you mean the hormones that cause heart failure. Okay.


They cause heart failure. And also for example, that would indicate a heart injury.


Yeah, it’s a good question. So in patients who have severe lung disease, there are a group of hormones released by the immune system called cytokines which I think the literal translation is foremost that affects cellular function. And those are particularly important in activating the immune system and when the immune system is active and when it’s overactive, our, our own immune system can attack basically any part of the body you can name can be subject to attack by the immune system. And so those are the hormones that I specifically mean when I say that there’s, you know, a propensity of this virus to cause damage to the hardest through immune system released cytokines. Now the, the lay press has commented a lot on this paper that came out of UConn looking at a bio marker or a marker of the body.


That’s a, that’s a bio marker called troponin. And the term Ponant is a, is a cellular protein within the heart that is released by dying heart muscle. It’s also found in every other muscle of the body. And so we think that we think that it’s, you know, specific to the heart 99% of the time, but 1% of the time it isn’t, but when the numbers get very high, that specificity, that ability to say this is solely from the heart is very, very difficult to do clinically. And so when we say that that’s a marker of heart injury, we have to take it into context of everything else. There are, there are a significant amount of patients that are walking around patients on dialysis, for example, who have an elevated proponent, just, and we have no idea why their heart functions. Normally they have no heart failure, they have kidney failure, but their true opponent as high, do those, do those patients have heart injury?


The textbook definition would say, well, because there’s, your opponent is positive. Their heart has to be being injured, but it’d be being injured basically throughout the duration of their lives. And then there are other there’s other science that supports that this molecule traponin is released in healthy hearts. For example, in a paper that was published in 2006, anybody who ran a marathon and had their blood drawn afterwards, had positive troponin levels. And so how do we interpret that paper for move on in the context of all of these other things is I think that one, it can be a very, very sensitive, or it can capture a lot of people who have the potential to have heart injury. Does that mean that their heart is injured or not functioning properly? No. We have to think about it and figure out what’s going on with the patient, but it’s a good, you know, like 20,000 foot view of this patient.


And what we see historically is that that marker is elevated and really sick people. And if somebody is in an ICU and has the propensity to develop multi-system organ failure, their treponema is very likely going to be positive. So what that paper for Mohan said is that inpatients who with COVID-19 who had a positive term opponent, they had a higher risk of death. And how do you interpret that whenever you read a paper like that and you interpreted, and you’re in an ICU taking care of patients, what you read is these patients that were in this paper were really, really sick to begin with.


And so whenever you read that paper and you wonder these patients were really, really sick to begin with, is it because of their heart was necessarily involved or is it because they were really sick to begin with? And we can’t really parse those things out, but that generated a lot of excitement in terms of looking for heart injury on these patients. And so I would say that if that paper did anything, it really, it reset the framework for us to be able to at least think about these patients differently. Now, what is thinking about these patients differently mean in New York city in the middle of the pandemic? Because if you’re going to look for hard injury in somebody, you should, the first test that you’re going to perform as a test called an echocardiogram, which is an ultrasound of the heart, basically tells you how the heart’s moving, what the muscle of the heart looks like how well that muscle is squeezing, what the pressures inside of the heart look like.


If there’s any damage to the valves of the heart, if there are blood clots in the heart, it can answer a lot of questions, but it requires exposing a technologist to that patient for upwards of 45 to 60 minutes, to be able to do that test. And there are ways to answer those questions kind of like by beating around the Bush circumferentially, to see how the hardest functioning without necessarily exposing one of your staff members to do that test and very early on in this pandemic, whenever we heard stories from Italy of multiple healthcare providers dying, multiple healthcare technologists, dying, multiple nurses dying it’s very hard to say, and this person who has a normal blood pressure who has severe lung disease, who only has an elevated traponin, but also has kidney failure and also has a bacterial infection in their lungs. Should we subject a technologist to go and do an echo on this patient?


If everything is fine, that didn’t, that doesn’t mean that the patient never got an echo. It just means that that generated a lot of excitement and people who are not actively taking care of COVID patients. And didn’t didn’t understand, I think the logistic challenges of being able to do testing on these patients and be confident that you’re not sending your echo echo tech of 10 years, who has two small children at home and the lay on a patient’s chest for an hour. And so I think in terms of interpreting the proponent data as a 20,000 foot view summary of that paper, I think what we took away from it is, is that these patients are really sick. And you have to look at it in the context of everything else that’s going on. And again, taking a step back, if you view that paper in light of the other papers that have come out on RDS in patients who have HRDs, who have an elevated deponent level, their proclivity for death is higher than the ones that don’t just as in the normal population. If you’re on dialysis and you’re having an elevated proponent, because your kidneys have failed and you’re on dialysis, your likelihood of death is higher than that than someone who doesn’t. And so it’s trying to figure out, kind of get through the hysterics and figure out clinically what’s going on with people.


So if I’m understanding you correctly, what you’re saying is that while under normal circumstances, the traponin would be a marker. So for example, somebody comes into the ER with chest pain, they look like they’re having an EMI traponin is going to point very specifically to that, but in this case, because the patients are so sick coming in and especially in New York, you know, I always say, if you aren’t going to die in the next six hours, you were basically sent home to fend for yourself. You’re saying that because so many systems were affected, the proponent level may not be specifically pointing to Hartford.


Yeah, correct. That’s exactly right. And I think that, I think that that’s, that’s very difficult for a lot of people to grasp especially cardiologists who have been ignoring traponin levels and ICU patients for years, because we know that every other organ system is sick, but now we have this new disease. You have to interpret every test that you do on a patient, as a doctor in the context of what’s going on. And so if you don’t have any context, it’s very difficult to know how to interpret that test. Be it an EKG,


A blood test, a white blood cell count enter Conant falls into that category. If I see a patient who has coronavirus and has a positive traponin and has the inability to maintain their blood pressure under any circumstances, I’m going to immediately do an echo on that patient and work them up for heart failure. However, if their blood pressure is normal and only their lungs are involved and they’re not on a ventilator yet. And they’re able to tell me that they don’t have chest pain and that they feel short of breath, but basically everything is okay, besides that. I’m probably not


As a, as a point of reference. Could you kind of walk us through the steps as if let’s say I come into the ER by ambulance tonight showing all the signs and symptoms that I could be having an acute EMI, what tests would I get in a pre COVID-19?


That’s a great question. So I’m trying the print, the first thing that the first test that should be done by the EMT is as an EKG at your house. And I, I don’t know of an ambulance system in New York that does not have that capability. That’s called to a chest pain call that wouldn’t have the ability to do an EKG. That EKG would immediately tell us the severity of the heart attack. If the heart attack look like it was a life threatening heart attack, the ER would be called to let the patient know, let the ER know that that patient was on the way and that we needed to be ready to accept that patient in the cardiology suite where we would do a procedure called an angiogram. And then that person would most likely get a stent. And we have optimized our care settings to get that time less than 90 minutes from phone call to stent. It needs to be less than 90 minutes. When you arrived in the ER, the first test that would be done would be blood tests to find out whether or not you’re prone to bleeding or clotting, what your kidney function looked like.


Sorry, but before you go on, so, so the reason I’m going to ask this next question is because people are having difficulty getting tested and getting worked up. So if you could, if you don’t mind, could you just say, like, when you say, okay, what is your blood blood tests? So what, what specific tests would you be getting?


Good question. I didn’t realize you wanted so much granularity.


The reason why, and it’s, it’s, it’s not, it’s because I’m, I’m taking these people on a trip to Kenya after this. But, but what it really boils down to is, and I believe I speak for many people in this group, there’s kind of this big mystery surrounding symptoms and patients go to an internist and you know, in at least in my experience I see the doctors that were on the front lines, who’ve seen a ton of really sick COVID patients. I’ve seen doctors who are now starting to see long haulers. And then I see kind of the majority of doctors who haven’t had any experience with COVID patients. So patients are coming into these doctors and they’re being told things like, well, it’s going to get better. Well, it’s been two weeks, give it one more week, or you don’t need to see a cardiologist.


You don’t need to see a pulmonologist. You don’t need to see a gastroenterologist or a hematologist, or maybe you should see a therapist because it’s probably anxiety. So part of what I’m trying to get here is I am trying to let people leave tonight with some questions that they can say to their doctor, you know, what may, what do you think it would be worthwhile for me to have an echo? Or do you think it would work be worthwhile to run these labs? So if you can kind of give us some breadcrumbs that we can take to our doctors,


That would be awesome. Yeah. Understand. So I think the first test that you need, or something called a basic metabolic panel, which gives you all of your electrolytes, which go along with the propensity to develop abnormal heart rhythms, a complete blood count, which lets, you know, if there is some smoldering infection that’s been missed or, or if there’s an Nemea which can cause a lot of these similar symptoms a two proponent, as we mentioned and then another test of the heart called a brain natriuretic peptide, a BNP and a BNP is a good if you use it in the right clinical context marker of heart failure. And so whenever the pressures inside the heart are high, which is what we call heart failure because of the pressures in the pumper too high, then the pump is failing is a BNP.


And so the, those are the tests that you should have done if you’re having these symptoms. Now there are other tests that ERs will do on you that are blood tests just to make sure that our procedures are safe. So like markers of bleeding will not tell you anything about these patient’s symptoms, but it will tell us if we’re going to stick a catheter into somebody’s groin, the likelihood that they’ll be able to clock whenever we pull that catheter out. And we hope that they’ll form a blood clot, we’re not going to do it on somebody who has the inability to form a blood clot because it put them at risk of bleeding. In addition to that, an EKG, INR and PTT. Yeah. I don’t think that those would be helpful necessarily in the clinic. But in terms of, if you’re being planned for a procedure, you absolutely need those tests.


And then an EKG is absolutely necessary in any patient who has chest pain, shortness of breath. Any symptoms that you, and look we miss as cardiologists. If you look at the science on how we practice medicine, we miss heart attacks and pre heart attack precursors and women all the time because their symptoms are not what you would say textbook. And so anybody who has any symptom that you could reason out could be related to the heart should have an EKG, anybody it’s a cheap test, it takes 30 seconds to do, and it can give you a lot of information about that. Patient’s heart. And if you have a completely normal EKG you can either be reassured based on your, what we call our likelihood of something going on. Like what’s your pretest probability that this person has a disease. If it’s a hundred percent, then you don’t need to do any tests.


You’ve diagnosed the problem. If it’s 50%, then a test can really help you increase or decrease your probability that something is happening and then based on the results of the EKG and echocardiogram. Absolutely. And then if you’re worried about the person’s ability to exercise, doing a stress test, just to see how long a person can exercise for is a very reasonable indication to do a stress test. You know, we do stress tests on people, largely to look for a disease called coronary disease, the number one killer of Americans however stress tests are kind of, so, so at our ability to diagnose coronary disease, because you have to, again, you have to put everything in clinical context. So the FAA, it makes us do stress tests on pilots that run marathons. That test is useless, but it tells you how long a person can exercise for. So if a person comes to you and says, I can’t exercise, I can’t walk around the block and you put them on a treadmill and they go for 24 minutes on a treadmill, you have two very disparate pieces of information, but also you can take somebody who’s afraid to exercise and exercise them and help them get through whatever’s going on and say like, look you exercise for 24 minutes on our treadmill exercise testing in general. Oh yeah. So


Are you using mostly Bruce protocol for, for, for people?


You know, Cornell is a very, is a very particular place. So we use the Cornell protocol. It’s just a little bit gentler on the patients, the Bruce protocol for everybody who’s unfamiliar with these terms, or is a, is a treadmill protocol where you put people on a treadmill and every three minutes, the incline of the treadmill and the speed of the treadmill will and will increase by around 1.5 miles per hour. Or, and what we’re trying to do is to see how far people can go on on this protocol and an effort to diagnose coronary disease or diagnose their inability to exercise the Cornell protocol instead of these three minute jumps increases every two minutes by half. So it’s just more gentle on the patient.


Okay. We, we use a protocol called the Benson protocol similar.


Yeah. Benson had not, and also a gentler protocols. Yup.


And, and one thing that, you know, I don’t know if you’re finding this as well, but one thing that we’re finding with a lot of the patients that we’re seeing are even rehab protocols that we thought were gentle before that we were seeing like 85 year old patients with COPD and pulmonary fibrosis and pulmonary hypertension are even a little bit much for patients who have had COVID and particularly the long haulers. So one of the things we’re trying as we’re scaling back, a lot of our, even our boot camp is being back to about a quarter, a quarter of intensity and we’re starting a brand new protocol based on one minute increments. It’s a very, you know, and I don’t know if that’s the dysautonomia or, you know, it doesn’t seem like it’s a particularly cardiac induced section.


Yeah. I don’t, you know what, in my experience the I’ve done, I’ve sent several of these patients to cardiac rehab cardiopulmonary rehab. And I do the exercise stress test on them in the beginning. And most of them can make it to the equivalent of stage two of the Bruce that I’ve seen. It’s the rare patient that can’t finish stage one, which for everybody on the call, that’s, that’s about the equivalent of doing light housework or playing singles tennis. If somebody’s shooting the ball at you and you’re not moving and you’re just standing there going like that, it’s a very, very low exercise level of stage. One of the Bruce I’ve had one patient who couldn’t complete stage one, most people can get into stage two, which is, you know, a brisk walk around the block, maybe go up six stairs or so, but no more than six years. And again, for people who were previously healthy before this virus, that’s a big change.


Yeah. We have very different patient populations because I see a lot of my patients and you say a ball being fired right at you. And, and you know, I’m looking around the face of that, the call. And I think people, you know, singles tennis, people are thinking like that would never happen to them.


Yeah. Maybe singles Dennis was the wrong, was the wrong example. What I need is somebody standing still and throwing a ball at you and you’re just hitting it back to them. And that would be the equivalent in my mind of about formats.


What what about like the, the role of so for patients here, like, do you think people should be getting stressed tested? When should that be,


Be happening?


Two are in the acute emergency room, just got over COVID and a lot of the people on this call are two months, three months out and their doctors are saying you don’t need a stress test.


Yeah. It’s, it’s very difficult to say right now, in terms of the post COVID syndrome that has been identified and that we’re trying to treat that you don’t need something because more information is going to be better than no information. And in terms of stress testing in particular, there, I wouldn’t send a patient just for an exercise stress test. I would send them for a cardiopulmonary exercise test where you can monitor their oxygen, uptake, their oxygen utilization, their respiratory ability while you’re exercising them. So you get the information on exercise, but you also get good information on lung function and oxygen utilization, which can kind of help you classify this person as are these symptoms coming solely from the lungs solely from the heart or some combination thereof. And I think a C pad cardiopulmonary exercise test is much more tests than just


An exercise stress test expired gases. Yeah.


Okay. So last stress testing question. Is there a role for a pharmacologic stress test in these patients?


I don’t think so. And I don’t think so. I say that one because of the dose of radiation is ridiculous. Like giving somebody a dose of radiation that’s that high, you really need a good reason to do it. And pharmacologic stress testing is excellent at diagnosing coronary disease. The test characteristics are great, but outside of that, the test characteristics are really not good for anything. And so if you’re not trying to diagnose coronary disease which I don’t think we are in this patient population, I think the utility of a pharmacologic stress test, or basically having somebody exercise the same treadmill protocol that you would do anyway, and then injecting them with radiation afterwards. I don’t know what that injection buys you. Gotcha. Okay.


Okay. Thank you. Can we just talk for a few minutes about let’s, let’s break it into electrical system circulatory system and mechanical system of the heart. So in terms of electrical system, are there a Rhythmia as you mentioned, a fib, are there other a Rhythmia’s that you’re seeing more, more like, what are you seeing in terms of arrhythmia


Patients? Afib is the big one. And so AFib is, is largely what we see. Now if you’re talking about in chronic patients who have had COVID and developed AFib in the context of COVID, that’s, that’s really the arrhythmia that we see in these patients who are recovering or who have recovered. And again, when you’re above the age of 65 and you’re develop a fib, the likelihood that ASAP won’t go away is very, very low. And so in the year, 2000, some somebody paid 20, you know, unsuspecting volunteers to participate in a research study where they brought them into the hospital and caused a fib and 20 out of 20 of them for 30 seconds, and then brought them back two weeks later and found that in these healthy people, 12 out of the 20, it had recurrences of a fib afterwards. So we know that if you have a fib, one time, the data supports that you’re going to have a fever again, it’s just a matter of time.


And so you may feel it and you may not feel it, it may affect you. It may not affect you, but if you have it, once you basically got it for life, because you’ve developed a substrate to have it. And so when patients have it with COVID the likelihood that they’re going to continue to have a payback, or this episode is very, very high, which has implications for stroke, because APM is one of the biggest causes of stroke that we’ve, that we see. And the American population, at least if it’s not number one, it’s number two.


So if I’m understanding you correctly, I think it sounds like you’re saying a AFib is on both sides of COVID. So for the patients who were in a fit before getting COVID is going to worsen their, their course, but also for patients who were previously healthy with no history of arrhythmia, we’re a fib in those patients.


I don’t think that we can say the evidence supports that patients who had a fit before COVID would worsen their course. Abe is a non life threatening arrhythmia, which can predispose patients to stroke. And if that stroke risk is lowered with a blood thinner, then their survival is equal to that of a patient without a fib. However I think that patients who have acute COVID and are in an ICU who develop a AFib, need to be monitored very closely after they leave the hospital, even if the eighth of goes away for it to come back and that in some sec, subset of that population, the aphid will never go away. Gotcha. Which depending on the online underlying heart disease can have implications for those patients. If you had high blood pressure for the majority of your life, that’s been untreated, AFib can cause heart failure in you. And we need to make, treat you to make sure that you feel better again, knowing that it won’t change the duration of your life. You can certainly improve the quality of somebody’s life


And prevent a secondary complication. Could I just by a show of hands, see how many people have been told they’ve had a AFib since developing COVID. Is there anyone here? Okay, so a couple, a couple Mary Lou ICU. Okay.


I’ll review as well. Yeah. That’s about in line with what with what we see, you know, it’s like 10% of patients. So like one out of 10 people will develop a fib during the course of COVID is what our Cornell experience has shown us.


Okay. So now patient has a new onset of a fib. What what does that patient need to do? What tests do they need? What medications do they,


So they, again, all of the same blood work that I mentioned earlier, because new onset AFib could be an underlay in one out of a thousand cases could represent a heart attack. And you don’t want to miss that one out of a thousand an echo to make sure that the hardest structurally normal and that’s the function of the heart is normal. And then you need to be able to give that patient a blood thinner to prevent stroke. Okay. And then if somebody remains any fit, then you want their average heart rate with walking and with exercise to be less than one 10. And the reason for that is because we know that patients who have elevated heart rates all of the time, if you have that elevated heart rate for more than three months, you can develop heart failure from just having that elevated heart rate, the heart doesn’t like to run marathons all the time while you’re sitting down watching TV. So you need to be able to control the heart rate in patients who have elevated heart rates for me. And you do that with beta blockers, like Metoprolol calcium channel blockers, like Delta is even if you fail those medications, a medication called Amniodarone, which is a medication that we use as a last resort, if you can’t tolerate any of the others.


So you’re saying any patient with AFib, regardless of age, regardless, you don’t want their heart rate going above


One 10.


Correct. So there was a large study that looked at and the number used to be 70. So there was a large study called the race to trial that was published in 2006 that compared her heart rates of one 10 versus heart rates of 70. Because the medications that you give to control these heart rates have side effects. You don’t want to load people up with meds for no reason. And, and keeping the average heart rate below one 10 is safe and you don’t overmedicate patients.


And that’s even with exercise.


That’s with exertion one 10 on average with exertion. Now you want, how do you calculate an average heart rate is that you look at the heart rate for 24 hours, usually with a Holter monitor or some type of other heart rhythm monitor to make sure that the average heart rate is below one 10. If you’re exercising in a gym and you’re on your fourth mile of running, which I don’t think many of our post COVID patients will be. But if you are then you don’t want that person to have a low heart rate. You want that person to be able to augment their heart rate appropriately and be on the one forties to one 50, is that way they can sustain their run. So it’s the average heart rate below one 10, not the, at one time, while in the gym exercising, but in a person who’s walking around and living their life. Normally with periodic exercise, you want the average heart rate below one time.


Okay. So for anyone who’s. So for those of you that don’t know, so normally a fit a fib is like we have, we have the atrial depolarization ventricular depolarization. So we have a nice give and take in a AFib. We have this kind of ACE. Atria is not really depolarizing, it’s doing its own thing. And then we have an irregular ventricular rate now. So for patients who have a fam anticoagulation, and you mentioned those beta blockers, we’re seeing a lot of patients now whose heart rates, they’re not in a AFib, but their heart rates are kind of running the gamut. So we’re seeing them cycle up from 70 to one 40, they’re coming down to one 20 for a few seconds, then they’re back at 70. And this can all be while sitting in a chair, unrelated to exercise.


Yeah. Yeah. That’s autonomic dysfunction. That is textbook autonomic nervous system dysfunction. And so, you know, as these, as the two hormones of the autonomic nervous system or adrenaline or epinephrin, or nor epinephrin, and and to CDOT Coleen, and those two heart rates basically dictate what those two hormones basically dictate what your heart rate and blood pressure do. And when those two hormones are unbalanced, we call that syndrome, autonomic nervous system dysfunction, and getting those hormones back in balance is a very challenging thing to do. And patients feel like they can’t exercise their heart rates go up spontaneously. They feel anxious because the hormone adrenaline causes anxiety. So you can’t say that it’s sick. This is all anxiety. If no hormone, if the hormonal system that causes anxiety is driving the problem. And you should anxious in this situation.


I mean, if you weren’t, I would be wondering why you’re not anxious.


And so those, those patients that we see, I think that’s that at the end of the day, the most debilitating outcome of this, this viral illness is going to be autonomic nervous system. Like the blood pressure drops in blood pressure spikes and heart rate drops in blood pressure drops in heart rate and the inability to exercise constant fatigue, the inability to sleep normally these are gonna end up being big problems.


You got it. Let me ask you this. So when somebody’s exercising and we’re seeing their heart rate run up. So, so they start thinking about exercise. They go up to one 10, they stand up and walk across the room. They’re at one 30 now, and then they start to do something they’re in there at one 50, one 62. Th does this have the same implication as if they didn’t have dysautonomia? Like in other words, are we supposed to take this with a grain of salt of dysautonomia and continue to move forward? Or do we kind of let the dysautonomia set the pace?


It’s a good question. If the PA it depends on how the patient feels. So patient feels like they can continue in my mind. There is no such thing as a maximum heart rate. Okay. Outside of April where I want your average heart rate below one 10, but in my mind, if you’re exercising for the purpose of exercising, your heart is doing what it needs to do to be able to supply blood flow to your tissues in a way that makes sense for your body. And if you feel like you can’t go on, if you’re reaching your limit, you should stop and rest, and then restart. You shouldn’t stop and rest, and then never exercise again, because you have to be able to train your body and the treatment, as you know, for audit dysautonomia on anomic nervous system, dysfunction is a structured regimented exercise program where you figure out what your limit is and incrementally push past that limit over time until the form is acetylcholine and epinephrin are back in balance. And so in those patients who have spikes and heart rate at the very onset of exercise, I would see how they’re feeling and I would try and push them.


You would try and push them. What I’ve seen with a lot of patients so far is definitely positional changes. So postural, or, you know, orthostatic hypertension patients go from lying down to sitting up their pressure drops. Their heart rate goes up, sit to stand pressure drops. Again, heart rate goes up. What we try to do, we try to, you know, assuming there’s no underlying danger, dangerous condition that we’re missing, or that we’re not seeing, or that’s explaining this compression stockings and or compression leggings gently, you know, pushing the calves and things like that to get that, you know, venous return. And then, you know, really trying to get people moving. The common symptoms we’re seeing are dizziness, a feeling like people are going to pass out extreme fatigue. And you know, it’s very similar to what pots patient, and very similar to a lot of the pulmonary hypertension patients we’ve seen. Are there medications that, that can affect the autonomic or that can, you know, you talked about acetylcholine and adrenaline, so is that any way to medicinally be treated or it’s a matter of retraining, the autonomic nervous system only.


It depends. And it depends on a contextual basis. If the, if the dysautonomia is, if the symptoms are driven by postural changes in blood pressure, then you know, there’s never been a good medical therapy for orthostasis. Okay. But if you were going to try anything, you should try midodrine because it’s basically oral epinephrin and you’d take it and it raises your blood pressure, and it will keep your blood pressure up and help you prevent you from passing out if your blood pressure is low. So, and I say that with a, with a very strong, if your blood pressure is low, because if your blood pressure is normal and you take midodrine, it will make your blood pressure really, really high, and you should not take it. And so because, and of course the downside of very high blood pressure being stroke because of that downside things like compression stockings make sense, abdominal binders can really help.


I don’t know how many of those you’ve used, but in the patients who are refractory to compression, stockings alone, I tend to recommend an abdominal binder. And then if a dominal binder fails, then I go to midodrine because what you’re going to want, you’re not going to be able to see when you’re seeing a patient every two weeks in clinic, every month in clinic from my side of things, which is not your side of things where you’re actively working with these patients all the time is at some point, they’re going to get better. If they’re doing everything that you’re doing with them, and they’re doing what I’m, and they’re doing what I recommend at some point, the patient is going to get better in their blood pressure. They’re going to get better. And then they’re going to take midodrine and they’re going to be hypertensive, and you don’t want them to have a stroke. And so I try and use that medication really, really, really is a last resort.


You’re confident that over time patients are gonna are going to get better from this.


Yeah, I think it depends. I think it depends. I think,


I mean, we’re not holding you to a prompt, but I think a lot of people just kind of breathe a sigh of relief when you said that, and


There’s no science, right. There is no science, but in the patients that I’ve seen from back in March who have been exercising for three months and gone through adequate rehab and retrain their bodies on how to live which is no small ask, by the way, as a doc, it’s like, that’s not a small ask. They get better. Yeah.


I agree. And ladies and gentlemen, by the end of this week, we will have the first week of boot camp ready for you, not regular boot camp covert boot camp specifically. Can


We talk a little bit about chest pain? So chest pain is something very common. Okay. Obviously in the EMS world, obviously in the ER obviously in the cardiology world, very concerning, but people are reporting very different types of chest pain. So some people say burning chest pain, some people say squeezing chest pain. Some people say it feels like an Elvin sitting on my chest, chest pain. And you know, then there’s the musculoskeletal chest pains. Can you talk a little bit about that? And when should we be concerned and when should we consider this an emergency that’s actually going to gain us admission into the ER, like this is more selective than studio 54 in the eighties. It’s like, you have to really know the bouncer to get in. So,


So I want to say outright that if you are worried about the chest pain that you’re having, you should go to the ER, there’s no question about that. If you have chest pain and you’re worried about it, you should go to the ER, because that worry it, or a sense of doom it’s been described in textbooks is one of the hallmark findings of a heart attack. Okay. And what we saw during COVID was that people based on the way that the news portrayed COVID in New York city, hospitals were afraid to go to the ER because they were afraid of catching coated. And we saw a big increase in heart attack deaths in home which is in my mind, unacceptable as a cardiologist, when you have a treatment that can cure the problem and less than an hour and a half. And you’re unwilling to go to the ER, because you’re afraid of the ER.


So do not be afraid of the ER, that there’s, there is no sense in dying from a heart attack based on a, at this point in New York city negligible risk of getting COVID in an ER, I mean, our case numbers are basically zero. Whenever you spread it out across the population of 12 million. So there’s that the chest pain that feels like. And again, we miss chest pain in women often because women do not have typical symptoms. So I’m going to describe typical symptoms with the caveat that these typical symptoms usually do not apply to women. Feels like somebody’s holding you up against a wall. That’s how it feels. It’s not pain. It just feels like somebody’s holding you up against a wall and won’t let go. Usually people, sweat, usually people feel short of breath. Usually people feel lightheaded most of the time people feel anxious.


And so that’s the kind of chest pain that makes me worry about a heart attack. Other kinds of chest pain that can happen, that could represent a problem with the heart, but aren’t necessarily life-threatening would be chest pain that gets worse when you lie down or lean all the way forward. That feels sharp, chest pain that happens every time you take a deep breath but won’t go away, but you take a deep breath that stops you from breathing in. If that happens like that, like a lightning bolt going off, then you should probably go to the ER to make sure you don’t have a blood clot in the lungs.


And then you mentioned musculoskeletal chest pain. And then I’ll finish with kind of in my mind, the worst possible chest pain that anyone could have musculoskeletal chest pain is usually reproducible. So you can touch the area that hurts on your chest and make that chest pain appear. That is not something to go to the ER for. And there were, I think there was one paper in 2004 and one of the emergency medicine journals that said that that chest pain could be consistent with a heart attack. So basically if you go to the ER and you tell them that you have that kind of chest pain, they’ll admit you to make sure you’re not having a heart attack, but there’s never been a cardiology journal article that supported that science. And but they, they hang their hats on that a lot. And do, does that patient have what we call costochondritis or inflammation of the chest wall with coronary disease and the tour unrelated?


We can’t answer that question, but if you can push the, push the pain on your chest, or if you take Tylenol and the chest pain goes away and you’re not worried about it, there’s really no sense. And you go into an ER and being evaluated for it. I’d be, you know, any cardiologists would be happy to see you in our office because we love nothing more than telling people they don’t have coronary artery disease. It’s like, it’s one of the joys of our day is telling people your chest pain is not from the heart. You don’t have to worry about it. Now that brings me to the most feared kind of chest pain that one can have. And that’s chest pain that feels like somebody is tearing you to your back. And I say the word tearing specifically, because tearing is what’s happening to the aorta. As you develop an aortic dissection and people describe it all the time as tearing or ripping like a sheet of paper ripping, and you feel it in your back, they always describe it as chest pain. The rare patient will only describe it as back pain, but if you have chest pain that feels like somebody is tearing you or it’s tearing toward your back or ripping to your back immediately go to an ER, do not question it just go. Because you need to make sure that you don’t have a problem with your aorta.


And I would say call nine one, one, and one of the, in a lot of these things.


Yeah, you shouldn’t in any of these situations, you shouldn’t be going to the ER because EMS can do an EKG on you. And, and in some situations administer the medications that you need upfront and the setting of a heart attack that are, that are life saving the earlier you get them.


Yeah. I mean, a lot of times I hear people who drive themselves to the ER or their family members drive themselves to the ER, my, my grandmother’s cardiologist once wanted it or drive from Brooklyn to Manhattan to go to his ER. And I said, well, you know, you have to think about, well, number one, getting to the ER, yourself, the physical activity, the emotional strain, the anxiety is going to increase and exacerbate anything that’s going on. And if you call nine one, one treatment begins right where you are. So they can already start to put out the fire to some extent. So don’t get the idea of driving in your car, because again, if something else goes wrong, you could be putting other people at risk as well.


If you’re considering driving yourself, then you should rethink either the severity of your chest pain. Okay? So either it’s not that bad or you need, you need to call a family member and have them talk you out of it, or you should not drive yourself to the ER if you’re having a heart attack.


So with, with COVID I are we seeing people who are having heart attacks because of COVID, who’ve never had any coronary disease before? Like I read where they were saying that fever and inflammation can make blood clot blood more prone to clotting intervene, interfere with the body’s ability also to dissolve clots. So a double whammy, and then also inflammation can, can destabilize plaque, right?


Yeah. All of those things are true. I will say that in our first thousand patients who came to Cornell, five of them had a heart attack, what I would call a heart attack and in the most traditional sense of the word. And so the rate is very low, but not zero. And again, it’s hard to know. It’s hard to know if that person was having a heart attack and that asymptomatic Kobe, do you call that because they weren’t short of breath. They were coming in with chest pain and then they had a blood clot in their coronary arteries. They had heart attacks. Is that asymptomatic COBIT or is that a manifestation of COVID? I would think that if it was a manifestation of COVID that we should see it in more than 0.5% of the patients who come in you know, like at least 1%, at least 2%, 3%.


And we didn’t really see that that much. But can a blood clot form when somebody is critically ill in the coronary arteries? Yes. When anybody is critically ill blood clots can form anywhere. They can form in the blood vessels of the brain, which caused stroke. They can form the blood vessels of the heart, which causes a heart attack. And, and again, being able to tease these things out in the setting of a new viral illness is very challenging, but the rates, at least we know from our own experience, which I, I really am finding a hard time trusting other, especially the Chinese experience because of what the rates of what they reported are inconsistent with everything that we saw Cornell. The rates are very low, not zero, but very low.


So you’re feeling that for the patients that maybe did have heart attacks, they had like a subclinical, maybe they had coronary disease before no symptoms, subclinical symptoms. And then this kind of just pushed them over the edge


Or they, or they just had acute MIS they had it, they had real coronary disease and they had plaque rupture and they, I mean, they had acute MIS there’s no doubt about that. But their question is what caused that? Am I very hard to know. You want to say that it’s, COVID, you know, you want to say that, but I don’t think that we have the scientific evidence to support that claim,


But, but we, but that is good evidence to say, check your heart out before you have a problem, right. Yeah, of course. So what about, can you just talk a little bit, you mentioned clots, can you talk a little bit about like what a lot of people describe as micro clots or a micro embolize because you know, especially in the dissection post-mortem studies, what’s your thought on that?


Yeah, I, and I think it’s, I think it’s good to, to approach this in a similar framework that I’ve been trying, you know, I think context is important and in anybody who has ERDs going back to the first paper on this was from 1978 patients who had a RDS had my growth rom by in their lungs. And that’s because those same cytokines that are released by the immune system in the throws of critical illness are cytokines that make the blood clot. And we know from decades of research on ARDSM that treating those patients with blood thinners did not improve their survival, did not make them feel better and may have worsened, but their survival decidedly did not improve it. Decidedly did not make those patients feel better and may have worse than their survival. And so in COVID there has been no randomized trial of blood, of, of anticoagulants, of blood thinners for COVID zero.


And in our experience at Cornell, we saw a lot of people who had markers that their blood was clotting at very high unusually high levels, but not unusually high levels. If you put it in the context of HRDs and how sick they were, because all of these things are also released in patients, cancer, patients who have liver disease, patients who have lung disease. And in, and specifically I’m talking about the D dimer level. So we saw D dimer levels in the eight to 10,000 range, which you can see in patients who have leukemia lymphoma you name the cancer, the D dimer is going to be elevated liver failure, et cetera. And in a lot of those patients early on, we would just throw blood thinners at them because the D dimer level was so high. And as a pulmonary rehab doctor, you know, or a therapist, you know, that when patients who have pulmonary embolize get blood thinners, they’re D dimers go down to basically zero, and then in cardiology clinic, we will stop their blood thinners.


And then the D D if the D dimer creeps back up, we’ll give them back to the patient to get it back down to zero. I don’t think that that same logic applies in this disease and I, and it may, but we don’t have any randomized trial data to support it. And whenever you have these numbers that are surprisingly high these lab values that are surprisingly high, and you have patients that you that are, it’s hard to get tests on these patients, because nobody wants to infect their staff. So it’s been, you know, it’s a phone call. Every time you get a cat scan on these patients you always wonder, am I missing a blood clot? So very early on in the course of this illness, we, the majority of providers would just give them blood thinners because you’re giving everybody in an ICU, some degree of blood thinners anyway, to prevent blood clots from forming because all of these people are in bed.


And so if you’re laying in bed and you’re not moving your legs, the likelihood you get a blood clot in your legs is pretty high and giving blood thinners to prevent those blood clots is important part of care at low doses. But whenever you ramp up the dose of those blood thinners, there’s a very, very, very at the, at the time underrecognized risk of bleeding and so bleeding from the gut, bleeding from the nose, bleeding from the ears, bleeding into the brain, bleeding into the muscles of lag people bleed. If you give them blood thinners, I mean, it’s the downside of the drug, and there’s no proven benefit of blood thinners in these patients. But certainly we saw patients who bled after we gave them blood thinners. And I think for those reasons we backed off pretty early on, on giving everybody blood thinners that came in with COVID and tried to really select patients based on evidence of a blood clot.


And we did find people who had evidence of blood clots that I’m not, I’m not sure changing that we definitely saw patients who had a higher risk, higher risk of blood clots, but, and maybe it’s higher than the generally critically ill patient population. We don’t know, but we definitely saw patients with blood clots. We gave those patients blood thinners, obviously, but in your mind is as a physician, you always want to weigh the risk of what you’re doing and the benefit of what you’re doing. If there’s no proven scientific benefit, but there is known risk, then you’re causing that patient harm. And so, which is like, it’s the antithesis of what we want to do as doctors. And so until there’s good data, I wouldn’t recommend throwing blood thinners at people unless you have a known blood clot based on elevated block, based on abnormal blood enzyme levels, because we have 30 years of ARDSM research that says, don’t do that.


And what are the blood vendors of choice like in the ICU and in the, in the outpatient environment. So in the outpatient environment the blood thinners of choice or something called [inaudible], which, which are the drugs rivaroxaban, or Xalrelto a pixel banner Eloquist and dabigatran or Pradaxa, those are the three that you would use. If you have a reason that you can’t get one of those three, then you would use Coumadin, but nobody really wants to use Coumadin unless you have a mechanical heart valve. If you have a mechanical heart valve, you, you have to be on Coumadin. There’s no question about that because the others are not as good at blood thinners, but because they’re not as good a blood thinners, they have a lower bleeding risk. And you don’t, you don’t want your patient


To ever bleed after giving them a blood thinner. And so those are tend to be the three first line, especially for AFib. There’s basically no reason anybody who, who has AFib, unless they have a mechanical heart valve or rheumatic heart disease, you know, from the Dominican Republic, from Puerto Rico, from Eastern Europe and have rheumatic heart disease specifically that they should get a blood thinner other than Coumadin. And then in the ICU, the, all of those medications ha have around today time that they’re in the body. So I have life of around 12 hours. So they’re in the body for at least two days. And if you have a bleed, you don’t want a blood thinner hanging around for two days in the body. And so we tend to use Lovenox, which is in a medication that’s injected under the skin or heparin, which is a continuous IB medication, which are easily reversible and in the body for no longer than six to eight hours. And so we tend to use Lovenox or heparin in the ICU, but in the outpatient setting, you really prefer Eliquis, Xarelto, Pradaxa Pradaxa being the most expensive and everybody hates paying for it. So we almost never use it. And then Coumadin is a last resort.


A lot of people hear this, this clotting story and they, they are having difficulty getting seen by specialists. And they’re asking, should I be taking aspirin? Should I be starting myself on aspirin?


Yeah, it’s a good question. I think that there are two different types of blood clots. There are arterial blood clots, and there are venous blood clots, venous blood clots, or blood clots that form in the veins, aspirin has never been shown to have any benefit in those, in those blood clots. You know, you can give aspirin for nobody would ever give aspirin for a DVT or a PE. You just wouldn’t do it. It’d be medical malpractice. If you tried to give aspirin for DVT, they just don’t work as well. However, if you have a blood clot in one of the coronary arteries, aspirin is probably the best drug that you could get. And so knowing that there are different types of blood clots in COVID patients, we really see more venous clots than arterial clots. And again, aspirin has never been trialed in these patients.


And so if there’s no trial, then there’s no known benefit. You can theorize all you want, but there’s no known benefit. And even where we thought aspirin was beneficial, which is in the patient who had high blood pressure, who maybe smoked for 20 years, whenever smoking was popular and has a dad that had a heart attack at age 50 for years and years, we would give those people 81 milligrams of aspirin to prevent a heart attack. However, in 2018, two big trials came out that showed that the risk outweighs the benefit and you cause more prevent heart attacks. And so we know for a fact that there’s harm, even from baby aspirin, with no proven benefit and a signal of harm, it’s hard to recommend that patient take a medication. What about an acute MIS they’ll one 62 of baby aspirin in the Honda 24, three 24.


Okay. Gotcha. Yeah, chewed. Gotcha. what about the role of a hypoxia? How much do you think that played in terms of heart complications, a fib heart failure? Hypoxia is a, is a huge one. I think that that’s probably the biggest thing that we saw. So I mean that, that’s the lung disease there and, you know, it’s causing hypoxemia. And if you asked how patients died of COVID, they had pea arrest, which is arresting from hypoxemia. And if you ask me what the biggest complication of COBIT is to PA or restaurant hypoxemia and no doubt, that’s the number one most feared complication is that direct cardiac injury. No, but it’s a cardiac arrest. The heart stops beating. So you have to wonder, I’m like, yes, that, that is obviously a cardiac complication, but does hypoxemia cause heart failure, not so much, does it cause a AFib maybe, but these people are really sick and they have cytokines that are also causing their APEB.


And does hypoxemia cause heart attacks? No, but it certainly makes them worse. And so if your blood oxygen level is low or you’re unable to provide oxygen to the area of heart that doesn’t get any blood flow, your outcome is going to be worse than not. Gotcha. So one thing we hear about a lot is the ACE two receptors. So can you just talk for a moment about that and is there a role for ACE inhibitors or [inaudible], it’s a good question. So early on, if you remember, the, the ACE inhibitors became very murky. And so we learned that SARS Kobe to the virus that causes COVID-19 finds to an interest lung cells through the H two receptor is being acetylcholine esterase which again, acetylcholine, one of the main hormones of the autonomic nervous system. And so the ACE two receptor we’ve w gets up regulated or there’s more of them around if you take blood pressure medications that affect that system, those blood pressure medications tend to be ACE inhibitors like life center, pro captor pro, and our pro Pendo pro Fasano pro.


I can go down a list of a lot of them or medications called angiotensin receptor blockers, low SAR, tan, Candice are tan Irbesartan, Valsartan OMA, star tan. Those are the big ones. And there was fear early on that you were allowing more viral entry if you were on these medications, longterm and again, all of this was kind of hypothetical and people just thinking outside the box there was no data, however, to suggest that you being on those medications longterm had any impact on your survival from the disease. And then in early may, May 4th, a guy named Mandy Mera from Harvard, published a paper in new England journal, looking at an absurd number of patients who had Corona SARS, Coby too, and asked specifically the questions about ACE inhibitors. And then he, he said that you actually had improved survival if you were taking ACE inhibitors and ARBs and had had COVID.


However, his paper was fraudulent. And they had made up all of the data, and yet he still has a job that paper has been retracted for fraudulent data from a company run by a vascular surgeon named supine decide called surgeon spear that could not vouch for the diversity of the data or the accuracy of the data. And so at that point, we were like, okay, well, this was a, this was a complete waste because obviously that paper made all of the major news outlets. I’m saying, please continue to take your lisinopril. Your low Sergeant you’ll survive if you get COVID. And then harmony Reynolds from NYU, published a paper, looking at all of the NYU hospital’s outcomes. And she obviously has control over all of their data, very thoughtful, well done paper and showed that there’s no increased risk of death in those patients.


And so taking an ACE inhibitor or an ARB for your high blood pressure, I think after we looked at Harmony’s data, we can be certain that it does not cause harm. You will not die more because you’re on used drugs. And her and her research group showed that very effectively. And so I would say probably continue your medications if you’re taking them. And then people started asking the question of, Oh, well this receptor, the ACE two receptor is also found in the heart. So is this virus getting into the heart and causing the heart heart failure that, that we, that we think that it’s causing. But again, nobody had any proof of this. And, and most recently, you know, just published online a couple of days ago was an autopsy series of 22 hearts from the ELA group at LSU in new Orleans.


And they new Orleans being one of the three biggest cities in the United States that were affected by COVID. And in March, if you guys remember because of the Mardi Gras parades, and there was no evidence of SARS Kobe to have that virus in the hearts of those patients. And so I think that though, it, it uses those receptors to get into the lung cells. The likelihood that it’s actually causing heart damage is probably low based on the available evidence that we have at this point. But that evidence is limited. The numbers of patients are low. That’s what I read. That’s what I have to about it. Just


Just very briefly, if you could just talk about how hydroxychloroquine and I mean, it doesn’t have to be major, but just, you know, and run best severe. So both of those have potential cardiac implications. They do. And I think that, you know, early on, there was a lot of excitement about hydroxychloroquine another paper mandate mirrors was on hydroxy cork, which was also retracted for fraudulent data. There have been a lot of there have been a lot of people that have gotten behind this. And then of course it’s been politicized to, I think everybody’s detriment because it made it much harder to figure out how to actually get people enrolled in clinical trials. If it’s been politicized, people either want to take it, or they don’t want to take it based on their party affiliation, which is stupid. And there’s no reason in my mind why Plaquinel should work on the virus or hydroxy chloroquine.


They tried, they’ve trialed it in many different viruses in the mid two thousands. There was a paper in the journal nature, which looked at Plaquinel and the virus chicken Gunyah, which is a virus found in the Caribbean, which causes longterm viral complications and patients very similar actually to what we’re seeing in our COVID patients in terms of prolonged symptoms, but in, in monkeys that were receiving plaque Plaquinel who they actively infected with chicken Granja plaque. Reno had no effect. Its ability as an antiviral was basically zero and then study after study, after study showed conflicting evidence. These patients live longer. If you take black one, all these patients don’t live as long as you take Plaquinel, but all of them had serious statistical flaws until a guy at the university of Minnesota, David vulvar published a randomized trial. And again, our randomized trial on medicine is kind of our gold standard of how we should treat patients.


It’s randomly assigning without knowing if it’s a man woman, what their age are, what their, what their medical conditions are to one treatment or another, and seeing if they live or die in the case of Plaquinel and the largest randomized trial showed that there was no benefit of Plaquinel, but also no farm from black window. And so I think hydroxyl cork, when we can put to bed does not benefit patients who have COVID. They just published another trial, looking at taking hydroxychloroquine to prevent infection. If you had a member of your household that was infected with Kobe, they gave it in a randomized fashion to other members of the households and they gave them, they didn’t give it to other members of households and study them. And then it had no effect. And so I think hydroxy chloroquine is a drug of the past that had a lot of excitement for no reason in my mind historically, and then you know, the most feared complication of hyper hydroxy chloroquine is that it can prolong an interval on the ECG called the QT interval. And the QT interval can predict if it’s prolonged, can predispose people to potentially life threatening heart rhythm abnormalities. That happens very rarely, but again, if there’s no proven benefit of the drug, then the risk outweighs the benefit. You shouldn’t give the drug, even if the rates of these complications are over here, you should change your name to Google.


So I have just a couple of more questions and then I’m going to go to audience questions. So Beth, if we could open up the chat to people’s questions so essentially patient patients here in this group, let’s say people are having some symptoms. They could be cardiovascular in nature. They may be dysautonomia in nature. What should they be going to their doctor if they haven’t had them yet? So you said EKG, halter monitor. Yep.


Well, their monitor is a great, it’s a great 24 hour view viewpoint of a person’s heart rhythm. It’s it’s cheap. It’s easy to do. And an echo. Yeah.


Overnight oxygen study where the whole,


So I don’t know that you can do the two at the same time. It depends on the sleep study lab. I actually think insurance won’t reimburse both tests. If they’re done simultaneously, they have to be done on different days. I would only do an overnight sleep study if somebody actually had, what if I thought they had sleep apnea,


Like a full sleep study in the lab? I just mean like an overnight oxygen, because one thing that a lot of people report is they’ll wake up from sleep. They’ll be immediately awakened. They check their, their heart rates are fast, their oxygen’s are low. Okay. I don’t know, just a thought


If that happened, that I would refer that patient for a full sleep study


Him for a full sleep study. Okay. What about bulging veins or veins that are very translucent through the, through the skin?


It depends on the person’s skin. So if you’re a thin person, you’re basically going to be able to see any veins, but if you notice a change in your, in your, in the appearance of your veins, then you should be scanned and make sure you don’t have a blood clot.


Okay. can you talk a tiny bit about Ray nodes? Lavato reticular Iris


And purple fee. Yeah. So again, all of these things have been kind of attributed to this disease in terms of blood clotting. And there’ve been case reports of libido reticularis and Ray nodes and, and this purple feet syndrome. But if you look at the rates of those complications and people who have, and don’t have COVID and the most recent dermatologic paper I read about the illness, the rates were equivocal. So the rates in the normal patient population versus a patient population, or I have COVID having purple feed or newly purple fi they happened at the exact same rate as whether you had the virus or not. And so I think that there was again, excitement early on about this blood clotting phenomenon of this disease that I think is just in line with the remainder of critical care literature.


Gotcha. Okay. So eight 15 we’re going to go to the speed round. So I have been seen one time by a cardiologist who was pretty quick to assume my change in heart rate is caused by anxiety. I believe it’s a possibility. I believe it is a possibility of different kinds of stress, not anxiety, but my body’s reaction to what I’ve endured. I am greatly affected by change in temperature, heat humidity in the sun. My heart rate immediately rises when I go outdoors. Even if just walking a few steps, steps out, back and sitting, this is not normal for me. It can cause a setback with symptoms for many days. Any thoughts?


Yeah. That sounds like textbook autonomic nervous system dysfunction. Yeah. Got it. Got it. Got it. And so, I mean, if, if that person were my patient, I would make sure that I enrolled them in an, either a pulmonary or cardiac rehab program to retrain them.


Gotcha. I have a couple of questions about shortness of breath and fluctuating heart rate. Some days are bad with me having to sit on the couch in order to breathe comfortably and control my heart rate to keep it below one 20 some days are almost fine. Why the fluctuation again, dysautonomia right?


Could be, it also could be a fit.


It could be a fit. Okay. it almost seems to follow sleepless nights like clockwork. Any, any information it could be either, either one, check it out, right? You can go check it out.


I mean, at least wear a Holter monitor to make sure there’s no way to live there.


I am a 58 year old woman with IPF. That’s not me. I’m speaking for someone else with, with heart palpitations. My pulse can go up to one 50 beats per minute with just standing it’s worst in the shower. It’s worse than the shower. I’m not on oxygen. I was tested for pods. However, my symptoms were not bad enough. Can this be a cardiovascular system, symptom of IPF?


Again? I think it’s probably dysautonomia, especially if it’s going up. When you get in the shower, everybody’s blood pressure is going to go down a little bit because the water is so hot. Your skin’s going to your blood vessels are going to dilate and it’s going to lower your blood pressure. It sounds like textbook dysautonomia. Yep.


If I ask you about your astrological sign and you tell me it’s dysautonomia, then I know that this thing is rigged. Okay.


That’s right. No, it’s Leo. It’s legal proudly.


That makes sense. There seems to be a big difference of opinion in the profession about whether you need to stay on these things. Oh, okay. So let me just say, so since being diagnosed with a fib in the hospital, I’ve been on Metoprolol and eloquence, as you mentioned, it’s been three months. I wore a halter monitor for 25 days. Take a Kardia mobile every day. And so far, no way fare, but I do have a sinus arrhythmia. Must I continue with either or both of these meds forever.


Good question. The first thing that I would ask is have they had any side effects? So usually if somebody has a side effect of bleeding from Alloquest, the drug would be stopped anyway. So if still on it, you probably haven’t


Had the side effect though, that having a bleed from Eloquist is a scary thing. The rate is very, very low, but the propensity for APM to come back is very, very high. And most of the times it comes back, people don’t feel it. So if you do a 32nd EKG strip on our cardio monitor, you have 24 hours of the remainder of the day, minus 30 seconds that you’re not looking at your heart rhythm. And you can’t look at your heart rhythm continuously, unless you get an implantable monitor called a loop recorder, which transmits automatic EKG recordings once a month to your doctor. And then they can look at your heart rhythm continuously over the last 30 days and say, yes, no to AFM, which I’ve done in some patients who refuse to take blood thinners. So, you know, competitive, downhill skiers or boxers, you don’t want that person on a blood thinner. They’re going to get punched in the head and have a bleed into the brain. You don’t want them on a blood thinner. So I’ll put in a loop recorder, which is a small electronic monitoring device and look at their rhythm continuously in the batteries last about three years. So then you can get three years of data on people and almost always the up comes back.


Do you trust those cardiac monitors, those little finger things? How do you like those?


It’s great because, and I’ll, and I’ll just, I’m not invested in the company, but I do know the founder of the company. And I think he’s not that nice of a guy, but I think it’s a good device because if you if you can take your heart rhythm, whenever you’re having symptoms, it’s a very good strip to let you know, if you have ACE overnight or other heart rhythm abnormalities, you can diagnose them very well. And oftentimes when you prescribe people, Holter monitors you only wear it for 24 hours, then you ship it back. And then the day they ship it back and they’ve taken it off, their symptoms immediately come back. And so it’s very frustrating as the cardiologist on the other side of that to go, okay, we’ve got to get another Holter monitor and see if we catch it that way. You know what you’re treating, but the cardio monitor for its price point can immediately tell you, yes, no, you either have an arrhythmia or you don’t. And if you don’t have an arrhythmia, then you need to look into other reasons that you’re having the symptoms.


Gotcha. And in hearing what you think about the owner of the company, I’d like to say the views expressed by dr. Mccullough do not necessarily know


That’s right. That’s right. That’s right.


I’m kidding. I don’t care. I don’t like him either. I don’t, I don’t know him, but I know if you don’t like them, I don’t like them in Brooklyn. So we formed a lot of companies. Can chronic fever affect any parts of the heart? 155 days of temperatures, 100.6 to 100, 2.9,


Chronic fevers can affect the heart because of the immune systems driving of that fever. So if the immune system is releasing cytokines and the setting of those fevers, then you can certainly have the heart be affected by those same hormones as they are when anybody else is critically ill for any different reason, though, the though the rare rate is low. It’s not zero. And if you have any heart-related symptoms, swelling of the legs, shortness of breath, low blood pressure, abnormal heart rhythms, then it deserves an echo.


Are there any supplements or other things you would recommend or foods that that could help people through this?


Honestly, the answer to that is no. And the answer to that is no, because by asking, by doing the research on diet, you’re biasing the research by asking the question. I think the, I think the thing that you can do to help people the most is try and get them to back to living as, as normal of a life as they can. And that means eating whatever they wanted to before. COVID like try and get their lives back as normal as they can make sure they’re getting good nutrition. That way they can support the metabolic needs of the exercise program that they need to, to undertake, to go on their journey. Don’t try and limit your diet or increase outer proportion. You know, strange foods that have no scientific benefit. I’m not anti supplement. I’ll never tell somebody to stop supplements, but I’m, I am a, a doctor that tries to make every decision that I make based on evidence available at hand. Because if you don’t have the evidence available at hand, then you’re just making things up, which has the potential for harm. And so there’s never been any paper that shows that supplements actually improve survival or symptoms in anybody. And they’re expensive and not regulated by the FDA.


That’s how the supplement industry works. So if you get a halter monitor result and the provider interprets results as normal based on average BPM, what verbiage can we use to ask our doctor to hint at dysautonomia? Oh, what’s the heart rate trend? It it’s nonspecific. It just says, you know?


Yeah. So you would have to ask, I want you to look at my heart rate trend when I’m moving around. My heart rate is inappropriately too fast when I’m sitting down, you know, at 4:00 AM my heart rate, shouldn’t be one 10 while I’m sleeping. Look at the actual times because the average BPM heart rate that’s reported on the Holter is just the average for the 24 hour period, which may be normal. And then you miss the granularity of the hour by hour or half hour by half hour data that’s provided. So you actually need to look at the heart rate trends. Gotcha.


Any connection of Wolf, Parkinson, white and or six sinus syndrome and Kobe


Wolf Parkinson white? No. Well, Parkinson white is something that you’re born with. You don’t, you don’t all of a sudden develop a bypass tract around the hearts conduction system, just because you get a viral illness. That would be very, very, you know, that’s, that’s like growing new heart and that’s, that’s one thing that the heart, unfortunately can’t do. And then the other question, six sinus syndrome is a hard one to answer because whenever you have low levels of oxygen, you can provoke sick sinus syndrome sick sinus syndrome, again, very common. And if you have low levels of blood oxygen, then your sinus node will act like it’s diseased. Also, if you have periodic aphid, then you can develop sick syndrome in the setting of having periodic APEC, but that’s called tacky Brady syndrome. It’s one of the most common indications for a pacemaker in the country is tacky Brady syndrome. And that’s it periods of very fast aphid followed by periods of very slow or diseased sinus node function


For those who are younger and have never had heart or vein issues. I heard a cardiologist say, don’t rely too heavily on compression stockings as we don’t want your veins to get lazy. We’ll compression stockings make a 32 year old vein lazy. And should I rotate on it?


There is no scientific evidence to support that statement.


Yeah. And let me also just say, when we talk about, you know, compression stockings, we’re not talking about for the rest of your life. Okay. we’re talking about, this is a bridge to get you to be able to do the exercise because as you start extra, like a lot of people, especially with dysautonomia position change is a big thing. So they’re lying down. Their blood is flowing sideways. They go from lying down to sitting at the side of the bed and the blood pools in the legs. Then they go from sit to stand and it pools even more. So for me, the way we use compression stockings in our practice is we use it as a tool so that when you change position either a, you don’t feel like passing out, or it just gives you a little more support to get you up and moving.


And the way that we train the autonomic nervous system is by gradually increasing your exercise. So, you know, over time we hope that the autonomic nervous system is going to recover. And, you know, as I’ve said before, like I really view this as like a scorched earth type of situation where, you know, every system can be affected systems recover at different paces. So as inflammation goes away and as, as things start to heal, but the compression stockings are not like for the rest of your life, it’s a tool to help you move moving, you know, to get moving. Initially had a stress echo recently, I was told that I have mitral valve regurgitation. He said, it wasn’t significant. Should I monitor this? I’m 39 and otherwise healthy.


If it’s insignificant mitral regurgitation, you should have an echo probably once every 10 years, every 10 years. Yeah. 10 to 15 years


Walking in her hair that day. Do you still need it? All right. So other questions, my cardiologist plays the loop blink recorder in my chest to keep track of my heart rhythm. I can also alert the monitor. What are your feelings on this? And I think you mentioned that


I did. It’s a great way to help people who don’t want to take blood thinners for AFib and make sure that they don’t have a fab come back. That’s probably the most reliable method. Gotcha.


Since a probable COBIT episode in March, I’ve been prone to blood pressure fluctuations AFib, and by Gemini, if these symptoms are COVID related, would ablation help. That’s a great question, right? There would ablation help


If it’s Germany 24 hours a day, then that means that every other heartbeat is a, is a premature ventricular contraction. And I assume that they’re talking about ventricular by Gemini and not atrial by Germany. So if, if 50% of your heartbeats are premature ventricular contractions, then the first thing that I would do is try medicine to suppress them with the number being greater than 11. We all on average have around a hundred thousand heartbeats a day. So if you have 50% that you’re having 50,000, if you have more than 11,000 premature ventricular contractions in a day, for more than three months, the likelihood that you develop heart failure is present, but not zero. And so if you have more than 11,000 BPCs a day, I would try you on a drug called Metoprolol to suppress those PVCs. And then if the Metoprolol did not suppress them, I would monitor that patient very closely.


We’re talking like every two months, every three months with an echocardiogram and the second the ventricle started to fail, I would send them for an ablation. So then you ask the question, Oh, well, why didn’t you just do the ablation upfront? And that’s because it’s an invasive procedure and has associated risks that are, that go along with that procedure to where you should always try medications before you try invasive procedures, make sure you failed the medications or you are, you can’t tolerate the side effects before you go, have somebody sticking catheters inside of you. Absolutely.


All right. Just a couple more. Okay. So if I’m still having calf pain, shortness of breath during exercise and chest pain burning, mostly what tests should I ask my primary for? I have an appointment Tuesday.


No. Yeah. So probably almost certainly an EKG and an echo, just make sure that the burning Chino burning chest pain can be from a lot of different things. Not necessarily just the heart, but I would make sure that that person has had their cardiac system evaluated. And then if you didn’t feel satisfied after the EKG and echo, you could put that person on a treadmill and see how long they exercise for. So


Resting echo to begin with, and then,


Yeah, you don’t ever want to send a person for a stress echo until you make sure that their resting heart is normal and not every echo lab in the city. And I assume we’re talking about New York city, but also the country, not every echo lab will do a comprehensive, full echo first.


So you’re saying they won’t do a resting. They’ll just pop you on the treadmill.


No they’ll do for resting images, but they won’t interrogate the valves. They won’t look at the size of the word, all of these other, you know, there’s a lot that goes into it into our full resting echo and a stress echo is by no means should ever be considered a full resting echo. Gotcha.


Echo fine labs, all good EKG. Good. Sometimes blood pressure goes to about 90, over 50. I get dizzy and short of breath when that happens, what can I do to help the issue


Dysautonomia? You have to be retrained. Yep.


I’ve been recently prescribed colchicine for inflammation increases in my blood. I often wake up with the chest pain. Okay. I don’t know if that’s a, it’s not a question. My cardiologist did that one. What do you see the future of cardiology looking like in the next few months or years with Kobe?


I, I think that it’s going to be hard. I think that’s hard to say. I think that a lot of cardiac care went down during


COVID. And so, you know, there were fewer patients listed for heart transplant. There were fewer heart transplants performed. And I think in the next few months, I would hope that we could at least take care of some of our chronic patients that all got displaced, who have known heart disease, who haven’t been able to get in and see their doctors because all of their doctor’s have been redeployed to COBIT units and then incorporating and coming up with algorithms to treat patients who have longterm system symptoms of COVID are important, not only from a pulmonary, but also from a cardiovascular standpoint. And so we have a program at Cornell that we’re developing in terms of like trying to develop and think about what treatment algorithms, what diagnostic algorithms do we need to put these patients through to make sure that their heart and lungs are okay and make sure that we’re not missing anything. Given that we know so little about this virus in particular,


Are there any medications that can, can kind of mellow the recurring cytokine storm and, or lower the sympathetic output?


We don’t know how much cytokine storm is unique to COVID. And I would say every time that you give medications that suppress the immune system, you have to consider, which is what getting rid of cytokine storm is. And if you’re going to give a medication, that’s going to calm down the immune system, you have to take it in the context of what’s going on with that patient. If it’s a COVID patient, it’s a patient who’s actively infected with a virus. So you shouldn’t give medications to suppress the immune system in a person who is actively infected, unless you have a good reason and good data to do so. And they’re trialing those medications now, and most of the trials have failed for obvious reasons.


There’s a poll pulse rate of 48 to 50 dangerous.


Not if you feel fine, the lower it is, the healthier you are. Usually you see marathon runners have pulse rates in the 35 to 45 range. The better trained you are, the lower your pulse rate will be.


Can you just talk 30 seconds about viral cardiomyopathy?


Yeah. So viral cardiomyopathy or mild carditis is a diagnosis that’s based off of biopsying the heart and seeing viral particles with cell death. And so most commonly, we see this in patients who have been infected with a virus called Coxsackie virus, which is the same virus that causes hand foot and mouth disease and kids adults don’t really feel symptoms, or they may have viral like symptoms, you know, feeling like they’re crummy, having a runny nose, having a cough for a few weeks. And then three to four weeks later, they feel chest pain, particularly chest pain when they lean forward or lean back, which, which invokes assist a syndrome called pericarditis or inflammation of the SAC lining the heart. And then myocarditis is whenever you have that same syndrome, but the virus actually gets into the heart and causes cell death very early on in COVID.


There were reports out of China that said that this virus causes myocarditis which is a very specific term. Okay. Very specific term, which that you have a biopsy, which shows that there’s a virus on the heart, but they didn’t have any biopsies. They just commented on patients who had heart failure in the setting of a very critically ill viral illness. And then case report application port after case report came out with very little evidence to support that there’s actually mild carditis going on. And so in terms of coping specific related myocarditis, the question is still out. We don’t have any autopsy or proof or proof that it exists. And we certainly don’t think that it exists in, in outer proportion to what we see in other patients who are critically ill. And in terms of traditional myocarditus usually you get symptoms of chest pain a few weeks after you have a nonspecific viral illness. Usually it’s because you’ve come into contact with a small child. Who’s been sick usually with hand foot and mouth disease.


You’re good for like five more minutes. We got just two or three more cards.


Yeah. I should probably turn on a light. It’s getting dark,


If not, just move your mouth and we’ll pretend we can’t hear you quite yourself out. And we’ll say it was a glitch. My echo showed mild concentric left ventricular hypertrophy. LVEF ejection fraction, 55, 60 mild diastolic dysfunction. My cardiologist says I shouldn’t worry because I’m young. Sure. We’re not, should I see another doctor?


Yeah. I mean, that’s a normal echo basically. And, and diastolic dysfunction is nothing that’s ever been shown to shorten people’s life. And usually doesn’t cause people’s symptoms. And so I don’t, I don’t know anything about what went into the interaction that that person had with that doctor. But reassurance, I think is appropriate. If that’s the only test that was done,


I have what seems to be musculoskeletal pain on my left chest, near the sternum, putting pressure on it does not replicate it. But if I stretch my chest or bend over, I will notice the pain a little. It seems like potentially costochondritis, but no markers of inflammation are present


And you don’t have markers of inflammation present whenever you have costochondritis ibuprofen, as you need to for the pain. And it goes away and you have a medical condition that prevents you from taking ibuprofen. Yeah.


Yeah. And don’t forget, you know, for many people you were in the hospital, you were in bed. Even if you weren’t in the hospital, you were in bed, you weren’t taking deep breaths. That could also be muscular as well. It could be tight intercostals or, you know, pain spasm cycle for Matt. And that I think is a wrap. Thank you so, so much that was super enlightening. Good looking, super smart. A lot of the ladies and some of the men want to know if you’re single. If you tell me you’re either an artist or musician, I will be jealous. But I just want to say, thank you so much. We covered a ton of them.


No problem. Look at what we can do to help.


And you’ll be seeing my patients. So thank you so much. Ladies and gentlemen, I’m going to unmute you all so that you can in an audio logic manner. And if there’s anything I can do to return the favor and it doesn’t have to be anything related to medicine or rehab, I washed cars, walked dogs. Thank you so much greatly appreciate it, dr. Mccullough, thank you for having me. Alright. Thank you everybody. So this Wednesday we’re hitting the neurologic system and just a reminder, we have a couple of webinars coming up, support groups coming up. Our team is doing consultations with people. If you would like and are interested in that, helping you get situated with respect to who should you see? What should you see them for? Just shoot me an email. And I think that’s it. And I would be doing the foundation a disservice if I did not say everything that we are doing is for free based solely on donations. So if you have been helped by this and you have a few extra nickels dimes thousand dollar bills, million dollar bills, pulmonary backslash donate. Thank you so much for being here. Feel good, ladies and gentlemen, and look out for COVID boot camp coming up very, very soon. Have a good evening, everybody. Thank you, Beth. Thank you, Karen.