In this must-listen episode of Long COVID The Answers, host Funmi dives deep with expert Erica into a groundbreaking study that reveals COVID-19 may elevate the risk of heart attack and stroke for up to three years after infection, especially for people with non-O blood types. Could COVID-19 be as serious a heart disease risk factor as smoking or high cholesterol? Erica shares eye-opening insights on how the virus impacts cardiovascular health and explores innovative recovery strategies tailored to long COVID patients. Join us for this essential conversation that could redefine how we understand COVID’s long-term effects on the heart.
Guest – Dr Erica Spatz MD, MHS
Note: The podcast has no bias. All conflicts of interest are highlighted with individual guests.
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Podcast Overview:
Long-Term Cardiovascular Risks of COVID-19: Key findings from recent research showing that COVID-19 can increase risks of heart attacks, strokes, and other cardiac issues for up to three years after infection, with elevated risks for those with non-O blood types.
ABO Blood Type Interaction: Discussion of how non-O blood types may experience higher cardiovascular risks post-COVID, regardless of hospitalization, highlighting the need for targeted approaches.
Revisiting COVID as a Cardiovascular Risk Factor: Debate on whether SARS-CoV-2 should be classified as a risk factor for heart disease, alongside known factors like high cholesterol, smoking, and diabetes.
Preventative and Rehabilitation Strategies: Innovative recommendations for preventing heart damage and managing cardiovascular health post-COVID, including the role of exercise, rehabilitation for the autonomic nervous system, and personalized approaches for patients with long COVID.
Future Research Needs: Emphasis on the urgent need for expanded studies to better understand and treat cardiovascular complications in the post-acute and long COVID phases.
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Podcast Transcript:
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Episode 18 – The Cardiovascular Effects of Long COVID ft. Professor Erica Spatz MD
[00:00:00] Funmi Okunola: The information in this podcast is provided for informational purposes only. You should not use any information discussed in this podcast and related materials to make medical or healthcare related decisions. Always consult your physician or other qualified healthcare providers with regards to diagnosing and managing your medical condition. Any medications or treatments, including any discussed in this podcast, should be initiated and managed by a qualified healthcare professional
Funmi Okunola: Welcome to Long COVID – the Answers. Today’s Episode is called “The Cardiovascular Effects of Long COVID”. I’d like to introduce Professor Erica Spatz, MD. Professor Spatz is a cardiologist and clinical investigator at the Center for Outcomes Research and Evaluation. She is the Associate Professor of Cardiology and Associate Professor of Epidemiology at Yale School of Medicine in the U.S.A.
Professor Spatz is the Director of the Preventative Cardiovascular Health Program. Her clinical and research interests include the development of individualized approaches to preventing and managing cardiovascular disease, along with tools to help patients become more active in their healthcare decisions.
Welcome, Erica.
Erica Spatz: It’s great to be here, Funmi. Thank you so much for having me on your show.
Funmi Okunola: Thank you for coming. Erica, do you have any conflicts of interest to declare?
Erica Spatz: I am a principal [00:01:00] investigator on a study that is funded by the U.S. Center for Disease Control and Prevention called INSPIRE. This is a government funded study to evaluate the long-term effects of COVID. Other than that, no other disclosures.
Funmi Okunola: Thank you. I’d like to approach this interview differently. From my own personal analysis of research articles and interviews with clinicians and scientists, I’ve come to understand that a SARS-CoV-2 infection results in a Post COVID condition for a significant proportion of the population, which I understand is as follows:
One – organ damage from hospitalisation, namely ICU admission, affecting around 13% of the population.
Two – Long COVID, an ME/CFS stroke complex chronic disease state, a relapsing and remitting illness found largely in about 10% of the population of non-[00:02:00] hospitalised people infected with SARS-CoV-2, mainly affecting women.
Three – COVID-19 is a systemic disease, meaning it affects the whole body. The coronavirus infects and is thought to cause an inflammatory process in multiple organs, increasing the incidence and/or worsening chronic diseases in the community. For example, with the heart, increasing all types of cardiovascular disease.
With the lungs, causing respiratory disease – for example lung fibrosis with the pancreas, diabetes, damage to the lining of blood vessels or the endothelium, leading to blood clots and strokes with the brain, cognitive impairment and dementia. Today we’re going to focus on the damage done to the heart.
We will try to understand the functional changes associated with COVID-19, i.e. the pathophysiological mechanisms, and discuss how we can prevent, treat and possibly cure the cardiovascular issues. [00:03:00] Erica, can you please describe the different categories of cardiac injury caused by a SARS-CoV-2 infection?
Erica Spatz: Thanks, Funmi, for that overview. When we think about cardiovascular disease, either during Acute COVID infection as well as Post COVID infection, there are a few big umbrellas that we want to think about. So, one is there an increased risk? Is my patient presenting with classic cardiovascular conditions, but which are heightened during COVID or especially in the immediate aftermath of COVID, and those include conditions like arterial or venous thrombosis that can lead to myocardial infarction also known as heart attacks, strokes.
Venous thromboembolism leading to pulmonary embolism or PEs. These are conditions that [00:04:00] we can see during the acute phase of COVID but are also present at an increased rate in the year and even years following COVID infection. So, categorically it is an arterial and venous thrombosis, another category that is affecting the structure of the heart through mechanisms that are usually inflammatory, like myocarditis, and we’ve heard a lot about myocarditis in the early stages of COVID both in relation to the infection itself, the SARS-CoV-2 infection, as well as in relation to vaccination. Some of these presentations of myocarditis were acute and diagnosed in the hospital at the time of COVID, and we also realized that sometimes we were seeing patients after having a COVID infection and detecting signs of potential prior [00:05:00] myocarditis or present myocarditis that was a little atypical for our usual presentations.
In addition to this, SARS-CoV-2 can lead to arrhythmias like atrial fibrillation, ventricular tachycardia. So, we’ve talked about the vascular system, we’ve talked about the heart structure, as well as the electrophysiology of the heart. We really want to make sure that we’re evaluating patients for the traditional cardiovascular diseases that we see day in and day out in any person and recognize that they can be heightened even in a person without prior cardiovascular disease.
If they’ve had a COVID infection Funmi, there are also some conditions that particularly present in the Post COVID phase and are not typical of the cardiovascular disease organ damage that [00:06:00] we see in some of these. They are related to more what I would call functional disorders, where there is dysregulation of the autonomic system or dysregulation of the vascular system, and there can be presentations of tachycardia or POTS, which is postural orthostatic tachycardia syndrome. There can be inappropriate sinus tachycardia, so the heart rate is increased. At times, when you’re at rest, there may also be chest pain syndromes related to coronary vasospasm or impaired relaxation.
So more of the functional aspects of what our cardiovascular system does as opposed to identifying organ damage. That’s a lot. Let me stop there and we can hopefully dig more into those.
Funmi Okunola: Yeah. That’s a lot and actually quite scary. What are the [00:07:00] mechanisms of these injuries, bearing in mind that this podcast is directed at both a medical and non-medical audience?
Erica Spatz: So, there can be direct injury from SARS-CoV-2 that enters into the cells through a spike protein and can cause direct damage from the actual virus. In addition, SARS-CoV-2 elicits an incredible immunologic response and an inflammatory response, and a lot of the conditions that we’re seeing are manifesting from our own body’s immune and inflammatory response.
There’s been a lot of research that has evolved in the last few years to understand variation in immune responses, which may explain why some people go on to develop Long COVID and [00:08:00] others don’t. This may have to do with the immunobiology, and that differs from person to person.
As you mentioned, we know that the immune system is different between men and women. We know that, for example, women have higher rates of autoimmune disease, and that probably relates into the different patterns that we see in terms of sex differences. There is also some research that is looking at metabolomics, especially related to gut metabolomics and seeing changes in gut metabolites.
There may also be some remnant or persistent virus in the system that never cleared. We also see some reactivation of some latent viruses like Epstein-Barr Virus, EBV, and the problem for me is that it may be different for each person, so the same pathophysiology may not [00:09:00] explain all people’s presentation of Long COVID. Although we’re learning a lot in the research setting, a lot of that has not yet come to bear in the clinical settings so that we can treat the underlying ideology, which may be different for me and for you and for someone else.
Funmi Okunola: Yeah, incredibly interesting. Can you please talk about the mechanism by which there is an increased frequency of arterial and venous and the outcomes of this?
Erica Spatz: Sure. You know, with any infection, we do see a heightened risk of arterial and venous thrombosis, particularly so with COVID, and frankly some of the studies that are showing the rates of arterial and venous thrombosis, both during acute infection, for example, during hospitalization, as well as in the very early phase and [00:10:00] even years out Post COVID are frightening because the risk is significantly elevated.
Some studies show two times the risk, and other studies show up to 20 times the risk of developing arterial and venous thrombosis. We know that the risk is higher in people who are hospitalized, and, in fact people who are hospitalized with COVID-19 infection, who do not have a history of coronary artery disease or other kind of vascular disease, they have the same risk of developing a heart attack or stroke as a person who has cardiovascular disease, but doesn’t have COVID, is not hospitalized with COVID. So, in some respects, we are seeing the very acute hospitalized patient with COVID as having an equivalent risk as somebody who has known cardiovascular disease and is at [00:11:00] higher risk for recurrent events.
Funmi Okunola: Yeah, all the more reason to protect yourself from the infection. What you’ve disclosed today is really quite shocking. So, I have two extra questions. What proportion of increased risk is there in the non-hospitalized patient which is the majority of us? I mean, people are getting infected and reinfected with SARS-CoV-2 daily.
Erica Spatz: So, the risk is much lower if not hospitalized, but it still needs to be considered. I don’t have a specific rate of increased risk. A lot of it has to do with people’s underlying health status. We know that people who have underlying cardiovascular disease and people who have obesity, for example, are at higher risk of having complications of COVID itself as [00:12:00] well as its secondary effects on the heightened risk of thrombosis. So, we need to be in closer touch and have a keener eye and thinking about what are our patients presenting with, who have had a recent COVID infection because we may not see them as having a high risk for a heart attack or stroke, but that risk is heightened following COVID infection, not nearly as much as for the hospitalized population.
Funmi Okunola: Yeah. My second question was why is there so much ignorance of this? Do you think – I’m finding with colleagues that questions around SARS-CoV-2 infection don’t even enter the differential diagnosis when they’re taking the clinical history. Why do you think there’s so much ignorance of what you’re saying?
Erica Spatz: I think to some degree we’ve become a bit complacent with the idea that [00:13:00] so many of us have had COVID, have had recurrent infections, and there’s been a bit of a numbing effect of that so that having COVID is not as unique or identified as a unique risk factor as in the past.
Another thing is that I think clinicians are by and large scared to ask because they don’t know what to do with the information, and there can be concern that there may be an over estimation of the effects of COVID on that person’s health or health status for which they do not know how to mitigate, myself included, which is to say that should we be treating somebody different who is presenting with symptoms? And recently had COVID infection, vs somebody who didn’t? How does that come into our diagnostic evaluation and treatment? And I [00:14:00] think we’re still lacking that clinical acumen to really target what the unique biology that may be presenting, but it’s an important part of people’s history because we should be on heightened alert for a whole range of cardiovascular conditions that are at much higher risk following COVID infection.
Funmi Okunola: Yes, it seems that we need more targeted research looking at the non-hospitalized population, taking into account their SARS-CoV-2 infection.
Erica Spatz: And you know, Funmi, it’s also a good place to say that a lot of times, for the non- hospitalized patient, maybe even somebody who hasn’t even had a severe COVID infection, but is presenting with new cardiac symptoms, [00:15:00] often times our testing is normal.
So, we may do an echocardiogram to look at the structure of the heart, we may do a cardiac MRI, we may do a stress test, and the tests often return normal. We are not seeing, at least at the macro level, evidence of organ damage. But our patients are still suffering from symptoms that we may not have the right diagnostic tests to identify, and we’ll talk a little bit more about some of the unique work that we’ve been doing around identifying those different kinds of presentations.
However, I think when clinicians receive test results that are normal they’re more likely to dismiss their patient’s symptoms as not being cardiac or maybe being in somebody’s head or having a different explanation, and I think that our diagnostic testing hasn’t really caught up [00:16:00] with the diversity of presentations of cardiovascular symptoms that we’re seeing, and there’s an enormous opportunity to improve on that and to not dismiss people.
Symptoms are real. We just might not have had the right test to label what is the actual etiology of that person’s symptoms. But in most of the cases that I see, there is a cardiovascular etiology. I’m just lacking the tools to be able to accurately diagnose it.
Funmi Okunola: Thank you, Erica. That was a fantastic answer. How does heart damage caused by COVID-19 present in the community, i.e. the non-hospitalized patient?
Erica Spatz: We see increased blood pressure following COVID-19. We may see increased insulin resistance and glucose intolerance with COVID-19 and even some dyslipidemias. In our prevention space, we are seeing people [00:17:00] who have higher incidence of cardiovascular risk factors or even poor control within an underlying cardiovascular risk factor. That is very common. If we start to think about Long COVID, a term that has been used pretty broadly to identify people who are often times struggling with profound fatigue, post exertional malaise, so they feel exhausted, totally gassed after any kind of physical or mental activity. They may have some cognitive impairment, often referred to as brain fog.
People who are struggling with Long COVID are really at risk for other kinds of cardiovascular manifestations because they don’t feel well sometimes standing up, or they don’t feel well doing any kind of physical activity. So, they’re more likely to be sedentary. With [00:18:00] sedentary lifestyle there may be weight gain, and that can worsen the cardiovascular risk factors that we were talking about. There may be overlying depression which increases cardiovascular risk. Some of their symptoms may also be cardiovascular driven, right? We’re regulating heart rate, regulating blood vessel diameter and such, so there’s a lot for us to dig into as cardiologists in a person who has Long COVID, because we need to think about what their symptoms are today and what they’re at risk for in the future. How do we help them in a way that’s not going to exacerbate some of their Long COVID symptoms?
Funmi Okunola: Thank you. In your case report, “Chest Pain and Coronary Endothelial Dysfunction After Recovery From COVID-19”, a case series published in Wiley in February 2022, you look at two previously healthy middle-aged individuals who survived COVID-19 and presented with [00:19:00] chest pain with no clear cause. After extensive and specialized testing that would not be done for people ordinarily presenting with chest pain, they were found to have significant damage to major blood vessels of the heart, thought to be due to damage to the lining of these blood vessels or endothelium caused by a SARS- CoV-2 infection. Can you explain the mechanism of your discovery?
Erica Spatz: Absolutely. So, we had patients presenting with chest pain, and not only these two patients, but in these two particular patients, we brought them to have the gold standard for testing of endothelial function, which is performing an invasive, cardiac catheterization, or what would otherwise be called an angiogram.
Typically, this is the procedure that’s done with catheters, either going in through the radial artery in the wrist or the femoral artery in the groin, typically [00:20:00] to inject contrast dye to look for blockages in the heart arteries and maybe to put in stents. We do this procedure if somebody’s having a heart attack and are racing to the catheterization lab to do an angiogram and open up that blood vessel and restore blood flow.
We’ll do it for people who have abnormal stress tests or who are suffering from chest pain. In a lot of people, and Funmi, especially women, independent of having COVID, many women we find come to the catheterization lab for good reason. They’ve had a heart attack, or they have an abnormal stress test, but we don’t find any blockages of heart arteries. So, something happened. Something is happening. Why are they having chest pain? What we’ve been doing along with several centers throughout our country and really across the globe are adding on coronary physiology testing. This is testing the physiology of the blood [00:21:00] vessels. So, we actually don’t directly see damage, but we are seeing an abnormal response of the blood vessels for example in coronary vasospasm. We provoke the blood vessel to dilate, to open up, relax.
We use something called “acetylcholine” in people who have endothelial dysfunction. The blood vessel does not open up. It doesn’t dilate. It actually does the reverse. It constricts and this is one of the diagnostic tools that we can use to identify coronary vasospasm. Increasingly, we’ve been using coronary physiology testing in women who have no obstructive coronary artery disease when we do our catheterization.
We also hypothesize – that maybe that same physiology was happening in some of our Long COVID patients who [00:22:00] had chest pain and many of whom had abnormal stress tests, not everyone, and we have lacked a diagnosis for what was explaining their chest pain. So, we brought them to the catheterization lab. Lo and behold, there were no blockages. The arteries looked healthy, but when we put them to the test to see how they would respond to different triggers, they did not respond appropriately. There was dysregulation, this endothelial dysfunction, and we know that SARS-CoV-2 enters the endothelium through an ACE – 2 receptors that are on endothelial cells.
So, the endothelium is a prime place for SARS-CoV-2 to enter and to cause damage. Again, we’re not seeing that damage, but we’re seeing the end result of that which is this abnormal response to triggers, and interestingly that endothelial damage that we think is happening is probably what’s at play for the thrombotic [00:23:00] complications that we were talking about earlier – the arterial thrombosis, which can lead to heart attacks and strokes even arterial damage at the level of the lungs. In autopsies, we have seen the lung architecture be destroyed by SARS-CoV-2, so the endothelium is a prime target for SARS-CoV-2, and in the cardiovascular world, we’ve seen it manifest as endothelial dysfunction presenting as chest pain, which we were able to identify as coronary vasospasm.
For me today, we don’t bring everybody to the catheterization lab to do invasive testing, but that has formed a lot of our approach to people who have chest pain, which is to say, let’s still do our testing, our non-invasive testing. Let’s make sure you don’t have the other kinds of traditional cardiovascular diseases, and if those are normal, let’s not stop there and chalk this up as being non-[00:24:00] cardiac. Let’s try some medications that can particularly target the endothelium and see if we can help improve symptoms, thereby working backwards to say, ah, I think that’s the mechanism that’s explaining your chest pain.
Funmi Okunola: That’s fantastic, Erica! That’s so enlightening. So, could this be an explanation for the common symptom of chest pain affecting Long Haulers that is very often ignored?
Erica Spatz: Absolutely. I think we need to do our due diligence, and again evaluating every person according to what’s appropriate so not think that all of our tests are always going to come back normal and are always going to be this entity of endothelial dysfunction, but I think it needs to be front and center, especially as you noted.
So many people with Long COVID are women, young women. Their tests are coming back normal, their traditional tests are coming back normal, but they’re having [00:25:00] real chest pain, and that chest pain can be triggered by exertion, it could be triggered by emotional stress, and we’re using a lot of medications to relax the blood vessels, dilate, the blood vessels and finding that that helps.
I mean, most women don’t want to be on heart medication, but actually they’re finding relief. So, if not having relief, okay, let’s move on. Let’s think about what else might be contributing to the chest pain, but it’s a good concept and a proven diagnosis that we should keep in our pockets to think about in our Long COVID population.
Funmi Okunola: Well, fantastic Erica. Speaking as a family physician, I find that the cardiologists that I deal with are really not as enlightened as you are. So, how do we approach this? If we don’t have a cardiologist that’s enlightened, and I find that’s more than 90% of [00:26:00] cardiologists that I and colleagues come across, do we just try the medication ourselves in the community? Like I am thinking of calcium antagonists, or could you give me an idea of how we would approach this?
Erica Spatz: Absolutely. I think one of the reasons why I’m in this space, Funmi, is that early on in the pandemic, we had a COVID team that came together, and we benefited, right? Our patients are teaching us all the time about what symptoms they’re having. What’s the pattern? What are the diagnostic tests looking at and how are they responding to different medications? We forget that this is a really new disease, and many people don’t have that experience. What we’ve been doing here at Yale is trying to educate our community, and also our providers. Currently, we have a Long COVID clinic that is run by [00:27:00] primary care, and they are taking on the bulk of treatment, and the treatment that we’re talking is ABO. Sometimes nitroglycerin, and these medications are relatively safe and benign, and will start with low doses, and could be used by family medicine and primary care.
In fact, we’ve come up with some algorithms to help at least get people started, and then if people are not responding or having partial response and there needs to be more nuance treatment, that might be a good time to bring a person to a cardiologist, but I think we have a lot of work to do.
I think that there’s nothing too overly specialized in what we’re doing, and if we have a community of people who feel comfortable prescribing these medications and get experience doing so, I think it will help a lot more [00:28:00] people.
Funmi Okunola: This is such a brilliant interview, Erica. Thank you so much for joining us.
I know we’re running out of time. So, I’d like to draw your attention to the following paper published two weeks ago on the 9th of October, entitled “COVID-19 is a Coronary Artery Disease Equivalent and Exhibits a Genetic Interaction with ABO Blood Type” by J. R. Hilzer, et al, published in “Atherosclerosis, Thrombosis, and Vascular Biology”.
The main findings of this paper were SARS-CoV-2 raised the risk of heart attack, stroke, and death for up to three years after infection, particularly in individuals hospitalized for COVID-19, regardless of whether the person had a history of heart disease or other risk factors for heart disease, such as pre-existing diabetes or obesity, which you’ve already mentioned in the interview, and also when people were hospitalized for COVID-19, there was an increased risk of heart attack and stroke for those with non-O blood types than those with O blood [00:29:00] type. Could you please comment on these findings?
Erica Spatz: I was just as fascinated by these findings. For me, and the things that were notable in this study, it is the extended risk out to three years following Acute COVID infection and that differed from prior studies, which showed a real tapering of the risk. A higher risk in the immediate post acute phase, but a tapering down over years.
This study showed a persistent elevation in risk out to three years. The interaction with ABO blood type is really interesting. So, as you noted, they found that the non-O blood type was associated with higher risk of heart attacks and strokes. Interestingly, there was no interaction with whether or not a person was hospitalized for COVID, only the secondary [00:30:00] outcomes of that. I don’t know enough about the genetic loci to say why that is the case, that there was a higher risk for arterial thrombosis in people with COVID and non-O blood types. But it’s super interesting and really speaks to the complexities of this virus, and how much further work we have to do to understand who’s vulnerable, who’s not, who should we be using anti-platelet agents in the Long COVID population.
For me, so many of our studies were testing anti-platelet, anti-coagulation in the hospital setting, but we haven’t really thought about trials in the post-acute setting. If we have somebody, potentially, who has the non-O blood type, who has other risk factors for cardiovascular disease, they may not meet our current guidelines for anti-platelet therapy, but maybe we should be thinking about that [00:31:00] to help prevent myocardial infarction and stroke.
We need a lot more studies in this area of Post COVID infections – Post, Long COVID and Post COVID, cardiovascular disease to really strengthen and provide a much more targeted and nuanced approach to cardiovascular risk in the Post COVID setting.
Funmi Okunola: Thank you, Erica. People infected with SARS-CoV-2 are more likely to develop almost any form of cardiac problem independent of age, race, gender or cardiovascular risk factors and whether or not they are hospitalized.
This condition can occur one to three years after being infected. As a result, should a SARS-CoV-2 infection be formally recognised by the medical profession as, and publicised, as a risk factor for heart attack, similar to high cholesterol, hypertension, family history of heart disease, smoking or diabetes?
Erica Spatz: That is [00:32:00] such a fantastic question for me, and I think that is a question that we need to answer. Is all COVID infection created equal? Is it always contributing the same amount of risk? What’s the variance of the COVID infection? You know, is this in a person who’s been vaccinated, and where are they in their vaccination status? What other factors should we be taking into account – ABO blood type? We haven’t answered that question as a community, and I think you’re 100% right to ask that question. The answer is, I don’t know. I don’t know if we should put it into our risk models, and if so, how much attributed risk should we give it? So, I look forward to hopefully having more data to answer that question.
Funmi Okunola: Thank you. Finally, Erica, do you have any suggestions for the prevention, treatment, or cure of heart damage resulting from a coronavirus [00:33:00] infection?
Erica Spatz: I think that controlling cardiovascular risk factors is important. We don’t want to have cardiovascular health snowball out of control while a person is suffering. So, even if it means temporarily treating high blood pressure, hoping that the blood pressure will come down as Long COVID resolves, I think there is still value, especially knowing that people are at risk for major cardiovascular events.
Funmi Okunola: Thank you. I also think we need to help guide how we can help people recover from Long COVID.
Erica Spatz: There’s a lot of controversy in the community around exercise in people who have chronic fatigue. There’s a lot of controversy about how to help people rehabilitate from endothelial function, and we’ve been using modified protocols to [00:34:00] help people gain back their endurance, giving, I always call it exercise for the arteries – retraining our arteries how to behave when we want to walk and exercise, how to dilate, autonomic nervous system control. How do we regulate our heart rate? How do we regulate our breathing? These kinds of functional, physiological processes which have been disrupted. So, I think we need to be more expansive in our approach. That’s not all going to be medication, but the rehabilitation needs to be nuanced.
It’s not your classic physical therapy strength and conditioning approach to a person who is deconditioned or sedentary. They need to be mindful of the physiology and other aspects of chronic fatigue syndrome that may be working against that person so that we can figure out how to best rehabilitate people to full cardiovascular health.
Funmi Okunola: Thank you, Erica, for such a [00:35:00] wonderful and informative interview and for furthering our understanding of the cardiovascular effects of Long COVID.
Erica Spatz: It’s my pleasure to be here. Thank you so much for having me, Funmi.
Funmi Okunola: Please join us for next week’s Episode of Long COVID – the Answers.
Funmi Okunola: Some questions for listeners to consider.
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SHOW NOTES:
Professor Erica Spatz MD talks to Dr Funmi Okunola MD about the effects of Long COVID on the heart. Professor Spatz is a cardiologist and clinical investigator at the Centre for Outcomes Research and Evaluation. She is the Associate Professor of Cardiology and Associate Professor of Epidemiology at Yale School of Medicine in the USA and is the Director of the Preventative Cardiovascular Health Program.
REFERENCES
