Chapters Transcript Video Pericarditis for the Primary Care Provider Back to Symposium Click Here to View Presentation Deck Today we're gonna be talking about pericarditis for the primary care physician. All right, so I have no disclosures. Uh, what are the objectives? We're gonna talk about normal pericardial anatomy, the pathophysiology and definition of pericarditis, how to diagnose pericarditis, and how do we treat acute and recurrent. So the pericardium can be essentially broken down into two layers. You kind of have this fibrous pericardium layer, and then you have the inner layer, the serous, which is the parietal and the visceral pericardium. The edge of the parietal pericardium basically begins the beginning of the fibrous pericardium. Inside the pericardium is the myocardium and the endocardium. Um, You know, uh, the way I describe it to my patients, I'm like, you know, the pericardium is basically like the skin around the heart. Um, it provides kind of like a. I don't know, like a, a, a place for it, uh, so to speak, and it's supposed to be flexible enough to allow the heart to do what it has to do. And if it becomes too stiff and inflexible, that, that leads to problems which we'll discuss. So this is kind of a gross anatomy slide of the, uh, of the pericardium, um, and how it basically, uh, encases the heart and kind of like a little cocoon for it. And then what is pericarditis? So pericarditis is an itis of the pericardium, uh, basically as simple as that. So, something causes some sort of inflammatory stimulus, and, uh, due to that inflammatory stimulus, you get the development of the, uh, inflammosome. And you get further inflammation. And, uh, that then can lead to, you know, uh, pain, um, from the inflammation. And then also, uh, fibrocalcific changes, uh, in certain cases, or just fibrous changes and thickening of the pericardium, um, you know, with the recruitment of fibroblasts and such. This is a nice slide because it shows you kind of where our treatments for pericarditis, uh, can, uh, act on the patient. Uh, so, you know, uh, colchicine, which we'll talk more about, uh, aspirin and NSAIDs on the COX-2, um, uh, pathway, corticosteroids, and then, of course, um, you know, our IL ones. So what's the pathophysiology? So like I said, basically you, um. You have, uh, inflammation, damage, inflammosome, more inflammation, more damage, more inflammasome, more inflammation, more damage. And that's why once it starts to spiral, it can be a really, really nasty illness. Um, and that's why recurrence rates are as high as they are, um, and complications can, can really be devastating. And it's one of those things that, um, because of the etiology, it can really affect anybody like of, of any age. The most common cause is infectious, uh, autoimmune is very common, metabolic, uh, traumatic or iatrogenic, you know, post-cardiac surgery, post-cardiac procedures. Um, and then neoplastic and drug-related are rare, but, you know, they do occur. So what are the most common infectious? So, uh, think of your most common, uh, GI and URI type bugs. They can certainly cause it, you know, think of influenza, enterovirus, um, a herpes virus, patients who might have reactivation of their HSV. Uh, bacterial is, is less common here in the, in the western part. Uh, but, you know, uh, tuberculosis is certainly a cause, and it's, uh, one of the ones that can cause, uh, you know, some fibrocalcific changes and some really nasty pericarditis. Uh, autoimmune, lupus, uh, vasculitis, uh, sarcoid, metabolic, extremely common, especially, uh, uremia. Uh, so think about your, uh, your, um, renal patients. Um, and then traumatic, so our patients who undergo EP procedures are at risk. Patients who undergo various cardiac procedures, uh, patients who are post cardiothoracic surgery, AVR, CABHG, uh, etc. Uh, so this is kind of just, um, uh, a little bit more. So again, Coxsackie, herpes, influenza, adenovirus, HCV, HIV, Parvo, big one that's not on this list, COVID, right? COVID, COVID certainly caused a lot of pericarditis, especially when, uh, when we were first seeing it, um. So what is the prevalence? So about 27. so about 30 cases per 100,000 subjects per year, uh, and about 3 of the 100,000, uh, admissions per year. So it's not uncommon, you know, and I would, you know, I think this number is really an underestimation of the, of the truth because it is 100% underdiagnosed, you know, because it's not your classic type of symptoms. And so what are the symptoms? How do you diagnose it? So basically, one, pleuritic chest pain, or equivalent, which is a little vague. But pleuritic chest pain, you know what I think of it, and, you know, with cardiology and, you know, even just going through internal medicine and, and primary care, you know, there's really a lot of different kinds of chest pain. The pericarditis chest pain is not that classic anginal. Uh, exertional, uh, deep cardiac chest pain. This one really is, you know, patients, they can't feel comfortable, right? They're like, if I, you know, I sit like this, like that, I have to lay down, I have to sit up, I take a deep breath, I'm uncomfortable. I, I kind of move like this, I'm uncomfortable. It's really hard even for them to describe what their symptoms are. Um, and it's, it can be difficult for us to kind of pick them up. But I think one of the things that are more common is kind of having that respiratory variation in symptoms. Ask your patients, take a really deep breath, see if that gonna affect the, the, the character of their chest pain. Do some positional stuff, sitting up, laying down. So that's number one. Then you need one more finding. So one more finding can be on physical exam, the pericardial friction rub. Uh, it can be the EKG changes, which Doctor Talreia showed us earlier today, and we're going to take another look. Inflammatory biomarkers, extremely important, especially CRP and ESR. Those are the two that really we should be ordering every single time that we're suspecting it. Uh, cardiac imaging, especially echo, um, and, um. And an advanced cardiac imaging, basically CMR and uh NCT. What are the definitions of it? So there's acute. Acute is, you know, uh, within 4 to 6 weeks of symptoms. Icessant, it's going on for greater than 4 to 6 weeks. Recurrent, it comes back after an, uh, you know, a pain-free period of 4 to 6 weeks and chronic, lasting over 3 months. So again, history, what are we asking? We gotta ask our patients, what is the character of your chest pain. We talked about the different kinds of pleuritic chest pain. Now knowing what the most common causes are, we should really dig into, hey, have you had any recent diarrhea, vomiting, any URI symptoms, any sick contacts, fevers, chills, any recent vaccines, you've been feeling off, recent travel history. Um, history of autoimmune disorders? Do you have lupus? Do you have rheumatoid? Uh, have you ever been told you had a pericardial effusion or pericarditis in the past since recurrence rates are really high? So it's important to ask these questions. Physical exam, the pericardial friction rub, or you can also see, you can also potentially hear distant heart sounds that you can hear with the pericardial effusion. Uh, other findings can be more, you know, can, you know, more of what you think about like a pericardial effusion. So I'm not gonna go in there, but the pericardial friction rub is a very unique sound. Um, if you YouTube it, you can, you know, there's a lot of examples of it. But obviously, the sensitivity of these, you know, physical exam findings, you know, they're really quite low. Labs, ESR CRP for every single patient with pericarditis every time, you know, and if you're expecting a recurrence, get it again. There's really no reason not to cause these are your kind of just your super, super general inflammatory markers, right? Uh, troponin, I, I put in here because why? So, you know, troponin's secreted by what the cardiac myocytes. However, it's not uncommon to have the entity of myopericarditis, right? If you're having a lot of itis of the pericardium, it's not. You know, crazy to suspect that the myocardium is feeling a little bit of it too. And if so, it kind of changes the prognostic implications and also perhaps the urgency in which this patient's going to be treated and perhaps even in the way the patient's treated. I also would get anti uh NTro-BMP because if these patients are also having, you know, heart failure or even subclinical heart failure, that can also kind of increase what is the urgency and the severity of the patient's, you know, symptoms, right? Cause you might be suspecting this from the outpatient setting, right? So not necessarily you're meeting them in the ED or in the hospital. So, you know, if you're suspecting these things, it's not, not a bad idea to get these. And then also, if the diagnosis is confirmed, or if it's really high on your differential, and you're just like, man, I really know it because of other things, uh, the history, the EKG, whatever, you can go ahead and get some autoimmune markers, you know, on a case by case basis, you know, certainly an ANA is not gonna, uh, is not gonna, you know, hurt. So the EKG findings, you know, the PR depressions, the diffuse ST elevations, they're kind of more smiley face as opposed to the concave tombstone. Ah, shape of uh of your classic stem MI. Echo. So what do we look for an echo? We're looking for an effusion. We're looking at the pericardial thickness, we're looking at the annular motion. We're looking for annulus reverses, we're looking for septal motion, we're looking for a septal bounce. So this is one of the most uh. Impressive, uh, examples of, of a pericarditis and pericardial effusion I've ever seen. I actually asked one of my colleagues, I was like, what do you think is the cause of this? And they're like, Stranger Things. This is literally the, this is literally the upside down. So this is actually a case of uh of uremic pericarditis. And so you can see it's a very complex, um, effusion with fibrinous strands, very bright, thick pericardium. And then here on echo, these are some examples of what we're looking for on Doppler. So now, the pericardium, as we remember on some of the earlier slides, it's, you know, adhered to the outer surface of the heart, right? So not the intraventricular septum, right? The interventricular septum has absolutely no contact with the pericardium, but the lateral wall does. Now, in a normal heart, when the heart squeezes your. Uh, your lateral wall is typically going to have more motion towards the apex than your septal wall. That's just normal. What happens with pericarditis, and especially if there starts to get early cases of constriction, constriction, the pericardium constricting the normal function of the heart, it prevents some of that apical motion of the lateral wall. Now, the intraventricular septum, also known as the medial annulus, kind of compensates. And so if you start seeing that the motion of that. septum towards the apex is greater than, than the lateral towards the apex. This is very, very specific for, uh, for constrictive physiology, and which is frequently a feared sequela of pericarditis or recurrent pericarditis. I know it's a little bit in the weeds, but I know we have some, uh, echo sonographers here. So I wanted to put that in here. And it's also kind of just interesting cause When you understand the pathophysiology of something, it's a little bit easier to kind of, uh, you know, explain things to your patients and stuff. So other things is you're gonna see, you can see a plethoric IVC, a hepatic vein diastolic flow reversal, um, on expiration. So these are all important things for our echo sonographers to be sampling. So when we do these pericardial studies and we read these pericardial studies, we can kind of give the best possible diagnosis. Uh, so this slide is also kind of, uh, a little bit for them. So, again, we're really looking for that septal motion. We're looking for respirophasic variation. Um, if the mitral medial E is, you know, high, and we're suspecting it, and we have an E over A of greater than 0.8, and we have respirophasic, uh, septal motion, this is really consistent with constrictive. Um, whereas, you know, if our annular velocities are kind of, uh, normal with the lateral being greater than medial, then it's very unlikely for the patient to have constrictive. I'm not going to go in the weeds. I kind of put the slide here because I think it's cool for, you know, the, the small sub, uh, section of, uh, you know, uh, people here. MRI. So MRI we really get to see things very beautifully. I think, you know, most patients, unless it's like a very simple pericarditis that the patient like immediately responds to treatment, should get a cardiac MRI. Um, I think for several reasons. One, the spatial resolution is better, so you can actually measure the thickness of the pericardium. You can see what the effusion, which you can also see on echo. You can see annular motion, septal bounce. But the big thing is you can see signs of active inflammation, right? So you can, you can see is the patient having active inflammation now. You can repeat it later. Has the inflammation resolved? Are they responding to treatment? Is the pericardium getting thinner? Is it getting thicker? Is there involvement of the myocardium? And so how does it look? So on cardiac MRI, so this is like a nice example. Like over here, like you can kind of see how thick of a rind. The pericardium is uh is around the heart uh and you really just can't get that on, on echo or really anything else. And so this is, uh, some MRI images of a patient. You can see the effusion there. Uh, you can see, uh, how thick the pericardium is. And it's kind of cool cause you can really see the split and also the, the enhancement of both the, um, The, uh, the outer layer, basically your parietal and your visceral pericardium are both, both thickened in that particular case. Uh, on your T1 imaging, you can get your thickness. On your T2 imaging, you can get signs of, uh, edema. T2 really measures the water content, right, of, of things. So, uh, the brighter it is on these T2 images. The higher the water content. Why would you have water in myocardial tissue and pericardial tissue? It's a sign of edema, right? Whenever there's inflammation, you're having edema, cells are bringing in all sorts of like fluid and, and, uh, and, and inflammatory, uh, stuff. So that's gonna increase the T2 time. And you can really kind of get a sense of the degree of inflammation. And then you have lake adolinium enhancement, which shows scarring and fibrosis. So this is just an extremely. Scarred and fibrotic pericardium here. Uh, and again, you're just not gonna appreciate that on anything other than MRI quite, quite as much. This is a pretty cool case and why I think MRI is important and how you can have serial imaging. So this is a patient who had an MRI before an EP procedure, after an EP procedure, clear signs of pericarditis. And then after treatment, you can see that the thickness of the pericardium. Uh, does respond and it does go down. And also the T2 member, as I said, is, uh, is a sign of inflammation. You can see that the inflammation goes down too. So MRI really kind of provides this degree of granular information that really nothing else is gonna provide in the setting of, uh, pericarditis. Non-contrast CT can show calcifications. Uh, calcifications can, can kind of help in the differential diagnosis of what's the cause of pericarditis, tuberculosis infamously is kind of classic for causing this kind of sort of calcific, uh, pericardial, uh, disease. All right. So now, treatment. I think this is very important for the primary care providers because sometimes you'll be the first ones to see them. You can get them started on treatment as they're waiting for a referral, or also for you guys to know like, hey, why did they start him on this? How long is this going to be on, and what kind of side effects should I expect from my patients because of, you know, the, the, the treatment. So the standard of treatment is colchicine. Colchicine, colchicine, colchicine. Colchicine is the most important therapy that we have for pericarditis. It's the first thing that we treat with. So with colchicine, we start and we're treating, uh, anywhere from 3 months if it's acute first time or 6 to 12 months if it's recurrent. I put all my patients with pericarditis on at least 3 months of colchicine. Then you have some sort of anti-inflammatory, typically NSAIDs. So. I usually use ibuprofen cause most people have it at home and it's cheap. And, uh, you know, uh, patients typically are less afraid to take medications when they've heard the name of it before, as opposed to like indomethacin or something like that. So I usually just go ahead and I use ibuprofen. If they have renal disease and I can't, then I use aspirin. The doses of the ibuprofen is really high, as is the aspirin, 600 to 800 mg TID or 500 to, uh, uh, 1 g of aspirin TID really high doses. So you're going to tell your patients you want them to eat, and you want them to drink plenty of fluids, and you want to monitor for side effects of colchicine, GI dysmotility, uh, some diarrhea. Which is typically self-limiting, or it can be treated with some Imodium. Uh, these are some things to consider. For recurrent pericarditis, the treatment is colchicine, but you also wanna really think about using your IL-1 inhibitors in the, in these cases because, uh, if you look in, in, uh, uh, at, at this pathophysiology slide, the IL one really, uh, inhibiting IL one really inhibits, you know, aggregation and formation of the inflammosome which then, uh, really kind of spurs on further inflammation. So, uh, you know, there's been. A lot that's kind of looked at it, but, but typically the way it goes is the first time is colchicine and NSAIDs. Anytime that there's a recurrent, you really wanna think about, you know, Arcoli or, uh, or Anakinra, uh, your IL-1 blockers, and at this point, obviously the patients are gonna be referred, but I think it's good for, for you guys to know because you guys will be, you know, co-managing these patients and, and it's important to know that they're on these immunologic agents and of course they have their own side effects. Um, Steroids are typically not routinely recommended. The time that I see that they are is if the patient has like an autoimmune disease, like say they have lupus. Lupus is a common one. And uh they need, they're having a lupus flare and they're gonna be on steroids for the lupus flare anyway so of course then you know, you're not gonna stop the steroids and it's really where the cross section of cardiology and rheumatology meet and I think it's very important to have a close uh connection with uh with the rheumatology colleagues to, to make sure patients are getting appropriate care. So I'm not gonna go uh too much into these slides, but basically this looked at, um, uh, treatment of recurrent pericarditis to prevent recurrences and, and you have several studies that basically showed that, uh, you know, compared to placebo, um, you know, uh, the probability of remission is, is much greater than, you know, than placebo and it's, it's almost perfect in, in, in some cases so. Um, it's not a surprise that, you know, instead of steroids, really the next line after colchicine that we're really thinking about is these IL-1 inhibitors. So in summary, uh, think about your pleuritic chest pain, know your EKG and lab findings, ESR CRP, uh, get an echo, refer for cardiac MRI, or if you feel comfortable, go ahead and order the cardiac MRI. And then it'll get on the table of, of me or Doctor Ver's desk or, or Doctor Zubatowska's or Doctor Cohen's desk. And like if we see some signs of pericarditis, like, you know, we'll be able to kind of, uh, link them into the system pretty quickly. Uh, CT can be helpful, especially non-con, colchicine, NSAIDs, and IL-1 blockers. Uh, and this is just, uh, a case that, that was, that we recently had. And this is a picture of, of a case that Doctor Pienta did, a pericardectomy. And as you can see, this patient's pericardium reached 1 centimeter. Normal is less than 4 millimeters. So you can imagine this patient's heart was literally encased in a rind that just did not allow it to function and the patient basically presented in, in pretty much extremists. And honestly, if this went missed. Uh, a non-diagnosed, this patient definitely would not have made it. Um, and if the patient, perhaps if this was caught earlier, then maybe it could have been stopped. Who knows how many recurrent episodes of pericarditis this patient had prior to, to the pericardium getting so thick. So, uh, you know, keep, keep your, uh, antennas peeled for pericarditis. Um, and, uh, thank you. Published Created by Related Presenters Denis Yusupov, MD Cardiology View full profile
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