Echocardiographic Differences Between Constrictive Pericarditis and Restrictive Cardiomyopathy

 Watch These two cases before we start our discussion on two very important diagnosis on Echocardiography and the major distinguishing features of these:

Echocardiographic Differences Between Constrictive Pericarditis and Restrictive Cardiomyopathy

Cardiovascular diseases encompass a wide array of conditions affecting the heart and its surrounding structures. Among these are constrictive pericarditis and restrictive cardiomyopathy, two distinct entities that can present with similar clinical features but have fundamentally different underlying pathophysiology. Echocardiography, a non-invasive imaging modality, plays a crucial role in the diagnosis and differentiation of these conditions. This article aims to elucidate the echocardiographic disparities between constrictive pericarditis and restrictive cardiomyopathy.

Constrictive Pericarditis:

Constrictive pericarditis is characterized by the thickening, fibrosis, and calcification of the pericardium, resulting in the rigid encasement of the heart. This restricts cardiac filling during diastole, leading to impaired cardiac output. Echocardiography serves as a frontline tool in diagnosing constrictive pericarditis and differentiating it from other cardiac pathologies.

  1. Pericardial Thickness and Calcification:

    • Echocardiography reveals a thickened pericardium (>4 mm) with varying degrees of calcification, which appears as bright echoes on the echocardiographic image. This calcification is often seen along the atrioventricular grooves and the posterior wall of the left ventricle.
  2. Respiratory Variation in Inferior Vena Cava (IVC) Diameter:

    • One hallmark echocardiographic finding in constrictive pericarditis is exaggerated respiratory variations in the diameter of the inferior vena cava (IVC). During inspiration, the IVC collapses significantly (>50% reduction in diameter) due to decreased venous return, while it distends during expiration.
  3. Septal Bounce:

    • Another characteristic feature is septal bounce, where the interventricular septum paradoxically moves towards the left ventricle during inspiration instead of the normal rightward motion. This occurs due to the rigid pericardium limiting ventricular filling, resulting in increased septal interaction.
  4. Dilated Inferior Vena Cava:

    • Echocardiography often demonstrates a dilated IVC with blunted respiratory variations in patients with constrictive pericarditis. This differs from the findings in restrictive cardiomyopathy, where the IVC size may remain normal or be minimally dilated.
  5. Pericardial Effusion:

    • While pericardial effusion can occur in both constrictive pericarditis and restrictive cardiomyopathy, its presence is more commonly associated with pericarditis. Echocardiography can assess the size and characteristics of the effusion, aiding in the diagnosis.

Restrictive Cardiomyopathy:

Restrictive cardiomyopathy involves myocardial stiffness, impairing ventricular relaxation and filling. Unlike constrictive pericarditis, which primarily affects the pericardium, restrictive cardiomyopathy directly involves the myocardium itself.

  1. Biatrial Enlargement:

    • Echocardiography typically reveals biatrial enlargement, with both the left and right atria exhibiting increased dimensions due to elevated filling pressures. This is a nonspecific finding but is more commonly seen in restrictive cardiomyopathy compared to constrictive pericarditis.
  2. Normal or Thickened Pericardium:

    • Unlike constrictive pericarditis, where the pericardium is thickened and often calcified, the pericardium in restrictive cardiomyopathy may appear normal or thickened due to inflammation or fibrosis. However, calcification is not a prominent feature.
  3. Pulsed Doppler Assessment:

    • Pulsed-wave Doppler interrogation of mitral and tricuspid inflow velocities provides valuable information in differentiating restrictive cardiomyopathy from constrictive pericarditis. In restrictive cardiomyopathy, there is typically reduced E/A ratio (early diastolic filling velocity/late diastolic filling velocity) with prolonged deceleration time, reflecting impaired ventricular relaxation.
  4. Normal Respiratory Variation in IVC Diameter:

    • Unlike in constrictive pericarditis, where exaggerated respiratory variations in IVC diameter are observed, patients with restrictive cardiomyopathy often exhibit normal or minimally dilated IVC with preserved respiratory variation.
  5. Myocardial Speckle Tracking:

    • Advanced echocardiographic techniques such as myocardial speckle tracking can assess myocardial deformation patterns, providing insights into myocardial stiffness and diastolic function. In restrictive cardiomyopathy, abnormalities in longitudinal strain are commonly observed, reflecting impaired myocardial relaxation.

In conclusion, while constrictive pericarditis and restrictive cardiomyopathy may share similar clinical presentations such as exertional dyspnea and peripheral edema, echocardiography plays a pivotal role in distinguishing between these entities. By carefully evaluating specific echocardiographic features including pericardial thickness, respiratory variations in IVC diameter, and Doppler-derived parameters, clinicians can arrive at an accurate diagnosis and implement appropriate management strategies tailored to each condition.


i'd like to summarize the imaging criteria and also the hemodynamic criteria for diagnosis and then describe a spectrum of constricted pericarditis and recognize a distinction between the restriction and constriction and then we'll review with you a treatment of a constriction and provide you with the important prognostic parameters in this disease so in constricted pericarditis is a predominantly right heart failure and you'll see in patients with a constriction most likely ascites in the edema and also a jugular venous pressure as you see in this patient as most of the patients do have elevation of jugular venous pressure with acoustimal sign and then early diastole the white descent is quite rapid because of the high right right or pressure at the opening of the tricuspid valve and then makes the third heart sounds called pericardial knock and also the subset of patients will present with the plural effusion so uh if you look at this slide showing the constriction and restrictive cardiomyopathy.

Again i emphasize that they may present similar way clinically but the underlying mechanism is quite different because both will present with heart failure because of the limited diastolic feeling but in constriction the limited diastolic filling happens because of the thicken or fibro scarred or calcified pericardium limiting the filling and then that creates the interventricular dependence with this very characteristic septal motion and echocardiography and also cardiac mri but in patients with a restrictive cardiomyopathy whether thick walls hypertrophy or fibrosis the diastolic filling is limited because of the muscle problem not the pericardium and then you see the more slow relaxation of the heart not like the patients with the constricted pericarditis in echocardiography and cardiac mri so traditional imaging and hemodynamic features are listed here pericardial thickness is increased and then subset of patients has a pericardial calcification you can tell in chest x-ray or ct and also there are a stat gold standard the hemodynamic criteria by cardiac catheterization as i listed here and i'll go over that individually although we emphasize the increased pericardial thickness i just want to want to remind you that the normal pericardial thickness cannot exclude cannot exclude the constrictive pericarditis because when we looked at our 143 patients with constriction surgically proven and when we look at their surgical specimen on the microscope the uh 18 of them did have pericardial thickness of a two millimeter or less normal pericardial thickness and the 82 percent had the thickened pericardium so subset of them can present with the relatively normal pericardial thickness especially in patients with the mixed meaning superimposed myocardial disease and such as in radiation therapy or previous cardiac surgery or myocardial infarction they can present through the constriction and relatively normal pericardial thickness and this is an interesting data we just published a year ago and showing the uh relationship between the right atrial pressure [Music] over pulmonary artery wet pressure ratio and then pericardial thickness is over here and the the patients with a relatively normal pericardial thickness here those are the patients with the mixed constricted pericarditis they actually have a lower right atrial pressure over the pulmonary artery weight pressure ratio here meaning uh the right atrial pressure indicates the intrapericardial pressure and that pressure is relative somewhat lower in patients with a mixed constricted pericarditis rather than primary primary or pure constrictive pericarditis i'll get back to this particular parameter when we discuss the prognostic features in patients with a constriction and also what about calcification uh they used to be all related to uh tuberculosis it is quite uncommon uh in this country uh but the in developing countries still tuberculosis constriction is tuberculosis is one of the more common cause of constricted pericarditis it's already 20 years ago when you look at this uh look at our population with constriction but 27 of them had the calcification and chest x-ray but whether they had the calcification or not their outcomes are quite similar after pericardectomy and also i'd like to emphasize that even having pericardial calcification may not be diagnostic for constricted pericarditis so we got to make sure that we come up with the hemodynamic criteria for constriction to make the diagnosis of a constrictive pericolitis and the uh you know orables consider the invasive hemodynamic pressure tracing as a gold standard for diagnosis of constriction and the first report of right-hand cath pressure tracing construction was published in 1946 from nyu and these investigators are very prominent in that they all they receive nobel prize for their work in cardiac catheterization and when they present uh uh this uh patient uh out of a 77 case illustration that's a number 64. with a constriction they've reported the correctly increased right atrial pressure and then normal rbc static pressures and increase rv diastolic pressure because of the limited diastolic filling and also very rapid rise of the early diastolic filling with a plateau and creating the square root deep in plato sign as you see in this pressure tracing uh there was 1946 but the uh uh soon after that uh for many papers uh came out as you see uh uh i'll show you later that similar things been presented in patients with a restrictive restrictive cardiomyopathy and also when you when you see this uh square root sign you see the very early diastolic dip rapid the rise of the filling during diastole early diastole and then plateau and then you can see that in the m mode echocardiogram because this is a very rapid early diastolic filling and then plateaus and this is when the when we hear uh a third heart sound uh called a pericardium because of the uh very rapid flow coming from the the uh the atrium to the ventricle and hitting the wall of the ventricle and then plateau and that's when we hear the third heart sound we call pericardial knock in patients with the constriction but we also hear that not the same sounds about the third heart sounds in patients with the restrictive cardiomyopathy because of the similar type of rapid feeling of the of the ventricle and then again this is a one of those articles i just mentioned that similar pressure tracing deep in plateau and then this is the uh atrial pressure tracing uh not from constriction in this case although similar but in patients with with the cardiac amyloidosis so they realize uh in 1950s and 1960s that the restriction and constricted pericarditis can present with a similar hemodynamic pressure tracing and they try to figure out what features can distinguish one from the other so uh this is the one attempt that when we compare the constriction and restriction and the simultaneous lv and highly pressure tracing and in restriction more of patients with the restriction had the higher lv diastolic pressure than rv diastolic pressure so the uh the difference of a more than five millimeter mercury between lv and rb edp became one of the diagnostic criteria of restriction distinguished from constrictive pericarditis however when our group look at the many patients for the construction and restrictive cardiomyopathy patients that equalization of lv and rv edp and also phc static pressure of a 50 millimeter mercury or less for constriction that's one of the hemodynamic diagnostic criteria and then rbdp over a ph static pressure greater than one-third all of them had about eighty percent overlap with the restrictive cardiomyopathy so this is really challenging for us to use the traditional hemodynamic diagnostic criteria for constriction and differentiate that from restrictive myocardial disease so uh if you look at the this uh square root sign or rapid rise of the diastolic pressures and this happens in patients with the restriction in patients with the constriction and that can be also detected by doppler echocardiography this is a pulse wave mitral infill velocity showing the early die study filling which is rapid filling and then the lower filling with the atrial contraction because of the increased the diastolic velocity at the mid to lastly hr contribution is relatively less and because of the rapid rise of the uh uh early diastolic filling we have a very short deceleration time meaning the from the time of the peak velocity to the time it reaches the baseline we call that as a deceleration time and usually it is a longer than uh 200 millisecond but in patients with the high feeling pressure and very rapid rise of the early diastolic pressure we have a shorter decel time as you see in this diagram i think that the characteristic uh really characteristic hemodynamics hemodynamics of constriction was really uh uh uh uh provided by dr lip hadley uh when she was the she was a visiting professor at stanford and working with dr christopher appleton and as you see here on your right side in patients with the restricted for cardiomyopathy when you see the intra-thoracic pressure the pulmonary capillary wedge pressure and then left ventricular pressure during diastole when we [Laughter] breathe in during inspiration the intrathoracic pressure meaning pulmonary capillary pressure falls uh here falls here for the inspiration and that pressure change or the drop in blood pre the intrathresh pressure transmitted equally fully to the left ventricle or intracardiac cavity so the lb diastolic pressure also falls so that the pressure gradients driving pressure gradient to the left side chamber does not change with the inspiration or expiration but in patients with the constriction there's a dissociation between the intracardiac and intrathoracic pressure let me just show you that a little more clearly on next slide and when uh dr liv hadley uh finished her professorship uh at stanford and lucky for us so she came to mayo clinic to spend another year with us and we were very interested in this uh non-invasive hemodynamics and also constriction and restriction and the dr nishimura very interested in hemodynamics and he is doing the cardiac cath radiations and i'm doing the simultaneously doing double echocardiography much info velocity in a patient with a constricted pericarditis so with inspiration again intrathoracic pressure falls so pulmonary capillary or pulmonary artery wedge pressure falls a few millimeter mercury but led diastolic pressure does not fall too much much less than intrathoracic pressure so as a result you have a marked decrease driving pressure gradient to the left side chamber so that if you the mitral infill velocity e velocity decreases from expiration and when you have expiration then the pulmonary wave pressure goes up again and then without a significant change in the left ventricular pressure change you have an increased driving pressure gradient to the left side chambers so let me just show you one more time because this is a crucial point of the hemodynamic hemodynamic mechanism of constriction and we want to add one more characteristic uh that is interventricular dependence which is unique to constriction because because of the thickened pericardial layer as the illusory is with the yellow line here they combine cardiac volumes left and right sides are constant so if you increase feeling to the left side chamber that'll decrease feeling to the right and vice versa so let me just show you this animation then with the uh uh pressure tracing on the top with the uh intrapulmonary uh intrathoracic pressure in purple and intracardiac pressure lv pressure as a blue so with the inspiration you can see the intrathoracic pressure falls but the lv diastolic pressure stays similar not without significant change that decrease filling to the left side chamber allowing septum to deviate left more filling to the right side chamber so pulmonary vein the diastolic velocity and mitral inflow velocity will decrease with over the expiration or inspiration excuse me and tricuspid inflow velocity will increase and hepatic vein doppler fourth flow velocity will increase but reverse is much less with expiration you have the increase intrathoracic pressure with a minimal change in the cardiac pressure increased pressure here flow and the septal deviates the right and more filling you see the pulmonary vein and mitral infill velocity with the expiration and you can see that reduction in trichos and then significant flow reversal with expiration uh as you i show you in this uh animation so we need to demonstrate these two features whether you do by uh echocardiography or by cardiac catheterization to diagnose constriction correctly and separate it or distinguish it from restrictive myocardial disease so another important [Music] diagnostic parameter for echocardiography came from this observation the e prime velocity that is the early diastolic velocity of the mitral annulus that is uh the parameter that corresponds what reflects the lb relaxation very well so normally uh in normal individuals with the normal myocardial relaxation e prime velocity is about 8 to 10 or sometimes young individuals up to 15 centimeters per second but in all individuals or all patients with the myocardial disease the relaxation is the first property one of the first properties to become abnormal so e prime velocity then by double equal cardiography by tissuedoplecocardiography from the medial annulus in this case that decreases to three four five six centimeters compared to the normal uh e prime velocity of eight to twelve sonometer per second but in patience for the constriction because of the uh uh lateral confinement here you cannot have much of a lateral move the but the only way this heart with the constriction the way to increase cardiac filling is increased movement of the mitral annulus so that e prime velocity is actually increased in patients with a constriction there are significant it's a paradoxical very opposite between the restriction myocardial disease and constricted pericarditis so this is the data that we put together although this initial observation was made by dr maria garcia when he was at cleveland clinic and he's now at the einstein in new york we look at this parameter in constriction cardiac amyloid and restrictive cardiomyopathy as you can see there's really little very little overlap between the myocardial disease and pericardial constriction when we use e prime velocity of eight or nine cylinder per second as you can see so this has become a very important parameter to distinguish between two conditions and also diagnose constrictive pericarditis so with our extensive experience almost more than 20 years of experience of using double eco cardiography we established and they published this echocardiographic diagnostic criteria for construction they are septal motion abnormality i already showed you why that happens because of the interventional dependence uh more feeling to the left uh with the expiration then less feeling to the right and vice versa with inspiration and you're gonna see this uh the the septal motion change to the left with the inspiration to the right or the expiration as you see and the mitral input velocity is very restrictive although most of them has a respite variation of 25 or greater from inspiration to expiration but 20 to 30 percent of them may not have any uh raspberry variations at all an e prime velocity of eight centimeters per second or greater and the most uh specifically hepatic vein doppler uh diastolic flow reversal as you see here with expiration not inspiration so if you uh uh uh if in someone with the jugular venous distension the right heart failure and echocardiography show these fe these uh features and we can be quite sure that the patients uh uh uh uh do have the uh constrictive pericarditis and i'm just showing you importance of hepatic vein um i'm not sure whether you're gonna be asked this type of thing in the heart failure board about the echo cardiac echocardio people they'll be asking you but the clinical practice wise is very important because this is normal hepatic pain with a minimal diastolic flow diastolic fluid reversal in constriction and exploration but in myocardial disease you also have a diastolic fluid reversal but with inspiration opposite paradoxical right this happens because the venous return will increase as you know with inspiration and with the disease myocardium that increased venous return of blood flow cannot be accommodated so it has to go back to the hepatic vein and then sometimes a severe tr can be confused clinically but they have the flow reversal back into the hepatic vein during systole not diastole so this is a very good uh things to do clinically when you take a cardiogram to separate different types of right out failures and this is an example of a myocardial disease and again similar my mitral inflow velocity very restrictive uh the uh ld function is preserved but the strain imaging is a very characteristic for cardiac amyloid we call this as a apical sparing the red is normal but all does the basal portion and the mid portion of the heart is quite reduced in the myocardial thickening and also the mitral annulus velocity is markedly decreased to four centimeters per second so a constriction really cannot have e prime over four cylinder per second has to be most of times it has to be more than uh eight centimeter per second or so so this is a typical restrictive cardiomyopathy and as a doctor leave hadley initially showed uh this uh you know interventional dependence and she got the idea actually from cardiac head radiation that nobody else uh recognized and we did the further studies to confirm that in restriction and constriction if you look at the both pressure tracing one from restriction and one from constriction both the equalization of dislike pressures really uh superficially they look quite similar you really cannot tell one from the other right but in a restriction when you have the simultaneous left ventricular pressure and the right ventricular pressure those pressure changes concordantly they drop or decreases with inspiration and increases with expiration but in patients with the constriction it's interesting that led pressure falls with inspiration but the rb pressure increases and also the width of the pressure is an increases with the uh uh inspiration here in rb and then decreases uh with the uh expiration as you see uh and then those changes are quite opposite in the left ventricular pressure tracing so that's that's the most specific changes we're looking at in patients who undergo cardiac catheterization for diagnosis of constrictive pericarditis or restrictive cardiomyopathy and this is also interesting the quite opposite because and i already told you that the e prime velocity should be very low in patients with the myocardial disease whether it's a cardiac amyloid or it is ischemic cardiomyopathy hypotensive heart disease or hypertrophy cardiomyopathy any myocardial disease myocardial relaxation is reduced especially when they're in heart failure right but in patients so the e-prime velocity is usually uh you know four five six nanometers per second but in constriction e prime velocities uh is about uh nine centimeters per second or greater so we now have a situation uh even in constriction you have the mixed disease because now the radiation induced patients with the previous myocardial infarction or cardiac surgery they have a myocardial disease and constricted pericarditis so when you look at this two-patient group the the blue is the pure primary constriction without myocardial disease their e prime velocities or almost all of them is a greater than nine cylinder per second but in patients with a mixed disease these are red dots and some of them actually do have the e prime velocity of lower than nine it can be a you know six seven eight centimeter per sec second so it may be sometimes a tough to separate this patient from myocardial disease and because of the high e prime velocity eoboy prime which is estimate of the pulmonary capillary pressure in myocardial disease it goes up because of the eob prime is linearly correlated to the e by prime ratio but here is a again the the is a paradoxes annulus paradoxes we're calling it but primary constrict constriction with no uh myocardial involvement eoa prime is a much less than 15 but the majority of patients with mixed constricted pericarditis has the not majority almost half of them do have the eob prime of 15 as you see here so it's very very uh interesting concept and that's why that when you see the uh uh high e prime velocity meaning pure uh constricted pericarditis and the low eob prime ratio as you see here low e prime velocity here and also the normal ph static pressure they have much better prognosis after constricted pericarditis and we just published that a couple months ago and then this will be very helpful for us to managing our patients with the constricted pericolitis and here again i i returned to this right atrial pressure over the pulmonary artery wave pressure ratio and i i know that the this ratio when it's high in patients with a restrictive cardiomyopathy they have a worse prognosis right because of the you know by ventricular involvement with the myocardial disease but in patients with the constriction actually the higher ratio median values of 0.77 0.77 to 1.0 the higher ratio those are the patients with the pure constricted pericarditis with the thicker pericardium they have a much better prognosis than the low ratio patients over here and that's the patients with the low eoa prime ratio as i shown you in this slide so if i can just summarize the last few slides of separating the primary from mixed constriction in pure primary constricted pericolitis the pericardial thickness is a greater thicker pericardium the mixed constriction has relatively normal pericardial thickness not all of them but the a lot of them a lot of patients and the rna pressure is higher in pure constricted pericarditis close to wedge pressures and then e prime is higher in primary computed mixed and eo prime is lower and also physical pressure is relatively normal in the pure constriction compared to a mixed constricted pericolitis so let me just then uh share with you a clinical uh spectrum of pericardial disease there are many different ways that the constriction can present the most common cause now for us in our practice is a cardiac surgery okay it used to be tuberculosis and there's still a lot of developing countries and also a lot of idiopathic or another common cause is the previous history of pericarditis they present with constriction 10 20 30 years later and or someone with a pericardial diffusion or tamponade they can present as a constriction as a par as a effusive constriction which can resolve spontaneously in some patients but they may go to the constriction may require a non-steroidal or steroidal medication or sometimes even cardiac surgery this is an example of a 54 year old physician with a history of acute pericarditis many years ago and now he presents with the increasing dyspnea and edema no diagnosis of five years and i saw him about three years ago and an echocardiography shows you right away the septum motion change here and ivs is a plethora you have to think about constriction whenever you see a patient with hep path or patients with a preserve or normal ejection fraction constricted pericarditis has to be a differential diagnosis and if you see the see any septal motion change i think you're close to the diagnosis of constriction okay because not many patients with the preserve ejection fraction heart failure injection hepatic patients has a septal motion of melody unless they have a conduction delays and other things like that and especially when you have the plethoric ibc then you know you are even closer to the diagnosis of constriction then you need to demonstrate the characteristic hemodynamic hemodynamics of constricted pericolitis and he has a restrictive filling with some variation not 25 percent but the hepatic vein which is most specific uh criteria of the constriction by doppler cardiography has the diastolic how do you know diastolic uh expiratory excuse me because the fourth flow velocity is lower in in exploration than inspiration you have a significant flow reversal here very diagnostic for constrictive epicolitis and also it's interesting that the myocardium is here then the pericardium is a tethered in constriction laterally and inferiorly posteriorly so when you look at the strain imaging meaning the myocardial thickness the the shortening with the with the contraction is a markedly reduced in the area of a tethering usually lateral or uh posterior segment of the of the heart and that's why the e prime velocity from the lateral is actually lower although it's very high i mean usually it's about you know 10 to 12 but it's now 16 still increased laterally but it's lower than the medial over 20 which is quite opposite to the myocardial disease myocardial disease is a lower but it's a is a it's a higher at the lateral low at the medial level so again this is a paradoxical nature of those uh relationship there's and we call this as a annulus reverses because it's a reverse to the normal uh situation as we see and i think that you probably will be uh using it in heart failure patients pattern recognition apical sparing for the cardiac amyloid hypertrophy cardiomyopathy uh for the decreased strain at the basal septum uh here entry wall and also the posterior wall there and then this is the uh patients with the apical infarct or stress cardiomyopathies even apical hypertrophy cardiomyopathy with a marked reduction in the strain at the apical segment and the lateral and the posterior myocardial strain is reduced in patients with the constricted pericarditis in that so uh i think it's important that we also recognize effusive constriction some of them return to normal spontaneously but we want to treat uh them with a nsaid or steroid unless they have a significant chest pain because we don't want to take any chance that they move to the chronic constrictive phase and this is an example we now have a lot of device you know ep device and we have the interventional structural heart disease device these patients getting both tablet and pacemaker implantation uh two manages uh severe aortic valve stenosis and patients unfortunately develop a coagulant tamponade they probably rupture the rb free wall and the we did the pericardial synthesis and bloody fluid and patients got better and discharged but two months later came back with more and more symptoms of heart failure and signs of heart failure and significant edema and you can say cardiac wise no fluid but the mark increase in pericardial thickness in this dark area there because of the inflammation of the pericardium so this is a very typical example of effusive constricted percolitis okay and we uh uh have adopted cardiography showing you know similar to constriction hepatic vein and then much info velocity we treat this patient with nsaid for two months with a cortisone and then a much info velocity and the hepatic vein all normalized and patient symptoms all went away so if we uh manage or identify patients with diffusive constriction early on we can actually manage their constriction by medical therapy we also publish this data uh not only the uh you know the efficient constriction but if someone has has the constrictive uh features by echocardiography or also clinically i think you can do most of diagnosis by echocardiography in clinical practice with the jugular venous pressure distension and then all the features i showed you but we do cardiac mri in most of patients to make sure that we analyze or assess the pericardial inflammation if someone has mock inflammation as you see here this is gadolinium delayed enhancement pericardium and that indicates that the constriction is not yet fixed it can be reversible with a medical therapy and then we treat uh with the nsaid with the cortisone or sometimes steroid causes it's really based on the levels of symptoms and you know hemodynamically unstable really a new heart three or four uh we like to go straight to the steroid but if much less than that we can try enslave with the colchicine and then a lot of patients can resolve their symptoms and we also found that the patients with a reversible a transient constriction by medical therapy they have much in more intense uh gadolinium take uptake there and also their inflammatory body markers like acetrate and cl crp they are all elevated computed the patients that uh who did not respond to our medical therapy so we usually do a cardiac mri for these patients not just for the diagnosis of constriction but i think looking at the reversibility of a constricted pericolitis so again we look at the pericardial inflammation and also we looked at septal motion change as you can see uh in uh by echocardiography also okay so this is a role of cardiac mri and the ct is the best for the structural delineation a thick pericardial layer here although as i mentioned before the normal pericardial thickness does not mean that patient does not even does not have a constriction but the thick pericardium really helps and we treat this patient with a steroid in one week everything is normalized pericardium is normal and no problem fusion and we usually uh continue our treatment for about three months with a good tapering uh strategy with the cold system and then a patient can recover from hemodynamically significant constricted pericarditis so this uh effusive constriction definition is you have an increase right atrial pressure and intrapericardial pressure uh at baseline after pericardiocentesis still uh rda pressure is elevated as you see here and then in this particular uh report the nine or nine of 13 patients required pericardectomy and we have this data uh uh 20 years later showing that only seven out of 15 that's 50 50 of patients and 8 of them after a pericardial synthesis had the effusive constricted pericarditis and they also they used the right-hand cardiac catheterization to diagnose that but we are now used echocardiography this is our data there are 205 consecutive patients and then we found that 16 of them has effusive constrictive pericarditis there so it's more frequent in patients with the hemopericardium especially with the during the device as i uh divided therapy as i've shown you before and in our practice though we treat most the patients have the pericardial synthesis with the nsaid or steroid nsaid and cultures in any way so only two patients required pericardectomy uh in 3.8 year follow-up as you see here this is another another example of a effusive constriction presents with the tamponade and the undoing pericardium window but patients still having trouble and then here is the uh jugular venous pressure elevation and then this is a double echocardiography showing marks septal motion of melody the m mode which is a most uh reliable looking at the separate motion abnormality hepatic pain much info velocity elevated e prime velocity we treat this patient with the steroid and the cold system did not respond so we had to go ahead with the pericardictomy and this is a intra the video of a pericardicum you can see the thickened pericardium and then the heart bulges through the uh the open pericardial layer there because of the constriction there and you can see our volume of constriction once we have the more understanding uh from dr lee hadley's visit in 1980s late 1980s an echocardiography and also a hemodynamic cardio catheterization all together and ctencaric mri we diagnose more patients and we are now doing 75 to 100 perce pericardectomies a year at the mayo clinic to deal with these patients and the radiation and post-op has much worse prognosis compared to idiopathic viral pericarditis and also important to note that the uh tricuspid regurgitation is important because the uh 53 percent of them with the constriction has no tr but once you have a even mild tricuspid regurgitation you have a much worse prognosis i think one of the reasons is also this is a patient with a constriction you can see the indented because of the pericardium mass there once you remove that your annulus is enlarged and you end up developing more severe uh tricuspid pelvic agitation so we have to make sure when you do intraoperative uh transition for the electrocardiography in patients undergoing pericardiactomy and this is a patient actually uh also having some indentation in the left side chamber and then this is a baseline of the mild mitral guard but after pericardectomy became severe that they have to do mitral valve repair so we have to really pay attention to the av valve regurgitation after pericardiactomy so uh if i can just summarize i think that the you know pericardial disease has a lot of spectrum inflammation with the pericarditis fluid with effusion and tamponade and then scar with constricted pericarditis and i think the multi-modality imaging is quite valuable and also the uh the constriction diagnosis really has to be based on hemodynamics whether you do echocardiography or cardiac catheterization you don't really have to do both once you're if you feel comfortable with one diagnostic hemodynamics for constriction and also you have to understand the effusive constriction it happens up to 20 and the medical therapy is possible but if nothing works then no medical therapy is helpful then you have to go through the pericardectomy as a choice but also the in your practice and also for the exam are they probably going to ask you about the mimicry because constriction can mimic some other disease and this is a patient who uh undergoing liver transplant you know they did the whole evaluation of transplant because of the liver function abnormal melody perimegaly and things but the during general medical examination you can see the acoustimal sign and all the echo mri all they're showing the constriction so constriction can be a diagnosis was a liver disease it happens very not infrequently and this is patient this is a patient i was seeing in velvet clinic came for the cbo aortic valve stenosis the low flow low gradient only at 26 millimeter mercury with the cbis but the much inflow is restrictive and the increased e prime velocity even with the you know cbas that's kind of unusual so when you look at the hepatic vein there is a typical diastolic flow reversible constriction so this is a patient of the radiation heart disease which caused the valve disease and also the uh constricted pericarditis so we've got to make sure that we uh discover this disease which can be sometimes quite uh quite uh challenging in our clinical practice so things to remember for your board in practice this is a really curable diastolic heart failure as i shown you and the phenotypically about the many features are quite similar to restriction myocardial disease but quite distinct hemodynamics as i shown you right the interventricular dependence in cath and echocardiography and also the diagnosis should be based on these features as i've shown you and this one again very paradoxical to the myocardial disease annulus paradoxes annulus reverses pressure change lvnrv discordance in this concordance and hepatic pain diastolic fluid reversal exploration not inspiration as in myocardial disease and also you have to understand the treatment based on the what you see in the cardiac mri and duration of disease and then clinical setting of that particular patients and also you have to pay attention to the uh uh tricuspid and mitral valve regurgitation intraoperatively and finally uh uh you know everybody knows dr paul de le white who really was a pioneer in construction uh in 1920s 1930s the mass general and then at that time he showed this a picture of a patient a society's improved [Music] after pericardectomy in 1930s and then he said that establishing the diagnosis of constriction is very very important in threefold and actually i was giving grand rounds at the mass general a couple years ago and i use this slide because we still have the same problems because it'll force the uh uh explanation of a group of patients with the symptoms in science of constriction which can be from some other disease too and also you know obvious confusion with other conditions we have seen patients coming towards it with a cardiac amyloid turned out to be constriction vice versa and also the most importantly experienced cardiac surgeons can now cure this problem that once thought to be hopeless disease so i think it's very very important that we diagnose constriction for us to do that we have to remember constriction as one of the conditions that cause right heart failure and heart failure with the preserved ejection fraction.


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