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Home , Acute pericarditis, Cardiomyopathy, Electrocardiography, Heart failure, Pericardial effusion, Pericardiectomy

Review Constrictive : diagnosis, management and clinical outcomes Terrence D Welch1,2

1Section of , Abstract 1.8% of patients have been reported to develop Dartmouth-Hitchcock Medical Constrictive pericarditis (CP) is a form of diastolic chronic CP.9 The incidence was lower in patients Center, Lebanon, New with idiopathic or viral pericarditis when compared Hampshire, USA failure that arises because an inelastic 2Department of and inhibits cardiac filling. This disorder must be considered with other aetiologies such as rheumatologic disease, Medical Education, Geisel in the for unexplained , malignancy or bacterial . The incidence School of Medicine, Hanover, particularly when the left ventricular of chronic, symptomatic CP appears to be simi- New Hampshire, USA is preserved. Risk factors for the development of CP larly low in patients who have undergone cardiac include prior and radiation , but surgery, with reported rates of 0.2%–2.4%.10 11 Correspondence to Dr Terrence D Welch, Section most cases are still deemed to be idiopathic. Making the of Cardiology, Dartmouth- diagnosis may be challenging and requires meticulous Hitchcock Medical Center, echocardiographic assessment, often supplemented The constrictive, inelastic pericardium is typically Lebanon, NH 03756, USA; ​ by cross-sectional and haemodynamic fibrotic, calcified and thickened, although CP may Terrence.​D.​Welch@​hitchcock.​ catheterisation. The key pathophysiological concepts, org occur with a pericardium of normal thickness in which serve as the basis for many of the diagnostic up to 18% of cases.12 A subset of patients with CP, Received 28 September 2017 criteria, remain: (1) dissociation of intrathoracic and typically those presenting subacutely, have inflam- Revised 2 November 2017 intracardiac pressures and (2) enhanced ventricular mation as the dominant pathological mechanism. Accepted 4 November 2017 interaction. Complete surgical is the Published Online First 25 November 2017 only effective treatment for chronic CP. A subset of patients with subacute inflammatory CP, often identified In contrast to the normal pericardium, the constric- by cardiac MRI, may respond to anti-inflammatory tive pericardium impedes cardiac filling. The ventri- treatments. cles are able to fill only as long as their volume stays below that allowed by the abnormal pericardium. Introduction Once that limit is reached, filling stops prematurely. Constrictive pericarditis (CP) is a form of diastolic Venous pressure increases, leading to congestive heart failure caused by an inelastic pericardium that symptoms and signs. volume and cardiac inhibits cardiac filling. Because its treatment differs output fall, leading to dyspnoea on exertion. markedly from all other forms of heart failure, accu- Because cardiac volume is limited by the constric- rate diagnosis is imperative. Making that diagnosis tive pericardium, the right (RV) and may be difficult, as CP may mimic other disorders. the left ventricle (LV) are noted to alternately fill This review is meant to summarise the state-of- at the expense of each other during the respira- the-art approach to diagnosis and management. tory cycle (figure 1). Recognition of this enhanced ventricular interaction is a key component of the diagnostic work-up.13 Aetiologies Under normal conditions, the pericardium has remains a dominant cause of CP world- little effect on haemodynamics. Changes in intra- wide. Case series from China, Iran and South Africa thoracic pressure to similar changes in pericar- have reported tuberculosis CP as the cause of CP in dial and intracardiac pressures, and cause a normal 22.2%–91% of cases.1–3 In contrast, European and slight variation in the LV and arterial North American series have reported much lower systolic .14 The negative intrathoracic rates of tuberculous CP (5.6% or less); most cases pressure of inspiration favours increased venous in these areas of the world are idiopathic or related return to the right heart and mildly decreases LV to prior cardiac surgery or chest irradiation.4–8 In filling and output through complex mechanisms a large series from the Mayo Clinic, 80% of cases unrelated to the pericardium. were classified as idiopathic or due to prior cardiac In CP, however, this respiratory variation in surgery, chest irradiation or prior acute pericar- cardiac filling and output becomes exaggerated ditis.7 When that cohort of patients was compared because of the pericardium. With inspiration, the with a historic cohort, a marked increase in the RV cannot expand to accommodate increased frequency of cases due to prior cardiac surgery or venous return. Rather, RV volume can increase was noted. Other possible causes only via encroachment into LV space, via a shift include rheumatologic disease, infection, malig- of the ventricular septum. This to decreased nancy, trauma and asbestosis. LV filling and output. Also contributing to this phenomenon is the insulating effect of the diseased Epidemiology pericardium, such that negative intrathoracic pres- Neither the prevalence nor overall incidence of CP sure during inspiration is not fully transmitted to To cite: Welch TD. Heart has been well established, but it appears to be rela- the cardiac chambers. Accordingly, the pulmonary 2018;104:725–731. tively rare. After an episode of , veins, which are extrapericardial, will experience

Welch TD. Heart 2018;104:725–731. doi:10.1136/heartjnl-2017-311683 725 Review

Figure 1 Enhanced ventricular interaction in constrictive pericarditis. Because of the volume-limiting effect of the constrictive pericardium, the ventricular septum shifts towards the right ventricle (RV) in expiration (A) and towards the left ventricle (LV) in inspiration (B) (apical four-chamber view). This phenomenon can also be recorded by M-mode (parasternal long-axis view); (C) shows movement of the septum towards the LV with each inspiration (arrows). a greater pressure decrease than the left heart chambers, and the pressure gradient to fill the left heart will diminish. This Elevated venous pressure is expected with CP.7 Exceptions to phenomenon has been termed dissociation of intrathoracic and this ‘rule’ would include patients with mild CP, or who are intracardiac pressures.13 The preferential filling of the right hypovolemic. Examination of the will heart chambers during inspiration then gives way to preferential reveal a steep, deep y-descent that signifies rapid early RV filling left heart filling with expiration, when increased intrathoracic that abruptly terminates when the volume limit imposed by the pressure decreases systemic venous return to the right heart and pericardium is reached. The jugular venous pressure may also restores the filling gradient between the pulmonary veins and rise with inspiration (Kussmaul sign). Chest and left heart chambers. Increased LV leads to increased may reveal a . Cardiac auscultation stroke volume. may reveal an early diastolic sound that is termed a ‘pericar- In some cases of subacute CP, a may be dial knock’. This sound occurs at the nadir of the y-descent and present between the layers of constricting pericardium. This corresponds to abrupt cessation of ventricular filling. Measure- situation is termed effusive-constrictive pericarditis and may ment of the systolic blood pressure may reveal an abnormal be recognised clinically when elevated venous pressure and (>10 mm Hg) decrease with inspiration, which is termed ‘pulsus constrictive haemodynamics persist despite removal of the peri- paradoxus’ and relates to enhanced ventricular interaction and cardial fluid. dissociation of intrathoracic and intracardiac pressures. Abdom- inal examination may show pulsatile with . Clinical presentation Peripheral oedema is often present. When advanced, CP may The haemodynamic derangements associated with CP may lead lead to . to a variety of symptoms and signs, as shown in figure 2. Evaluation History CP is usually not immediately evident on standard testing. Part Dyspnoea on exertion and oedema are the most commonly of the reason for the difficulty with diagnosis is that CP may 1 2 7 reported symptoms. Some patients present with chest mimic other causes of heart failure or even lung or liver disease. discomfort, , , abdominal symptoms, atrial The diagnosis should be considered in patients presenting with or congestive hepatopathy. otherwise unexplained heart failure, pleural effusion, jugular venous distension, oedema or liver disease. This is particularly true if there is a history of cardiac surgery, chest irradiation or pericarditis. The classic contending cardiac diagnosis is restric- tive . Initial evaluation should include an ECG, , laboratory assessment and echocardiogram.

Electrocardiography The ECG may be unremarkable. Low may be present in approximately one-fourth of patients.12 Atrial has been reported in up to approximately 20%–40% of patients.2 7 8 15

Chest radiography The chest radiograph may also be unremarkable, but might show a pleural effusion, pulmonary vascular congestion or cardio- Figure 2 Summary of the principal haemodynamic abnormalities and megaly caused by pericardial effusion. Pericardial calcification typical clinical presentations associated with constrictive pericarditis. on the chest radiograph is seen in only 27% of cases of CP, at See text for details and additional findings. least in areas of the world where tuberculosis is uncommon.16

726 Welch TD. Heart 2018;104:725–731. doi:10.1136/heartjnl-2017-311683 Review

Laboratory assessment Respiration-related variation in mitral inflow velocities Measurement of the plasma brain natriuretic peptide (BNP) Reduced left-sided cardiac filling during inspiration is also mani- level may be useful in the diagnostic work-up. As the BNP is fested by a reduction in mitral early (E) inflow velocities, when a marker of ventricular dysfunction and wall stretch, it is typi- compared with those during expiration (figure 3). E velocity vari- cally elevated in most forms of heart failure and cardiomyop- ation of 15%–35% is expected in CP, although 10%–15% vari- athy. CP, in contrast, should not cause wall stretch and appears ation is enough to differentiate CP from restriction.13 18 20 21 to yield smaller increases in BNP when compared with restrictive However, variation in mitral E velocity is not considered essen- cardiomyopathy, although significant overlap has been noted.17 tial to the echocardiographic diagnosis of CP, as it may be absent In some cases, hepatic function tests may be abnormal because when left atrial pressure is very high and it may be obscured by of congestion. atrial arrhythmias.

Respiration-related hepatic vein flow reversals Echocardiogram Reduced right-sided cardiac filling during expiration is also While a ‘standard’ echocardiogram will allow exclusion of other manifested by prominent reversal of hepatic vein flow during forms of heart failure, such as LV or RV systolic dysfunction late (figure 4). This flow reversal is less prominent or or valvular disease, a dedicated ‘CP protocol’ echocardiogram is absent during inspiration, when right-sided cardiac filling is necessary to identify CP and exclude restriction. favoured. Hepatic vein diastolic flow reversal during expiration A CP protocol echocardiogram should focus on the motion is a specific (88%) sign of CP.18 of the ventricular septum, variation in the mitral inflow velocity, variation in the hepatic vein profile, and Doppler assess- ment of mitral annular velocities. Myocardial strain imaging has Unique myocardial relaxation profile also emerged as a helpful addition. ►► Preserved or elevated e’: Most forms of heart failure are associated with abnormal diastolic relaxation of the myocar- dium, as measured by the early diastolic mitral annular Respiration-related ventricular septal shift tissue velocity (e’). CP, in its pure form, is unique in that The reduction in left-sided cardiac filling during inspiration the myocardium is capable of normal to supranormal relaxa- causes the ventricular septum to shift towards the left, allowing tion velocities.22 23 Therefore, if normal to high e’ velocities increased RV filling. The opposite occurs with expiration, with are recorded in a patient with heart failure, CP should be the septum shifting back towards the right. This phasic shift in strongly considered. A medial e’velocity of ≥9 cm/s appears the position of the ventricular septum may be observed with to be an optimal cutpoint for identifying CP, with a sensi- extended two-dimensional and M-mode (see tivity of 83% and a specificity of 81%.18 Some caution must figure 1). With a sensitivity of 93%, respiration-related ventric- be exercised, however, as the e’ velocity could be lowered ular septal shift may be the most important echocardiographic by mitral annular calcification or concomitant myocardial finding in CP.18 disease.18 24 Abnormal beat-to-beat ventricular septal motion may also be ►► Annulus reversus: Normally, the lateral e’ velocity is higher observed and likely relates to enhanced ventricular interaction than the medial. Uniquely, CP may cause reversal of this on a millisecond timescale.19 pattern, with the medial e’ being higher than the lateral.

Figure 3 Respiration-related variation in mitral early (E) velocity in constrictive pericarditis (Doppler interrogation from apical four-chamber view). With inspiration, left-sided cardiac filling decreases and is manifested by a reduction in mitral E velocity (arrow). With expiration, the mitral E velocity increases. See text for additional details.

Welch TD. Heart 2018;104:725–731. doi:10.1136/heartjnl-2017-311683 727 Review

Figure 4 Respiration-related hepatic vein diastolic flow reversal in constrictive pericarditis (Doppler and colour M-mode interrogation from subcostal view). With expiration, right-sided cardiac filling decreases and there are prominent reversals of diastolic flow in the hepatic veins (arrows). These reversals are less prominent or absent during inspiration. See text for additional details.

This has been called ‘annulus reversus’ and likely relates to Computed tomography restricted movement of the lateral myocardium due to peri- Computed tomography (CT) scanning of the heart allows cardial tethering.25 assessment for pericardial thickening and calcification, although neither is necessary for the diagnosis. In a study Mayo Clinic echocardiographic criteria of 97 patients with surgically confirmed CP, 35% had peri- The findings described above were evaluated at the Mayo Clinic cardial calcification and 72% had pericardial thickening on in a blinded comparison of patients with confirmed CP versus CT. 12 CT may also reveal deformation of the ventricular patients with restriction or severe tricuspid regurgitation.18 contour by the diseased pericardium and define the rela- Multivariable analysis yielded the three most important findings: tionship of the pericardium to the in those (1) respiration-related ventricular septal shift; (2) preserved or patients for whom surgery is being considered.31 increased medial mitral e’ velocity; and (3) prominent hepatic vein expiratory diastolic flow reversals. Finding a respiration-re- Cardiac magnetic resonance imaging lated ventricular septal shift in combination with either medial Like CT, gated cardiac magnetic resonance (CMR) imaging e’ ≥9 cm/s or prominent hepatic vein expiratory diastolic offers information about cardiac anatomy, including pericar- reversal yielded an optimal combination of sensitivity (87%) and dial thickening and calcification and presence of a pericar- specificity (91%) for the diagnosis of CP. dial effusion. CMR offers additional information, though, about pericardial-myocardial adherence, enhanced ventric- Myocardial strain imaging ular interaction and respiratory variation in flows across The use of speckle-tracking strain imaging has also been estab- the atrioventricular valves, and the tissue character of the lished as a useful tool in the diagnosis of constriction. CP, as pericardium.31 32 Delayed gadolinium enhancement (DGE) opposed to restriction, is generally associated with preserved (figure 6) of the pericardium is associated with increased global longitudinal strain and a distinct regional pattern of fibroblast proliferation and neovascularisation, as well as reduced lateral strain (with preserved medial), likely due to more prominent chronic and granulation the tethering effects of the constrictive pericardium on the free tissue.33 When DGE of the pericardium is present, the wall of the LV.26 27 Care must be exercised, however, to exclude constrictive process is more likely to be inflammatory and other disease states (such as ischaemic heart disease) that could modifiable with medical therapy.34 affect the myocardium and produce similar variation in regional strain. Invasive haemodynamics Haemodynamic catheterisation may be necessary when the Other echocardiographic findings non-invasive evaluation for CP is indeterminate. An intravenous Also expected, although not unique to CP, would be: fluid ‘challenge’ may increase the sensitivity of the evaluation, 1. A ratio of mitral early (E) to late (A) transmitral filling particularly if the mean is lower than velocities that is pseudonormal or restrictive (E/A>0.8), expected (below approximately 15 mm Hg).35 given elevated left atrial pressure.20 Expected ‘classic’ findings include: 2. Inferior vena cava plethora, indicating increased venous ►► Elevated central venous pressure and intracardiac pressures, pressure. with near equalisation of right and left heart diastolic filling 3. A ‘flat’ Doppler velocity profile (little pressures. change with inspiration), which can help differentiate ►► A steep, deep y-descent in the tracing true constrictive physiology from the changes that can be and ‘dip and plateau’ or ‘square root’ sign in the RV pressure produced by dramatic intrathoracic pressure swings in severe tracing, both signifying rapid early diastolic filling of the RV obstructive lung disease.28 with abrupt cessation due to pericardial constraint. Figure 5 shows a suggested diagnostic algorithm for the ►► RV systolic pressure that is <50 mm Hg. echocardiographic diagnosis of CP, based on the Mayo ►► RV end-diastolic pressure that is at least one-third of the RV Clinic criteria.29 30 Further assessment with cross-sectional systolic pressure. imaging and haemodynamic catheterisation will be vari- These features, however, may also be present in restrictive ably necessary thereafter to confirm the diagnosis or plan cardiomyopathy, making them insufficiently specific for the treatment. diagnosis of CP.36

728 Welch TD. Heart 2018;104:725–731. doi:10.1136/heartjnl-2017-311683 Review

Figure 5 Suggested diagnostic algorithm for the echocardiographic diagnosis of constrictive pericarditis (CP). The Mayo Clinic criteria for diagnosis of CP are incorporated into a practical algorithm that could be used as part of a comprehensive diagnostic work-up. A, late mitral inflow velocity; E, early mitral inflow velocity; e’, early diastolic mitral annular relaxation velocity; HV, hepatic vein; IVC, inferior vena cava; SVC, superior vena cava (adapted from Syed et al29 and reproduced with permission from Welch30).*Consider further imaging or invasive haemodynamics if constrictive pericarditis is still suspected.

The ‘modern’ catheterisation criteria for CP rely on the prin- concordant variation that is expected in other forms of heart ciples of dissociation of intrathoracic and intracardiac pressures failure. A larger RV pressure contour and a smaller LV pres- and enhanced ventricular interaction. sure contour during inspiration have been shown to have a ►► Simultaneous recordings of pulmonary capillary wedge sensitivity of 97% and a predictive accuracy of 100% for and LV pressures allow direct evaluation for dissociation of C P. 38 The use of these criteria may be difficult in patients intrathoracic and intracardiac pressures. When evaluating with irregular cardiac rhythms; temporary pacing may be the gradient between the pulmonary capillary wedge pres- required. sure and LV diastolic pressure, a difference of ≥5 mm Hg between expiration and inspiration was reported to be 93% sensitive and 81% specific for the diagnosis of CP.37 Biopsy and surgical exploration ►► Simultaneous recordings of the RV and LV pressure wave- There may be instances in which the diagnosis remains uncer- forms reveal discordant variation of the waveforms during tain even after exhaustive evaluation with echocardiography, the respiratory cycle (figure 7). This is in contrast to the cross-sectional imaging and haemodynamic catheterisation. Surgical exploration is sometimes offered in these cases. Endo- myocardial biopsy may be a reasonable option prior to proceeding with surgical exploration, though.39

Treatment Transient CP Some cases of CP may resolve spontaneously or with anti-in- flammatory treatment. Of 212 cases of CP at the Mayo Clinic, 36 (17%) were reported to have resolved without surgery after an average of 8.3 weeks.40 Most (67%) of these transient cases were effusive-constrictive. Transient CP occurred most commonly after cardiac surgery, and otherwise was deemed idiopathic or due to infection, trauma or malignancy. Treatment Figure 6 Cardiac MRI in inflammatory effusive-constrictive consisted of non-steroidal anti-inflammatory drugs or pericarditis. The left panel shows a four-chamber view of the heart with therapy in most cases. Subsequent studies showed that patients thickened parietal and visceral pericardial layers (black) and pericardial who responded to anti-inflammatory drug treatment were more fluid in between (white). The right panel shows delayed imaging after likely to have elevated serum inflammatory markers and more the administration of gadolinium. The pericardial layers appear white DGE of the pericardium on CMR.34 41 Recent evidence suggests due to delayed enhancement, which is indicative of inflammation. that positron emission tomography could provide another means The is black. LV, left ventricle; PP, parietal pericardium; of assessing pericardial inflammation and predicting response to RV, right ventricle; VP, visceral pericardium; PF, pericardial fluid. anti-inflammatory therapy.42

Welch TD. Heart 2018;104:725–731. doi:10.1136/heartjnl-2017-311683 729 Review

When the patient presents subacutely and pericardial inflam- mation is evident, it is reasonable to attempt a 2 to 3-month trial of anti-inflammatory therapy.43 A typical regimen would include along with a non-steroidal anti-inflammatory drug or an oral steroid, but this is an area that warrants further study.34

Chronic CP In the majority of cases, CP is chronic and progressive. therapy is strictly palliative. The only definitive treatment is surgical pericardiectomy.43 This procedure should entail removal of as much pericardium as possible, including the diaphragmatic and posterolateral pericardium.29 Incomplete resection is associ- ated with increased risk for recurrent CP and reduced survival rates.44 Several large-volume centres have published perioperative mortality rates of 6%–7.1% for surgical pericardiectomy.4–7 Longer term survival after pericardiectomy is not as good as that of an age and sex-matched cohort, but varies widely depending on the aetiology and patient characteristics.7 For example, patients with idiopathic CP have the best outcomes, with survival rates of ≥80% at 5–7 years.4–6 Those who survive to long-term follow-up appear to have sustained symptomatic benefit, with >80% reporting mild or no symptoms in one study.7 Conversely, patients with CP due to chest irradiation have very poor reported outcomes, likely due to the damaging effects of ionising radiation on other parts of the heart and . Figure 7 High-fidelity pressure tracings in a patient with (A) Reported survival rates for these patients at 5–10 years have constrictive pericarditis and (B) restrictive cardiomyopathy. (A) In ranged from 0% to 30%.4–7 constriction, the area under the right ventricular (RV) systolic pressure Prognosis after pericardiectomy also appears to worsen with curve (orange shaded area) increases during inspiration and the area more advanced New York Heart Association functional class, under the left ventricular (LV) systolic pressure curve (yellow shaded older age, impaired renal function, pulmonary , area) decreases. This discordance is due to enhanced ventricular decreased LV ejection fraction and increased Child-Pugh liver interaction. (B) In restriction, the areas under the RV and LV systolic disease score.5 7 45 pressure curves decrease concordantly during inspiration (reproduced Figure 8 provides a suggested clinical algorithm for the diag- 38 with permission from Talreja et al ). nosis and treatment of symptomatic constrictive pericarditis.

Figure 8 Simplified diagnostic algorithm for the diagnosis and treatment of symptomatic constrictive pericarditis.*Based on time course and clinical assessment that may include CMR imaging and inflammatory markers.

730 Welch TD. Heart 2018;104:725–731. doi:10.1136/heartjnl-2017-311683 Review

Conclusion 20 Oh JK, Hatle LK, Seward JB, et al. Diagnostic role of in CP is a form of ‘diastolic heart failure’ with a distinct patho- constrictive pericarditis. J Am Coll Cardiol 1994;23:154–62. 21 Rajagopalan N, Garcia MJ, Rodriguez L, et al. Comparison of new Doppler physiology and treatment. Because it often mimics other forms echocardiographic methods to differentiate constrictive pericardial heart disease and of heart failure and requires a specialised work-up, the diagnosis restrictive cardiomyopathy. Am J Cardiol 2001;87:86–94. may be difficult to make. A meticulous echocardiogram allows 22 Garcia MJ, Rodriguez L, Ares M, et al. Differentiation of constrictive pericarditis initial detection of dissociation of intrathoracic and intracardiac from restrictive cardiomyopathy: assessment of left ventricular diastolic velocities in pressures and enhanced ventricular interaction and may be suffi- longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol 1996;27:108–14. 23 Ha JW, Ommen SR, Tajik AJ, et al. Differentiation of constrictive pericarditis cient to make the diagnosis of CP. Cross-sectional imaging as from restrictive cardiomyopathy using mitral annular velocity by tissue Doppler well as haemodynamic catheterisation may be necessary in some echocardiography. Am J Cardiol 2004;94:316–9. cases to confirm the diagnosis. CMR provides the opportu- 24 Sengupta PP, Mohan JC, Mehta V, et al. Accuracy and pitfalls of early diastolic motion nity for characterisation of the pericardial tissue, with DGE of of the mitral annulus for diagnosing constrictive pericarditis by tissue Doppler the pericardium signifying inflammation and the potential for imaging. Am J Cardiol 2004;93:886–90. 25 Reuss CS, Wilansky SM, Lester SJ, et al. Using mitral ’annulus reversus’ to diagnose response to medical therapy. Complete surgical pericardiectomy constrictive pericarditis. Eur J Echocardiogr 2009;10:372–5. remains the only definitive treatment for patients with chronic 26 Sengupta PP, Krishnamoorthy VK, Abhayaratna WP, et al. Disparate patterns of C P. left ventricular mechanics differentiate constrictive pericarditis from restrictive cardiomyopathy. JACC Cardiovasc Imaging 2008;1:29–38. Contributors TW is the sole author of this manuscript. 27 Kusunose K, Dahiya A, Popović ZB, et al. Biventricular mechanics in constrictive pericarditis comparison with restrictive cardiomyopathy and impact of Competing interests None declared. pericardiectomy. Circ Cardiovasc Imaging 2013;6:399–406. Provenance and peer review Commissioned; externally peer reviewed. 28 Boonyaratavej S, Oh JK, Tajik AJ, et al. Comparison of mitral inflow and superior vena cava Doppler velocities in chronic obstructive pulmonary disease and constrictive © Article author(s) (or their employer(s) unless otherwise stated in the text of the pericarditis. J Am Coll Cardiol 1998;32:2043–8. article) 2018. All rights reserved. No commercial use is permitted unless otherwise 29 Syed FF, Schaff HV, Oh JK. Constrictive pericarditis--a curable diastolic heart failure. expressly granted. Nat Rev Cardiol 2014;11:530–44. 30 Welch TD. Practice of clinical echocardiography chapter 28: pericardial disease. 5th References ed. Philadelphia Pensylvania: Elsevier, 2016. 1 Lin Y, Zhou M, Xiao J, et al. Treating constrictive pericarditis in a chinese single-center 31 Klein AL, Abbara S, Agler DA, et al. American society of echocardiography clinical study: a five-year experience. Ann Thorac Surg 2012;94:1235–40. recommendations for multimodality cardiovascular imaging of patients with 2 Ghavidel AA, Gholampour M, Kyavar M, et al. Constrictive pericarditis treated by pericardial disease: endorsed by the society for cardiovascular magnetic resonance surgery. Tex Heart Inst J 2012;39:199–205. and society of cardiovascular computed tomography. 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Welch TD. Heart 2018;104:725–731. doi:10.1136/heartjnl-2017-311683 731