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STATE OF THE ART REVIEW

Role of Echocardiography in the Diagnosis ofConstrictive Pericarditis

Jacob P. Dal-Bianco, MD,* Partho P. Sengupta, MBBS, MD, DM,**Farouk Mookadam, MD, Krishnaswamy Chandrasekaran, MD, A. Jamil Tajik, MD, and

Bijoy K. Khandheria, MBBS, FACC, FESC,Rochester, Minnesota; Scottsdale, Arizona

The clinical recognition of constrictive pericarditis (CP) is important but challenging. In addition to Dopplerechocardiography, newer echocardiographic techniques for deciphering myocardial deformation have facilitatedthe noninvasive recognition of CP and its differentiation from restrictive cardiomyopathy. In a patient with heartfailure and a normal ejection fraction, echocardiographic demonstration of exaggerated interventricular interde-pendence, relatively preserved left ventricular longitudinal deformation, and attenuated circumferential deforma-tion is diagnostic of CP. This review is a concise update on the pathophysiology and hemodynamic features ofCP, the transmural and torsional mechanics of CP, and the merits and pitfalls of the various echocardiographictechniques used in the diagnosis of CP. (J Am Soc Echocardiogr 2009;22:24-33.)

Keywords: Constrictive pericarditis, Echocardiography, Doppler tissue imaging, Restrictivecardiomyopathy, Left ventricular deformation

Constrictive pericarditis (CP) is characterized by impaired diastoliccardiac filling and elevated ventricular filling pressures (Figure 1) dueto a rigid pericardium with fusion of the visceral and parietal layers.1,2

Patients present predominantly in heart failure with elevated jugularvenous pressure, dyspnea, peripheral edema, hepatomegaly, andascites.3 Pericarditis, cardiac surgery, and mediastinal irradiation arethe leading identifiable causes of CP in the developed world. How-ever, pericardial fibrosis and calcification are often idiopathic inorigin.3 Pericardiectomy relieves pericardial restraint and, in theabsence of concomitant myocardial dysfunction, effectively restoresdiastolic filling.4-6 CP due to cardiac surgery, especially coronaryartery bypass grafting7 and mediastinal irradiation,3,8,9 can involvethe pericardium and also the myocardium.3,10,11 Determining therelative contribution of pericardial restraint versus myocardial dys-function in such patients remains a diagnostic challenge.

PATHOPHYSIOLOGY OF CONSTRICTIVE PERICARDITIS

In CP, the visceral pericardium and the parietal pericardium arefibrosed and fused together,2 although not necessarily always thick-ened (Figure 2A).12 Calcification can result in the formation ofpericardial calcium plaques (eggshell appearance), which may pene-trate into the myocardium.2 The incidence and prevalence of peri-

cardial calcification is dependent on the underlying cause of CP andis less commonly encountered in developing nations as the incidenceof tuberculous pericarditis has declined. A recent series of 136patients reported radiographic evidence of pericardial calcification inapproximately one third of patients.13 The myocardium is usuallynormal in CP, but concomitant myocardial involvement may be seen,for example, following mediastinal irradiation.14 Epicardial involve-ment may also result from subpericardial myocarditis.2

Characteristic hemodynamic changes in CP are attributed toisolation of the cardiac chambers from intrathoracic respiratory pres-sure changes and a fixed end-diastolic ventricular volume (Figure 2B).Although normally, the pressure gradient between the pulmonaryveins and the left atrium and left ventricle is relatively constant duringrespiration, this pressure gradient decreases with inspiration in CP,leading to reduced diastolic pulmonary vein flow and left atrial andleft ventricular (LV) filling (Figure 1). The rigid, noncompliant fibrouspericardial sac couples both ventricles. Consequently, an increase infilling on one side of the heart impedes contralateral filling throughthe motion of the interventricular septum (IVS), thereby making bothventricles markedly interdependent.15-17 The inspiratory reduction inLV filling is therefore associated with a simultaneous increase in rightventricular (RV) diastolic filling and an IVS shift toward the leftchamber.18 The opposite physiologic effects on filling gradients andIVS shift are seen in expiration, with increased pulmonary venouspressure and an attendant increase in LV diastolic inflow. This isassociated with simultaneous decrease in right-sided filling. Becauseof elevated atrial pressures, ventricular filling is very rapid andpredominantly in early diastole, abruptly declining by middiastole.19

This hemodynamic pattern is reflected in the jugular venous and rightatrial pressure waveforms as elevated mean filling pressure with aprominent “a” wave, a sharp “y” descent reflecting early diastolicresistance-free rapid RV filling, and as well as a preserved “x” descentdue to accelerated atrial relaxation. The RV hemodynamic waveformwith a dip-and-plateau, or square root, pattern reflects rapid ventric-ular relaxation, with a subsequent sharp increase in filling pressure asthe expanding ventricle meets the pericardium (Figure 1A). Atend-diastole, the end-diastolic right atrial, RV, wedged pulmonary

From the Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN(J.P.D.); and the Division of Cardiovascular Diseases, Mayo Clinic, Scottsdale, AZ(P.P.S., F.M., K.C., A.J.T., B.K.K.).

This work was supported in part by a grant-in-aid to Dr Sengupta from theAmerican Society of Echocardiography (Morrisville, NC).

Reprint requests: Partho P. Sengupta, MD, DM, Mayo Clinic Arizona, Division ofCardiovascular Diseases, 13400 East Shea Boulevard, Scottsdale, AZ 85259(E-mail: [email protected]).* Drs Dal-Bianco and Sengupta contributed equally to this work.

0894-7317/$36.00

Copyright 2009 by the American Society of Echocardiography.

doi:10.1016/j.echo.2008.11.004

24

arterial, and LV pressures are equally elevated. These physiologicabnormalities that occur as a result of the ventricular interdepen-dence and respiratory influenced changes are the fundamental pro-cesses that account for the clinical, hemodynamic, and echocardio-graphic findings of CP.

It is important to distinguish the hemodynamic features of CP fromthose of cardiac tamponade, a condition characterized by excess fluidin the pericardial sac that hinders diastolic filling. In cardiac tampon-ade, the intracardiac volumes are decreased on both sides of theheart, with elevation and equalization of diastolic filling pressuresthroughout the cardiac chambers, reflecting increased ventricular

interactions between the right and left heart. Importantly, however,although early ventricular filling is resistance free in CP, the effusionin cardiac tamponade imposes pandiastolic resistance to ventricularfilling.

ECHOCARDIOGRAPHIC DIAGNOSIS OF CONSTRICTIVEPERICARDITIS

The echocardiographic diagnosis of CP was originally based onM-mode echocardiographic findings and subsequently on 2-dimen-sional echocardiography and Doppler hemodynamics in response tothe respiratory cycle. More recently, newer echocardiographic tech-niques, such as pulsed tissue Doppler, color Doppler tissue imaging(DTI), and speckle-tracking imaging, have been used to assess theunique changes in global and regional myocardial function seen inCP. However, while interpreting the role of various echocardio-graphic techniques and comparing individual studies, several factsmust be kept in consideration: (1) CP is a heterogeneous disease, andstudy populations vary significantly regarding the distribution ofunderlying CP etiologies; (2) the confirmation of a firm diagnosis ofCP is based on different “gold standards” (eg, surgical confirmation vspericardial thickness on computed tomography); and (3) pericardialconstriction may be localized, affecting the right ventricle more thanthe left ventricle or vice versa. Data on generalized versus localizedpericardial constriction are sparse.

Doppler HemodynamicsMitral inflow as assessed by Doppler echocardiography demonstratesan increased early diastolic filling velocity followed by rapid deceler-ation, leading to a short filling period. Early mitral inflow decelerationtime is usually, but not always, �160 ms.18,20

As first reported by Hatle et al18 and Oh et al21 in a larger cohort,dynamic changes with respiration occur in patients with CP (Figure 2D),but not in patients with restrictive cardiomyopathy (RCM; Figure 3B).Factors responsible for these respiratory driven changes are the dissoci-ation of intrathoracic pressure from intracardiac pressure and enhancedventricular interdependence. In CP, early diastolic mitral inflow is re-duced with the onset of inspiration, and isovolumic relaxation time isprolonged.With expiration, mitral inflow returns to normal, and isovolu-mic relaxation time shortens. Typically, patients with CP demonstrate anincrease in early diastolic mitral inflow velocity of �25% during expira-tion comparedwith inspiration.18,21 These changes can be seenwith thefirst beat of inspiration, when a decrease in transmitral flow velocity isnoted; the reverse occurs with expiration. Sensitivities and specificities ofDoppler assessment of respiratory changes have been reported to be ashigh as 85% to 90%.22 Importantly, the percentage of respiratorychange in patients with “mixed” constrictive and restrictive disease (eg,mediastinal radiation) is markedly lower.10 After complete pericardiec-tomy mitral inflow patterns return to normal, and little respiratoryvariation is seen on Doppler echocardiography.18 Accordingly, Dopplerassessment of respiratory variation has been reported to be useful forevaluating the outcome of pericardiectomy.21 Patients who hadminimalrespiratory variation after pericardiectomy were asymptomatic com-pared with those who continued to show respiratory variation.23

Patients with RCM (Figure 3) and up to 20% of patients with CPmay lack the typical respiratory changes in the presence of mixedconstrictive-restrictive disease and/or markedly increased left atrialpressure.21,24 Typical respiratory changes in the latter situation maynot be observed, because of mitral valve opening during the steepportion of the LV pressure curve, when respiration has little effect on

Figure 1 Cardiac catheterization findings in patients with CP.Respiratory changes in LV and RV systolic pressures (A) show areciprocal relationship throughout the respiratory cycle, suggest-ing increased interventricular interdependence. Similarly, the earlydiastolic transmitral pressure gradient as estimated from thedifference of pulmonary capillary wedge pressure and LV mini-mum pressure (B) shows a significant respiratory change, sug-gesting dissociation of intrathoracic and intracardiac pressures.Reproduced with permission from Circulation.17

Journal of the American Society of Echocardiography Dal-Bianco et al 25Volume 22 Number 1

the transmitral pressure gradient. In these patients, maneuvers thatdecrease preload (head-up tilt or sitting) can unmask the characteristicrespiratory variation in early mitral inflow velocity.24 Atrial fibrillationcomplicates the interpretation of respiratory variation of Dopplervelocities, but respiratory variation can still be appreciated regardlessof cardiac cycle length. Usually, this requires longer recording periodsof Doppler tracings.

Phasic, respiratory changes in mitral inflow are not unique to CP,however. Patients with chronic obstructive pulmonary disease orsevere RV dysfunction and large respiratory variations in intrathoracicpressure may also show inspiratory decreases in early mitral inflowvelocities. Typically, these changes are more gradual and occur laterin the respiratory cycle rather than during the first inspiratory beat. Insuch patients, a marked increase in inspiratory superior vena cavasystolic forward flow can be helpful to rule out CP.25 In chronicobstructive pulmonary disease, there is a greater decrease in intratho-racic pressure in inspiration, which generates greater negative pres-sure changes in the thoracic cavity. This augments blood flow to theright atrium from the superior vena cava during inspiration.

Inferior vena cava dilation (Figure 2C) and pulsed wave Doppler ofhepatic venous flow mirrors right atrial pressure. Pulsed Dopplerrecordings of hepatic vein flow in CP show marked diastolic flowreversal (Figure 2E), which increases in expiration compared with

inspiration.26 In patients with advanced constriction or with mixedconstrictive-restrictive physiology, it is not unusual to see significantdiastolic flow reversals during both inspiration and expiration. Incontrast, diastolic hepatic vein flow reversal is more prominent withinspiration in RCM.

Doppler evaluation of the pulmonary veins showsmarked respiratorychange in pulmonary venous flow inCP. The pulmonary venous systolicwave and early diastolic wave velocities, especially the early diastolicwave velocity, are increased during expiration and decreased duringinspiration.18 The changes in pulmonary venous flow velocities havebeen reported to be more pronounced than changes in mitral inflowvelocities.27 Similar respiratory variation can also be observed in patientswith CP and atrial fibrillation.28 In contrast, patients with RCM showblunting of the systolic wave velocity and a decrease in the ratio ofsystolic to early diastolic wave velocity throughout the respiratory cycle,with a large atrial reversal wave and without any significant respiratoryvariation. (Table 1 summarizes sensitivities and specificities for hemody-namic CP Doppler findings.)

Color DopplerPatients with CP typically demonstrate only mild mitral and tricuspidregurgitation. A pronounced increase in tricuspid regurgitant jetvelocity from onset to peak inspiration can, however, help diagnose

Figure 2 Findings in patients with CP. (A) Computed tomography in a patient with CP shows the extent of pericardial thickening(red arrows). Apical 4-chamber view of the left ventricle (LV) (B) and dilated inferior vena cava (C) with increased respiratoryvariations in transmitral early diastolic flow (D) and hepatic venous Doppler flow (E) are shown for the same patient with CP (redarrows in D and E indicate respiratory-dependent change in Doppler flow). Exp, Expiration; Insp, inspiration.

Figure 3 Echocardiographic features in a patient with RCM due to cardiac amyloidosis. Apical 4-chamber view shows thick walledleft ventricle (LV) (A) with a restrictive transmitral early diastolic flow pattern (B). Note the lack of increase in early diastolic transmitralvelocity with the onset of expiration (Exp). Insp, Inspiration.

26 Dal-Bianco et al Journal of the American Society of EchocardiographyJanuary 2009

CP.29 Severe mitral and tricuspid regurgitation speak against isolated orpredominant constrictive physiology and are markers for underlyingmyocardial disease. Color M-mode Doppler shows early-onset, elevatedmitral inflow velocities in patients with CP. Rajagopalan et al30 reportedsensitivity and specificity of 74% and 91%, respectively, to differentiateCP from RCM (mitral inflow slope �100 cm/s).

LV Mechanics

Radial motion of the IVS. Abrupt anterior or posterior motion ofthe IVS in early diastole is common in patients with CP (Figure 4). Thedirection of early diastolic IVS motion may depend on a number offactors, including uneven distribution of fibrosis or calcification in thepericardial sac, the timing of mitral and tricuspid opening, the relativecompliance of the right and left ventricles, and phase of respiration.31

In classic CP, the IVS shows a brisk, early diastolic motion toward theleft ventricle during inspiration, followed by a rebound in the oppo-site direction during expiration.32 This septal bounce reflects exag-gerated interventricular dependence combined with forceful earlydiastolic filling. Himelman et al33 reported in a large number ofpatients that an IVS bounce is the most consistent 2-dimensionalechocardiographic sign for CP, with sensitivity of 62% and specificityof 93%. Recently, Sengupta et al34 assessed IVS motion by color DTI

(Figure 4). In this study, the majority of patients with CP hadhigh-velocity early diastolic biphasic IVS motion (�7 cm/s), a findingwith 82.5% sensitivity and 92.7% specificity for CP (Table 1).

Radial motion of the LV posterior wall. In patients with CP, theLV posterior wall rapidly expands posteriorly during early diastole,followed by an abrupt cessation of such movement during middias-tole and late diastole (Figure 4), which corresponds to the abrupttermination of rapid ventricular filling.35,36 This lack of motion,termed “flattening,” of the LV posterior wall during middiastole andlate diastole can be best observed with M-mode echocardiogra-phy.37,38 Palka et al39 assessed relative subendocardial versus subepi-cardial LV posterior wall velocities using myocardial velocity gradientimaging. Patients with CP (n � 10) had markedly faster movingsubendocardium during rapid ventricular filling than normal subjectsand patients with RCM (Table 1).

Longitudinal LV mechanics. The quantitative assessment of lon-gitudinal mitral annular motion by pulsed tissue Doppler and colorDTI estimates LV relaxation.40-42 In patients with CP, mechanoelas-tic properties of the myocardium are relatively preserved in thelongitudinal direction, and therefore longitudinal deformation of theLV base (Figure 5) and longitudinal early diastolic velocities (Figure 6)

Table 1 Sensitivities and specificities of echocardiographic markers for CP

Marker Study n Secondary CP Sensitivity Specificity

Doppler echocardiography�25% respiratory variation of peak early diastolic MV inflow

velocity; augmented hepatic vein diastolic flowreversals after the onset of expiration; � 25% offorward diastolic velocity

Oh et al21 28 13 88% 67%

�10% respiratory variation of peak early diastolic MV inflowvelocity

Rajagopalan et al30 19 6 84% 91%

Color M-mode MV inflow propagation; first aliasing contour� 100 cm/s

Rajagopalan et al30 19 6 74% 91%

Respiratory variation in PV systolic/diastolic flow ratio �

65% in inspiration � % change of early mitral peakdiastolic flow � 40%

Klein et al27 14 10 86% 94%

Respiratory variation in PV peak diastolic flow velocity �

18%Rajagopalan et al30 19 6 79% 91%

Dilated hepatic veins, “W” wave pattern (reverse flow in latesystole and diastasis)

von Bibra et al26 13 8 68% 100%

LV septal/posterior wall radial motionIVS bounce

M-mode Engel et al31 40 NA 40% 80%M-mode Candell-Riera et al32 8 NA 88% NA2-dimensional Himelman et al33 39 NA 62% 93%

Biphasic early diastolic IVS motion by color DTI (�7 cm/s)motion

Sengupta et al34 40 30 82% 93%

Biphasic early diastolic IVS motion by pulsed tissue Doppler Oki et al46 12 9 100% 100%LV posterior wall flattening

M-mode Voelkel et al38 12 2 92% 100%M-mode Schnittger et al37 14 6 64% 90%M-mode Engel et al31 40 NA 85% 82%

Miscellaneous echocardiographic findingsPericardial thickening

M-mode Engel et al31 40 NA 53% 100%M-mode Hatle et al18 7 4 100% 50%2-dimensional Oh et al21 28 19 36% NA

Left atrial enlargement, M-mode Engel et al31 40 NA 75% 100%Premature PV opening, M-mode Engel et al31 40 NA 14% 100%

MV, Mitral valve; NA, data not available; PV, pulmonary valve.


are either normal or exaggerated. Conversely, patients with RCM andintrinsic myocardial abnormalities have reduced longitudinal defor-mation of the LV base and reduced early diastolic longitudinalvelocities. Pulsed tissue Doppler and color DTI have been shown tobe helpful to diagnose CP.30,43-48 A lateral or septal early diastolicmitral annular velocity of �8 cm/s on pulsed tissue Doppler is in

general the accepted cutoff value to distinguish patients with CP fromthose with RCM.Mitral annular velocities are particularly useful in CPwhen pronounced respiratory variations in peak early mitral inflowvelocities are not seen.49 The additional use of pulsed tissue Dopplerto hemodynamic Doppler and 2-dimensional and M-mode echocar-diography increases predominantly the sensitivity of echocardiogra-

Figure 4 Color-DTI for quantifying abnormal septal and posterior wall motion in CP. Characteristic findings on M-modeechocardiography (A) are septal notching (arrow 1) and the abrupt flattening of the posterior wall (arrow 2). Color M-modeechocardiography (B) shows high-velocity motion (arrow 3) in early diastole. Myocardial velocity tracings from the septum andposterior wall (C) identify components of abnormal septal motion in constriction. The posterior wall shows rapid early diastolic radialexpansion (blue tracing), which corresponds to the abrupt outward motion seen on M-mode. The septum shows high-velocity earlydiastolic fluttering (yellow tracing), which corresponds to the septal notching seen on M-mode. Am, Radial late diastolic velocity; Em,radial early diastolic velocity; Exp, expiration; LV, left ventricle; RV, right ventricle; Sm, radial systolic velocity.

Figure 5 Longitudinal deformation of the left ventricle in CP and RCM. Longitudinal shortening strains were obtained by2-dimensional speckle-tracking imaging. Speckle-tracking imaging is different from DTI in that strain data are angle independent.Myocardial deformation is computed from continuous frame-by-frame tracking of a small image block of “natural acousticmarkers.” Tracking is based on searching the new location of the marker in the subsequent frame using a block-matching algorithm.The basal septal and basal lateral wall segments show normal longitudinal shortening strains in CP (A, B) and reduced longitudinalshortening strains in RCM (C, D). Apical longitudinal shortening strains are reduced in CP (B), whereas longitudinal strain at the LVapical septum is preserved in RCM (D).


phy to diagnose CP.47 Table 2 summarizes studies that have exploredthe diagnostic role of early diastolic mitral annular velocity in CP.Attention needs to be paid to the differing patient age groups (mitralannular velocities decrease with age50) and different percentages ofunderlying CP etiologies, with varying patient numbers with pre-sumed “mixed” constrictive and restrictive physiology. These factors

may explain the spread of early mitral annular velocities and reportedsensitivities and specificities.

When recording and interpreting early mitral annular velocities,caution is warranted in the setting of extensive mitral annularcalcification, LV systolic dysfunction, or segmental nonuniformmyocardial velocities.47 Averaging additional mitral annular sites is

Figure 6 Longitudinal velocity of the left ventricle in CP and RCM. Longitudinal velocities were obtained by 2-dimensionalspeckle-tracking imaging. The basal septal and basal lateral wall segments show normal mean longitudinal early diastolic velocityin CP (�5 cm/s) (A, B) and reduced longitudinal early diastolic velocity in RCM (C, D). Em, Longitudinal early diastolic lengtheningvelocity.

Table 2 Studies assessing longitudinal early diastolic tissue velocities in CP

Study nMean � SD

age (y)Secondary

CPMitral annularsample site Comparison group

Cutoff value(cm/s) Sensitivity Specificity

Garcia et al44 8 62 � 13 6 Lateral* CA (n � 4), nonspecific fibrosis(n � 1), DM/small-vesseldisease (n � 1), cardiactransplantation (n � 1)

NA NA NA

Rajagopalanet al30

19 56 � 13 6 Lateral* CA (n � 8), advanced HTN(n � 1), DM/small-vesseldisease (n � 1), idiopathic(n � 1)

�8 89% 100%

Ha et al45 23 59 � 13 8 Septal* CA (n � 38), RCM (n � 14) �8 95% 96%Sohn et al48 17 46 � 14 10 NA Normal (n � 35) �(16 � 0.14 � age)

� 276% 82%

Senguptaet al47

45 24 � 12 30 Septal and lateral* RCM (n � 10), CA (n � 1) �8 89% 73%

Choi et al43 17 55 � 12 12 Septal* RCM (n � 12), normal (n � 15) �8 70% 100%Sengupta

et al5116 62 � 13 9 Septal* CA (n � 15) �6.6 93% 93%

Averaged from 4corners of MVannulus†

�5 100% 100%

Senguptaet al57

26 56 � 13 13 Septal and lateral CA (n � 15), RCM (n � 4) �5 92% 90%

CA, Cardiac amyloid; DM, diabetes mellitus; HTN, hypertension; MV, mitral valve; NA, data not available.*Pulsed tissue Doppler.†Mean velocity by color DTI obtained in 11 of the 16 patients.


of incremental value to differentiate CP from RCM.51 Althoughpatients with CP and RCM had overlapping values of earlydiastolic pulsed tissue Doppler velocities, clear separation ofgroups was evident with averaged color DTI early diastolic annularvelocities (averaged from 4 walls). However, when using colorDTI, one must note that resulting tissue velocities represent meanvelocities, which are significantly lower compared with peakvelocities derived on pulsed tissue Doppler.52 This is importantbecause most CP studies and early diastolic mitral annulus cutoffvalues are based on pulsed tissue Doppler velocities (Table 2).Furthermore, in RCM, mitral annular velocities may not be repre-sentative if the disease process is heterogeneous, as reportedpreviously in patients with endomyocardial fibrosis.53 Thus, hypo-kinetic areas accompanied by hyperkinesis in neighboring areascould result in relatively unaltered overall annular motion.47 Thislimits the ability of pulsed tissue Doppler to differentiate RCMbecause of endomyocardial fibrosis from CP.

Circumferential LV mechanics. Because of pericardial restraint44

and potential epicardial involvement,2,54-56 LV expansion in CP maybe limited in the circumferential rather than the longitudinal direc-tion. Accordingly, patients with CP were found to have reducedcircumferential strain in combination with preserved longitudinalearly diastolic velocities.57 This concept is further supported by thesignificant positive correlation of circumferential strain and radialdisplacement.

Torsional LV mechanics. By speckle-tracking imaging, Senguptaet al57 showed that patients with CP have significantly reduced netLV twist and torsion compared with normal subjects and patientswith RCM. While the base and mid cardiac rotation was relatively

preserved, apical rotation was markedly reduced, including thepeak systolic and diastolic rotation rates (Figure 7). Early diastolicrecoil, LV untwisting, and the magnitude of circumferential andlongitudinal expansion of the left ventricle are modulated bypericardial tissue properties.58,59 A recent study showed that thecongenital absence of the left pericardium results in reduced LVtorsion.60 The reduction of apical rotation in CP could be due toa lack of normal pericardium, enabling swift and friction-freeapical motion and potential scarring and inflammation extendinginto the epicardial layer of the myocardial wall.2,54-56 Pericardialtethering and/or diminished epicardial fiber function manifest asreduced basal, mid, and apical circumferential strain and alsoreduced longitudinal strain at the apex,57 which may be suscepti-ble to additional endocardial involvement due to the close spatialrelationship of epicardial and endocardial fibers.61 Table 3 sum-marizes LV mechanics in CP versus RCM.

Figure 7 Twist mechanics of the left ventricle in CP and RCM. Short-axis cross-sectional views are divided into 6 segments, and2-dimensional speckle-tracking imaging is used for computing LV rotation from 6 segments in each cross-sectional view. LV apicaland basal rotation is averaged from 6 segments in each view, and the difference of apical and basal rotation provides the net twistangle of the left ventricle. LV apical rotation and net twist angles are reduced in CP (A). Similarly, apical early diastolic untwistingvelocities obtained from 6 segments and the averaged value (dotted line) are also reduced in CP (B). Apical and basal LV rotationis normal in RCM with a normal net twist angle (C) and normal early diastolic apical untwisting velocities (D). Er, Early diastolic apicaluntwisting velocity.

Table 3 Myocardial mechanics in CP and RCM

Deformation parameter CP RCM

Longitudinal strain Normal* DecreasedLongitudinal early diastolic velocity Normal or increased DecreasedCircumferential strain Decreased DecreasedNet twist angle Decreased NormalApical untwisting velocity Decreased Normal†

*Except apical segments.†Although normal in magnitude, early diastolic apical untwisting veloc-ities may be delayed in timing.


ANCILLARY ECHOCARDIOGRAPHIC FINDINGS INCONSTRICTIVE PERICARDITIS

PericardiumThe detection of increased pericardial thickness may be of help inmaking a diagnosis of CP,35 but M-mode38 and 2-dimensional echocar-diography62 show poor sensitivity and correlation with pathologic spec-imen measurements. Transesophageal echocardiography, on the otherhand, because of superior resolution, showed high sensitivity (95%) andspecificity (86%) to detect a pericardium �3 mm thick.63 Nevertheless,about 1 in 5 patients with CP have normal pericardium,12 and theisolated finding of thickened pericardium does not imply constrictivephysiology.64

Recently, Lu et al65 evaluated the relative motion of pericardiumversus myocardium in patients with CP. By quantitative DTI, epicar-dial motion was found to be reduced, approaching that of thepericardium, whereas the endocardiumwas moving more vigorously.These findings are interesting because they seem to support theobservations on subepicardial involvement in CP.2

Cardiac ValvesA steep E-F slope on mitral valve M-mode tracing is suggestive ofrapid early diastolic filling and can therefore be seen in CP.66

Premature opening of the pulmonary valve due to increased middi-astolic RV pressure can be observed in patients with CP, if RVpressure exceeds pulmonary artery diastolic pressure.67

AortaAnother M-mode sign of the rapid early ventricular filling in CP isa sharp downward motion of the posterior aortic root in earlydiastole.68

Posterior LV Wall and Posterior Left Atrium AngleIn CP, the angle between the posterior LV wall and posterior leftatrium can be blunted, because the thickened, constricting pericar-dium affects the posterior left ventricle more than the posterior leftatrium, which then expands at a more acute angle respective to theLV wall.69

Interatrial SeptumDisplacement of the interatrial septum toward the left atrium duringinspiration is another reported sign of CP.70 (Table 1 summarizessensitivities and specificities for the miscellaneous echocardiographicfindings of CP.)

CONCLUSION

Multiple echocardiographic findings are used to confirm a diagnosisof CP, but demonstration of enhanced cardiac intracavitary bloodflow variations during respiration, abnormal interventricular septalmotion, and normal longitudinal mitral annular velocity provide thegreatest diagnostic yield. In the presence of a mixed physiology(pericardial constraint combined with myocardial dysfunction),the diagnosis and therefore referral for pericardiectomy remainchallenging. In such patients, the assessment of LV longitudinal, circum-ferential, and torsional mechanics by 2-dimensional speckle-trackingimaging can potentially decipher the extent of endocardial, midmyo-cardial, or epicardial involvement. Further prospective studies arewarranted to address the potential clinical utility of such diagnosticalgorithms.

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