Circulation: Cardiovascular Imaging

ADVANCES IN CARDIOVASCULAR IMAGING

Noninvasive Multimodality Imaging for

the Diagnosis of Constrictive Pericarditis
A Contemporary Review

ABSTRACT: There is a need to review the multimodality imaging Wissam Alajaji, MD

techniques, as well as the emerging role of the newer noninvasive imaging Bo Xu, MBBS (Hons)
modalities in the field of constrictive pericarditis (CP). Therefore, the aim of Apichaya Sripariwuth, MD
this review is to summarize the current available techniques that are useful Vivek Menon, MD
for the diagnosis and differentiation of CP from restrictive cardiomyopathy. Arnav Kumar, MD
Also, we provide illustrative images and videos of typical CP noninvasive Mary Schleicher, RN, BSN,
imaging findings, as well as a diagnostic and management algorithm. CP is MLIS
a challenging diagnosis; therefore, cardiologists need adequate knowledge Hussain Isma’eel, MD
Paul C. Cremer, MD
about the application of multimodality noninvasive imaging in a systematic
Michael A. Bolen, MD
and guideline-oriented fashion whenever CP is suspected.
Allan L. Klein, MD

R
Downloaded from http://ahajournals.org by on April 12, 2020

ecurrent pericardial inflammation may result in constrictive pericarditis (CP), char-

acterized by a noncompliant pericardium with impaired filling of both ventricles
and resultant diastolic heart failure.1–4 Often a diagnostic challenge, CP shares
hemodynamic features with other diseases, such as chronic obstructive pulmonary dis-
ease (COPD), severe tricuspid regurgitation, and restrictive cardiomyopathy (RCM).5,6
However, unlike other forms of heart failure, CP is potentially curable by pericardiec-
tomy1,7 or may even be reversed with anti-inflammatory therapy.8–10 Therefore, correct
diagnosis and prompt clinical management are crucial for improved patient outcomes.
Noninvasive imaging modalities, especially echocardiography, have characteristic find-
ings and play a critical diagnostic role when CP is suspected.1,2 Echocardiography is
consequently the initial test of choice, although cardiac magnetic resonance (CMR)
or computed tomography (CT) may be adjunctive if echocardiography is nondiagnos-
tic or if additional anatomic information is needed, such as the degree of pericardial
thickness, inflammation, or calcification.1 Recently, advances in echocardiography and
CMR have improved the noninvasive diagnosis of CP, demonstrated prognostic value
and informed subsequent management. Specifically, these advances have improved
the assessment of pericardial inflammation and fibrosis, as well as the hemodynamic
sequelae of constrictive pathophysiology. Yet, the emergence of the predominant role
of imaging in CP is often underappreciated. Therefore, this review has the following
objectives: (1) highlight the pathophysiology of CP; (2) emphasize updated echocar-
diography, CT, and CMR techniques to assess pericardial anatomy and hemodynamics;
(3) present typical imaging findings encountered in the noninvasive assessment of
CP; and (4) delineate the distinctive features in the evaluation of CP versus RCM. Key Words: algorithms ◼ cardiologists
◼ echocardiography ◼ multimodality
◼ pericarditis, constrictive

PATHOPHYSIOLOGY © 2018 American Heart Association, Inc.

The normal pericardium is thin, elastic, and split into an outer fibrous and an inner https://www.ahajournals.org/journal/
serous layers with <50 mL of pericardial fluid in between  the layers. Except for circimaging

Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878 November 2018 1

 Alajaji et al; Diagnosis of Constrictive Pericarditis
a small part of the left atrium (LA) and the pulmo-
nary veins, the pericardium encompasses the heart.
The diseased pericardium is noncompliant and encas-
es the cardiac chambers forcing the heart to operate
under a fixed volume. Consequently, ventricular filling
is impaired, despite normal myocardial relaxation.11,12
The characteristic hemodynamic features of CP are (1)
dissociation of intrathoracic and intracardiac diastolic
pressures and (2) exaggerated right to left ventricular
(LV) interaction known as interdependence.
During inspiration, the negative intrathoracic pres-
sure is transferred to the pulmonary veins but does not
affect the pressure in the constrained LA. This decreas-
es the pulmonary vein-LA pressure gradient leading to
underfilling of the LV. As a result, there is respiropha-
sic interventricular septal shift to the left, favoring the
right ventricular (RV) diastolic filling. This decrease in
the preload of the left heart is not mirrored on the right
side of the heart during inspiration because the infe-
rior vena cava (IVC), superior vena cava, and the right
atrium pressures are persistently high throughout the
cardiac and respiratory cycles and without significant
variations.13 In addition, the RV preload is augmented
by the negative intrathoracic pressure on systematic
venous return during inspiration, which supports RV
filling to the limits set by the constraining pericardium
and the space created by the degree of leftward shift
of the interventricular septum. The opposite occurs
during expiration when the positive intrathoracic pres-
Downloaded from http://ahajournals.org by on April 12, 2020
sure increases the pulmonary vein-LA pressure gradient
favoring LV filling. This increase in the preload of the
left heart causes a rightward respirophasic movement
of the interventricular septum. Consequently, there is
RV underfilling during expiration and displacement of
blood back to the hepatic veins, which causes the char-
acteristic late diastolic expiratory flow reversal.
Varying severities of CP physiology can occur. Early
on, impairment in diastolic filling leads to congestive
symptoms; however, when CP progresses to a state of
severely compromised diastolic filling, it leads to reduc-
tion in the cardiac index. In a subset of patients with
large pericardial effusions, constrictive physiology may
result, which is known as effusive CP. Effusive CP is char-
acterized by predominant visceral pericardial inflamma-
tion and persistence of constrictive pathophysiology
after drainage of a pericardial effusion.14
Basic Principles for the Noninvasive
Diagnosis of CP
CP is a hemodynamic diagnosis characterized by ven-
tricular interdependence and diastolic heart failure in
the absence of restrictive myocardial disease. Structural
alterations, such as pericardial thickening and calci-
fications, may lead to these hemodynamic changes,
although they are not always present in CP.15 In addition,
Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878
the finding of pericardial thickening is not equivalent to
CP.16 However, as pericardial thickening and calcifica-
tion become more extensive, constrictive pathophysi-
ology is more likely. Pericardial inflammation can also
impose constrictive pathophysiology and has important
management implications.8–10 The imaging evaluation
of the pericardium is consequently directed at hemo-
dynamic and structural abnormalities and the strengths
and weaknesses of echocardiography, CT, and CMR are
summarized in Table 1.
ECHOCARDIOGRAPHY
Pericardial Structural Evaluation
Pericardial Thickening and Calcifications
Echocardiography demonstrates pericardial thicken-
ing when there is parallel motion of both visceral
and parietal pericardium with increased thickness.1
The 4-chamber subcostal view is particularly use-
ful in detection of the motion between the pericar-
dial layers. Usually, transthoracic echocardiography is
less reliable than CT or CMR in detecting increased
pericardial thickness or calcification,1 although trans-
esophageal echocardiography has a reasonable corre-
lation with CT17 (Figure 1A).
Pericardial Tethering
Normally, the heart and the visceral pericardium move
within the parietal pericardium. When pericardial adhe-
sions are present, the normal independent motion of
visceral and parietal pericardium is lost. The demon-
stration of pericardial tethering by 2-dimensional (2D)
echocardiography can be difficult and may require
technical expertise (Movie I in the Data Supplement).
However, tissue Doppler imaging (TDI) and myocardial
Table 1.  Comparison of Multimodality Imaging to Study the
Pericardial Structural Changes and Hemodynamic Consequences of
Constrictive Pericarditis
Noninvasive Testing Target Echocardiography CT CMR
Pericardial structural target
 Thickening +* +++ +++
 Tethering +++ ++ +++
 Calcification ++ +++ +
 Inflammation + ++ +++
Pericardial hemodynamic targets
 Mitral/TV inflow respiratory +++ + ++
variation
 Respirophasic +++ + +++
interventricular septal shift
 Evaluation for RCM +++ + +++
(+) Poor; (++) good; (+++) excellent. CMR indicates cardiac magnetic
resonance; CT, computed tomography; RCM, restrictive cardiomyopathy; and
TV, tricuspid valve.
*Transesophageal echocardiography has improved sensitivity over
transthoracic echocardiography, which is unreliable.
November 2018 2
 Alajaji et al; Diagnosis of Constrictive Pericarditis

Figure 1. Pericardial anatomic abnormality detection by non-invasive multi-modality imaging.

Downloaded from http://ahajournals.org by on April 12, 2020

A, Transesophageal echocardiography (mid-esophageal 4-chamber view) demonstrating thickened, fibrotic pericardium (arrow) in a patient before undergoing
pericardiectomy. B, Noncontrast axial computed tomographic (CT) scan demonstrating prominent calcification anteriorly adjacent to the right atrium and right
ventricle (white arrow) and laterally adjacent to the left ventricle. C, Noncontrast axial CT and (D) cardiac magnetic resonance imaging axial black blood images
demonstrating circumferential pericardial thickening (white arrows). INF indicates inferior.

strain imaging are more reliable than visual assessment
for the detection of tethering. By TDI, the LV antero-
lateral wall may show pericardial tethering and can be
detected by the demonstration of a mitral annular later-
al e′ to medial e′ ratio <1, or annulus reversus, which is
a specific finding for CP.18,19 In addition, longitudinal TDI
has been used to study and compare the differences in
the inner to outer myocardium and the outer myocar-
dium to pericardial peak systolic velocities; tethering is
depicted by significantly higher ratio of inner-outer to
outer pericardial systolic velocities when compared with
controls.20 Alternatively, if annulus reversus is not pres-
ent, the anterior, inferior, and inferolateral mitral annu-
lar e′ velocities to medial e′ ratios may reveal tethering
in those walls, respectively; however, no data are avail-
able on its diagnostic utility.
Similarly, myocardial strain imaging by 2D speckle
tracking is useful. In the absence of other disease pro-
cesses that affect myocardial strain values, LV and RV
strain can demonstrate diminished (lower magnitude)
negative peak systolic strain in free walls when com-
pared with septal peak systolic strain, so-called strain
reversus (Figures  2 and 3). Our group has reported a
sensitivity and specificity of LV lateral wall strain to LV
septal wall strain ratio <0.96 of 89% and 96%, respec-
tively21 (Table 2). The LV and RV strain abnormalities are
also noted to resolve with pericardiectomy21 (Figure 2).
However, this study did not evaluate the incremental
value of strain on top of the simpler echocardiography
parameters; further studies may help in expanding the
data on our findings and evaluate the potential incre-
mental value of strain imaging in addition to simpler
echocardiography techniques. Lastly, tethering of the
LA free wall detection is possible by strain imaging,
which has a characteristic pattern of an impaired ear-
ly diastolic strain rate of LA superior and lateral walls
when compared with the septal wall in patients with CP
pre-pericardiectomy.22,23
Hemodynamic Testing
Abnormalities of Septal Motion
Respirophasic ventricular septal shift (VSS) is one of
the key noninvasive imaging diagnostic features of
CP1–4 (Movie II in the Data Supplement); it is well dem-
onstrated with a respirometer, 10-beat 2D cine clips,

Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878 November 2018 3

 Alajaji et al; Diagnosis of Constrictive Pericarditis
Downloaded from http://ahajournals.org by on April 12, 2020

Figure 2.  Two-dimensional speckle tracking echocardiography illustrating the left ventricular (LV) myocardial strain patterns derived from apical
three-chamber, apical four-chamber, and apical two-chamber images.
Pre-pericardiectomy strain patterns are demonstrated on the left, while post-pericardiectomy strain patterns are demonstrated on the right. Note the improve-
ment in lateral wall strain in the bull's eye plots (white arrow: pre-pericardiectomy; yellow arrow: post-pericardiectomy). ANT indicates anterior; ANT_SEPT,
anteroseptum; LAT, lateral; POST, posterior; and SEPT, septal.

and 50 mm/s sweeps of 2D and M-mode.1 Typically, ventricular septum shifting posteriorly into the LV with
using parasternal long- and short-axis views, ventricu- inspiration reflecting LV underfilling and anteriorly into
lar interdependence is characterized by diastolic inter- the RV with expiration (Figure 4A) reflecting recovery

Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878 November 2018 4

 Alajaji et al; Diagnosis of Constrictive Pericarditis

Table 2.  Summary of Useful Parameters in Patients With Suspected or Known CP

Parameter (Significance) Utility (Statistical Characteristics)

2D, M-mode, and Doppler echocardiography: key diagnostic finding

 Respirophasic VSS+medial mitral annular e′ ≥9 cm/s or expiratory Establish or confirm CP diagnosis (sensitivity, 87%; specificity, 91%)
diastolic hepatic vein flow reversal ratio ≥79%

 Respirophasic VSS+medial mitral annular e′ ≥9 cm/s+expiratory Establish or confirm CP diagnosis (sensitivity, 64%; specificity, 97%)
diastolic hepatic vein flow reversal ratio ≥79%
2D speckle tracking/strain echocardiography: key diagnostic finding if severe MV annular calcification or MV prosthesis is present; provide additional diagnostic
finding in patients without severe MV annular calcification and no prior MV prosthesis
 LVlateral wall/LVseptal wall ratio <96% Strain reversus favors CP diagnosis (sensitivity, 89%; specificity, 96%)
 LV GLS Normal GLS values favor CP diagnosis (CP [−15.8±2.8%] vs RCM [−9.8±3.7%];
P<0.05)
Cine cardiac MRI: additional finding
 Ventricular interdependence index=([cardiac area]end-inspiration/[cardiac Smaller [mean±SD] ratio favors CP diagnosis (CP [1.03±0.03] vs no CP [1.28±0.10];
area]end-expiration) ratio P<0.0001)
 Respirophasic septal shift index, %=(RV free wall to septum distance/ Larger [mean±SD] ratio favors CP diagnosis (CP [20±4.5%] vs RCM [4.2±1.7%])
biventricular distance)inspiration–(RV free wall to septum distance/
biventricular distance)expiration index
Velocity-encoded flow measurement across mitral and TVs by cardiac MRI: promising tool but limited and not widely available for clinical use yet

 Respirophasic variation in MV >25% inflow velocities Favor CP diagnosis (sensitivity, 100%; specificity, 100%)

 Respirophasic variation in TV >45% inflow velocities Favor CP diagnosis (sensitivity, 90%; specificity, 88%)

Volumetric and velocity-encoded flow measurements by cardiac MRI: promising tool but limited and not widely available for clinical use yet
 RVEDV
 TV (E/A ratio)
LGE by cardiac MRI: key finding for prognosis
 Quantitative pericardial LGE (median [quartiles]) cm3
Downloaded from http://ahajournals.org by on April 12, 2020
Smaller RVEDV favor CP diagnosis (RVEDV CP [120±21 mL] vs healthy control
[155±20 mL]; P<0.0001)
Smaller E/A ratio values favor CP diagnosis (TV E/A ratio CP [1.2±0.5] vs healthy
control [1.7±0.4]; P<0.0001)
Higher LGE values favor response to anti-inflammatory therapy (77 [43–15] vs 31

[17–23] cm3; P<0.001) and sparing from pericardiectomy (61 [38–95] vs 27 [15–39];
P=0.002)

2D indicates 2 dimensional; CP, constrictive pericarditis; GLS, global longitudinal strain; E/A, tricuspid valve inflow peak E wave velocity/peak A wave velocity
ratio; LGE, late gadolinium enhancement; LV, left ventricle; MRI, magnetic resonance imaging; MV, mitral valve; RCM, restrictive cardiomyopathy; RV, right
ventricle; RVEDV, right ventricular end-diastolic volume; TV, tricuspid valve; and VSS, ventricular septal shift.

of LV filling. Conversely, a septal shudder or bounce, septal fluttering motions by tissue Doppler M-mode
which is characterized by an abrupt displacement of and short-axis pulsed-wave TDI of interventricular sep-
the interventricular septum in early diastole during tum, respectively (Figure 4B, 4D, and 4E).25 Both tech-
each cardiac cycle is common in CP, although nonspe- niques may be used to improve the interpretation of
cific (Figure 4C).24 abnormal septal motion, especially when other causes
Septal shudder reflects the dip and plateau sign of of abnormal septal motion coexist, such as left bundle
ventricular pressure tracing by invasive hemodynam- branch block, paced rhythm, or RV dysfunction.25 In
ics. Unlike the ventricular free walls, the interven- left bundle branch block and RV pacing, there is a
tricular septum is anatomically not involved with the greater delay in the contraction and relaxation of the
pericardium and can, therefore, periodically bulge in LV compared with the RV. Consequently, in early sys-
and out of the LV cavity. The early rapid filling phase tole, RV pressure rise precedes that of the LV leading
is associated with abrupt pressure rise in the RV ini- to RV-LV pressure gradient and the characteristic 2D
tially pushing the interventricular septum toward the and M-mode echocardiography finding of early septal
LV. Then, the pressure rise is abruptly halted when motion into the LV. Similarly, in early diastole, the tri-
the intracardiac volume reaches its limits set by the cuspid valve (TV) opening precedes that of mitral valve
noncompliant pericardium and coincided with the causing RV-LV pressure gradient and early diastolic
pressure rise in the LV causing an abrupt anterior sep- septal shift, which may be confused with septal shud-
tal motion. Importantly, a septal shudder should not der. In RV dysfunction or significant tricuspid regur-
be misinterpreted as VSS, which is a more specific gitation, RV diastolic filling pressure and volume are
diagnostic finding. usually elevated, and this may lead to diastolic septal
In addition, the interventricular septum has a char- motion abnormalities mediated by TV inflow waves
acteristic early diastolic high velocity and polyphasic during diastole.

Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878 November 2018 5

 Alajaji et al; Diagnosis of Constrictive Pericarditis

Figure 3.  Right ventricular (RV) strain analysis in a patient with surgically proven constrictive pericarditis.
The RV strain pattern shows impaired RV free wall strain (black arrow) compared with ventricular septal strain because of RV free wall tethering. Note that RV
free wall strain is the highest at the apex and lower toward the base. Adapted from Kusunose et al21 with permission. Copyright© 2013. L/R invert indicates
left/right invert.

Mitral TV Inflow Pattern and Mitral Annular early rapid filling is abnormal leading to high E veloci-
Downloaded from http://ahajournals.org by on April 12, 2020

Tissue Doppler Velocities ties in both ventricles.2 Typically, there is ≥25% inspi-
Doppler findings are critical for CP diagnosis.1,2 Mitral ratory decline in mitral and ≥40% increase in tricuspid
E/A ratio >0.8 is essential for the diagnosis because E-wave velocities when compared with that during

Figure 4.  M-mode and tissue Doppler imaging (TDI) echocardiography (parasternal short-axis view) images from a patient with surgically proven
constrictive pericarditis.
A, M-mode image showing respirophasic interventricular septal shift. Note the interventricular septum shifts into the left ventricle (arrowhead) with inspiration
and into the right ventricle during expiration (arrow). B, Tissue Doppler M-mode image showing early diastolic high velocity motion of the interventricular septum
with inspiration (arrowheads). C, Septal bounce or shudder (yellow arrows) showing interventricular displacement in early diastole during each cardiac cycle. D,
Short-axis pulsed-wave TDI showing polyphasic septal fluttering during diastole (arrow). E, Short-axis pulsed-wave TDI obtained from a patient with restrictive
cardiomyopathy showing the absence of diastolic septal fluttering (arrow).

Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878 November 2018 6

 Alajaji et al; Diagnosis of Constrictive Pericarditis

Figure 5.  Pulsed-wave Doppler and tissue Doppler imaging (TDI in a patient with constrictive pericarditis; apical 4-chamber view) images.
A, Mitral inflow E and A velocities showing respiratory variation pattern. Note the inspiratory decrease (white arrow) with the first beat of inspiration and expira-
tory increase (yellow arrow) with the first beat of expiration in E-wave velocities in a patient with constrictive pericarditis (CP).1 B, Tricuspid inflow E and A velocities
showing respiratory variation pattern. Note the inspiratory increase (white arrowhead) and expiratory decrease (yellow arrowhead) in E-wave velocities.1 C and D,
Downloaded from http://ahajournals.org by on April 12, 2020

Mitral annular TDI velocities showing medial e′=14 cm/s (white arrow) and lateral e′=11 cm/s (yellow arrow); this finding is typical of CP and known as annulus
reversus. This Figure is adapted from Klein et al. 2013; ASE clinical recommendations for multimodality cardiovascular imaging of patients with pericardial dis-
ease.1 ASE indicates American Society of Echocardiography.

expiration1 (Figure  5A and 5B). Similarly, marked
respiratory variations are usually noted in pulmo-
nary venous flow.26 According to the 2013 American
Society of Echocardiography cardiovascular imaging
guidelines for the diagnosis of pericardial diseases,
the percentage of respiratory variations for the peak
E-wave velocity across both the mitral valve and the
TV should be calculated as ([peak Eexpiration−peak Ein-
spiration
]/peak Eexpiration)×1001; note that the mitral valve
E-wave respiratory variations yield positive values,
whereas the TV E-wave respiratory variations yield
negative values reflecting the typical discordant fill-
ing patterns.1 Because 30% to 50% of patients with
surgically proven CP lack significant respiratory varia-
tions,27,28 the demonstration of mitral and tricuspid
respiratory variations ≥25% and ≥40% is not required
for the diagnosis.2 Patients with either markedly ele-
vated filling pressures or reduced preload can have
less pronounced respiratory variation.29 In addition,
conditions such as COPD or tricuspid regurgitation
can induce mitral E-wave respiratory variation mim-
icking that of CP.6 The superior vena cava flow can be
useful in differentiating COPD from CP because of its
characteristic respiratory variation pattern. In patients
with COPD, the systolic forward flow increases with
inspiration in contrast to CP, which has little respira-
tory variations.6 This Doppler finding in the superior
vena cava may be equivalent to Kussmaul sign.
Another major finding in CP is the demonstration
of normal or high (≥9 cm/s) mitral medial annular
early diastolic velocity (e′) by TDI.1–4 Medial mitral
annular e′ ≥9 cm/s when combined with respira-
tory septal shift represents a robust combination for
diagnosis of CP with high sensitivity and specific-
ity >90%, respectively.18,30 Mitral annulus reversus
is highly specific for CP approaching 100%; how-
ever, this finding may be absent in about 25% of
patients18,19,31 (Figure  5C and 5D). In some cases,
especially when e′ velocity is borderline, medial
mitral annular peak systolic tissue Doppler veloc-
ity S′ ≥6 cm/s may provide a supportive parameter
for the diagnosis.32 Usually, medial, lateral, or mean
E/e′ cannot be used for filling pressure estimation
in patients with CP because it does not correlate
with elevated pulmonary capillary wedge pressure.33
However, in patients without myocardial pathology,
an inverse relationship termed annulus paradoxus is
often noted.34

Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878 November 2018 7

 Alajaji et al; Diagnosis of Constrictive Pericarditis

Figure 6.  M-mode echocardiography of the inferior vena cava and pulsed-wave Doppler (subcostal view) velocities of the hepatic vein and CT/CMR
Downloaded from http://ahajournals.org by on April 12, 2020

images of the inferior vena cava.

A, M-mode image showing dilated, plethoric inferior vena cava and no inspiratory (insp) collapse. B, Hepatic vein flow pattern showing systolic forward flow (S
wave), diastolic forward flow (D wave), and prominent late diastolic flow reversal at end expiration (exp; white arrow). This Figure is adapted with minor modifica-
tion from Klein et al. 2013; ASE clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease.1 C, Noncontrast axial
computed tomography demonstrating a dilated inferior vena cava (arrow) in a patient with pericardial constriction. D, Steady-state free precession bright-blood
axial cardiac magnetic resonance demonstrating a dilated inferior vena cava (arrow) in a patient with pericardial constriction. *Moderate-sized right pleural effu-
sion. ASE indicates American Society of Echocardiography.

IVC Size and Hepatic Vein Flow Pattern
Except in the setting of volume depletion, a dilated
IVC is invariably present (Figure  6A). Therefore, even
though it is nonspecific, a plethoric IVC is required for
the diagnosis of CP2. On the contrary, the diastolic expi-
ratory hepatic vein flow reversal ratio, which is defined
as the hepatic vein (diastolic reversal velocity/forward
velocity) in expiration (Figure 6B), is specific to CP,2,11,28
although it may be difficult to demonstrate since accu-
rate hepatic vein recordings are needed. A study report-
ed that the combination of VSS with medial e′ ≥9 cm/s
and hepatic vein expiratory flow reversal ratio during
diastole of ≥79% versus VSS and medial e′ ≥9 cm/s only
has a sensitivity and specificity of 64% and 97% ver-
sus 87% and 91%, respectively28 (Table  2). Note that
respiratory conditions with fluctuations in intrathoracic
pressure, that is, COPD, may produce similar patterns
of respiratory variations in transmitral and transtricus-
pid Doppler inflow patterns. In COPD, E/A is lower, and
deceleration time is more prolonged. Pulsed Doppler of
superior vena cava shows a marked increase in inspi-
ratory systolic flow, as opposed to diastolic prominent
flow in CP.6,13
Computed Tomography
Pericardial Structural Evaluation
Cardiac CT is not a first-line test for patients with
suspected CP.1 However, CT can be useful in preop-
erative planning for pericardiectomy, especially when
surgery is a redo-cardiac procedure.1,35 Multidetector
CT can offer valuable information, including location
of cardiac and vascular structures relative to midline
retrosternum, as well as aortic atherosclerotic chang-
es. Occasionally, especially in patients with predomi-
nantly abdominal complaints, when abdominal CT is
already available, there may be findings to suggest
the diagnosis of CP,36 which will require confirmatory
testing by echocardiography or CMR. CT is sensitive
for pericardial calcification or detection  of pericar-
dial thickening (Figure 1B and 1C). However, almost
one-third of patients with CP do not have thickened

Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878 November 2018 8

 Alajaji et al; Diagnosis of Constrictive Pericarditis
pericardium,36,37 and calcifications are only present in
about 25% of patients with surgical CP.15,38 There-
fore, absence of pericardial thickening or calcification
does not rule out CP. In addition, not all patients with
pericardial calcifications have CP; however, pericardi-
al calcifications represent abnormal pericardium and
may warrant clinical monitoring for the development
of CP symptoms or hemodynamic changes. CT can
have prognostic information, especially, if the pos-
terolateral wall is not visualized on CT, presumably
because of myocardial fibrosis or atrophy, pericardiec-
tomy is high risk.39 In our experience, we have often
observed that calcium in CP has a partial band-like
pattern (from basal anterolateral LV going inferiorly
and then encircling the heart to reach the RV out-
flow tract) with extension into the mitral and tricus-
pid annuli. There is often a sparing of the apex and
LV anterior walls. Further studies will be important to
study the pattern of calcification and correlate with
hemodynamic and prognostic findings.40
Hemodynamic Testing
As discussed, CP is a hemodynamic diagnosis, and CT
imaging is limited in this evaluation. The temporal reso-
lution that can be achieved with CT remains inferior to
CMR and echocardiography. In addition, breathing is
restricted during acquisition, and substantial radiation
exposure may be incurred. However, CT can be useful
in detection of IVC dilitation. Given the high sensitivity
Downloaded from http://ahajournals.org by on April 12, 2020
of a dilated IVC with CP, its absence by CT makes CP
less likely. Recent data suggest that dilated IVC by CT
(Figure 6C) in combination with pericardial thickening
can be useful37; however, because of the nonspecificity
of IVC dilation in CP, confirmatory testing by echocar-
diography or CMR is required. Occasionally, 4-dimen-
sional cine CT may be used to assess the septal bounce
in CP. However, given the radiation exposure concern
and the requirement for breath-held imaging, assess-
ment for accentuated ventricular interdependence is
not possible.
Cardiac Magnetic Resonance
Structural Imaging
CMR is a second-line imaging modality for the evalu-
ation of CP useful for both pericardial thickening
(Figure  1D) and hemodynamic change evaluation.1
Real-time CMR imaging can be performed during free
breathing and so can be used to assess the accentua-
tion of ventricular septal shift with respiratory maneu-
vers. In CP, the value of CMR is tissue characterization,
which can demonstrate pericardial edema and inflam-
mation (Figure 7A). Pericardial edema is suggested by
increased signal on edema weighted imaging using
T2 short tau inversion recovery sequence, and active
inflammation is demonstrated by late gadolinium
Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878
enhancement (LGE), which indicates ongoing fibroblast
proliferation with neovascularization10 (Figure 7B). The
finding of both edema and inflammation suggests an
acute or subacute active  process. Importantly, active
pericardial inflammation favors CP reversibility with
anti-inflammatory therapy.8–10 In addition, there is an
incremental value of the degree of LGE on the response
to anti-inflammatory therapy. A study suggested that
higher quantitative  pericardial LGE (median [quartiles]
LGE of 77 [43, 15] cm3) predicts improvement,8 and
lower LGE (<27 [15–39] cm3) is associated with poor
response to anti-inflammatories and the need for peri-
cardiectomy8 (Table  2). Another study reported that
CMR pericardial tissue tagging is highly sensitive in its
depiction of pericardial tethering.41 CMR can be useful
for simultaneous evaluation for myocardial infiltrative
diseases, which could suggest an alternate diagnosis of
RCM in the absence of CP.
Hemodynamic Testing
The application of relatively recent CMR techniques
allows not only structural evaluation of the pericardium
but also detection of the characteristic CP hemodynam-
ic changes. Like echocardiography, cine CMR video clips
during free breathing can be acquired in real time and
provide data for ventricular interdependence evaluation.
Visual assessment of VSS is possible by free breathing
cine CMR imaging with good sensitivity and specificity
for CP diagnosis.42,43 Also, if free breathing cine CMR
is not available, breath-held CMR may be used alter-
natively, with good diagnostic characteristics as well.44
In addition to the visual assessment, ventricular inter-
dependence can be quantitatively evaluated by CMR-
derived indices. From LV  ventricular short-axis view,
([cardiac area]end-inspiration/[cardiac area]end-expiration) is signifi-
cantly less in CP as compared with patients without CP
(1.03±0.03 versus 1.28±0.10; P<0.0001, respectively;
Figure  7C and 7D; Table  2).45 Another useful index is
the ratio of RV free wall-septum distance (distance A)
to that of biventricular distance (distance B) measured
from short-axis view, (A/B)inspiration−(A/B)expiration ≥11.8%
has been reported to favor the diagnosis CP (Figure 7E
and 7F; Table 2).43 Also, LAvolume/right atriumvolume index
tends to have a higher value in CP when compared with
RCM46; however, the mere reliance on LA/right atrium
volume index for differentiating CP from RCM can be
questionable because the study utilized other tools in
combination with this index, such as LGE.
Moreover, the use of velocity-encoded CMR allows
for assessment of mitral and tricuspid inflow veloci-
ties, and one group reported confident discrimina-
tion of CP from RCM47 based on variation of inflow
with respiration, although with limited sample size
and scanning technology that is not widely available
(Table 2). Another study using velocity-encoded CMR
signals reported that pericardial thickening with rela-
November 2018 9
 Alajaji et al; Diagnosis of Constrictive Pericarditis
Downloaded from http://ahajournals.org by on April 12, 2020

Figure 7.  Cardiac magnetic resonance (CMR; short-axis cross section views at mid-ventricular level) images.
A, CMR with T2-weighted short tau inversion recovery imaging demonstrating circumferential increased pericardial signal to suggest pericardial edema (white
arrow). B, Delayed-enhancement imaging demonstrating circumferential pericardial enhancement (white arrow). C, Short-axis cross section through the mid-
ventricular level with epicardial tracing in end inspiration and (D) end expiration patient with constrictive pericarditis showing heightened ventricular interdepen-
dence, and dissociation of intrathoracic and intracardiac pressures. E and F, Analysis of respiratory-related septal excursion. The relative position of the septum can
be obtained by dividing the distance between right ventricular free wall and septum (full black line) by the biventricular distance (dashed black line). The horizontal
dashed white line indicates the position of the left hemidiaphragm, which is used to determine the phase of the respiratory cycle.

tively lower RV volumes of RV end-diastolic volume
≤133 mL along with tricuspid inflow E/A wave ratio
≤1.3 can be useful for CP diagnosis48; similarly, the
data are limited, and currently, this technique is not a
part of routine CMR (Table 2). In addition, dilated IVC
detection by magnetic resonance imaging (Figure 6D)
can suggest the possibility of CP, especially when there
is pericardial thickening.49 Owing to the high sensitiv-
ity of dilated IVC in CP, its absence can nearly exclude
CP,49 although the nonspecificity of dilated IVC requires
other hemodynamic features to be present for the
diagnosis to be confidently made. Cardiac mechan-
ics by strain imaging CMR can be performed and can
help in differentiation of CP from RCM50; however,
this technique is not routinely done in CMR examina-
tions. Lastly, extracardiac imaging may provide hints
to the diagnosis, such as the finding of liver distension
with liver magnetic resonance elastography as surro-
gate for increased right heart pressure in patients with
CP50; however, this finding is of questionable use in CP

Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878 November 2018 10

 Alajaji et al; Diagnosis of Constrictive Pericarditis
Downloaded from http://ahajournals.org by on April 12, 2020

Figure 8.  Multimodality noninvasive imaging diagnostic and management workup algorithm for constrictive pericarditis (CP).
CMR indicates cardiac magnetic resonance; CT, computed tomography; E/A, mitral valve inflow E wave velocity/A wave velocity ratio; IVC, inferior vena cava; LGE,
late gadolinium enhancement; OR, odds ratio; RCM, restrictive cardiomyopathy; SVC, superior vena cava; and VSS, ventricular septal shift.

diagnosis given its nonspecificity and the challenge of
interpretation in primary liver disease.
Positron Emission Tomographic Imaging
Positron emission tomographic imaging can be useful in
the detection of pericardial inflammation. A limited sin-
gle-center study, which had 16 patients, suggested that
[18F]fluorodeoxyglucose positron emission tomogra-
phy may have utility in transient inflammatory constric-
tion. The study revealed that [18F]fluorodeoxyglucose
positron emission tomography/CT predicts response to
steroid therapy. The data are limited by sample size, and
the majority of patients had tuberculosis pericarditis.51
In addition, spatial resolution is a major limitation for
[18F]fluorodeoxyglucose positron emission tomogra-
phy currently, which would not allow adequate differ-
entiation of pericardium from myocardium.
CP Versus RCM Evaluation
Differentiating CP from RCM has major implications on
therapy and prognosis. Based on the 2016 American
Society of Echocardiography diastolic function guide-
lines, when mitral annular medial e′ velocity is >8 cm/s,
annulus reversus and hepatic vein expiratory flow rever-
sal are present, RCM can be excluded, and CP diagnosis
can be established with confidence.2 Using the current
understanding of the multimodality noninvasive cardio-
vascular imaging data, we developed a helpful algo-
rithm for CP evaluation and management (Figure  8).
Data suggest that even lower intensity of mitral E-wave
respiratory variations, as low as ≥10%, could favor
the  CP diagnosis because RCMs tend to have nearly
fixed ventricular filling.13 Also, hepatic vein flow reversal
tends to occur with inspiration in RCM.7
In special populations, such as patients with severe
mitral annular calcification, mitral valve prosthesis,

Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878 November 2018 11

 Alajaji et al; Diagnosis of Constrictive Pericarditis
severe tricuspid regurgitation, or RV systolic dysfunc-
tion, medial e′ may be reduced in the absence of RCM
or LV dysfunction. In addition, myocardial infiltrative
diseases can have nonuniform distribution.30,52,53 There-
fore, LV strain imaging may be a useful alternative
to overcome the limitations of tissue Doppler imag-
ing  because global longitudinal strain is significantly
higher in CP compared with RCM (−15.8±2.8% ver-
sus −9.8±3.7%; P<0.05), respectively.21 Similar results
have been reported with CMR.49 In RCM, there is pre-
dominant endocardial dysfunction and relative sparing
of epicardial function leading to impaired longitudi-
nal strain, relatively normal circumferential, and pre-
served twisting mechanics. However, CP predominantly
impairs epicardial fibers because of perimyocardial teth-
ering and leads to impairment of circumferential strain
and twist mechanics with relatively spared overall lon-
gitudinal strain.53,54
In addition, CMR can detect diffuse areas of myo-
cardial thickening or abnormal gadolinium contrast
enhancement and kinetics, which are often diagnos-
tic of RCM. Moreover, limited data suggest that pul-
monary regurgitation continuous wave Doppler has
a characteristic pattern for differentiating CP from
RCM.55,56 In CP, the pulmonary artery to RV pressure
gradient abruptly declines in early diastole reflecting
the rapid RV pressure rise (dip and plateau sign) and
remains low in mid and late diastole as RV pressure
plateaus, leading to the corresponding early reduc-
Downloaded from http://ahajournals.org by on April 12, 2020
tion in pulmonary regurgitation velocity. Whereas in
RCM, the pulmonary artery pressure is much higher
and the pulmonary artery-RV pressure gradient is usu-
ally more preserved in mid and late diastole, leading to
lower degrees of early velocity reduction on pulmonary
regurgitation continuous wave signals.
With the advent of computer-associated memory
classifier, echocardiography machines can use machine
learning to identify patterns and variables associated
with the highest diagnostic value based on memo-
rized data sets stored from patients with known CP
and RCM.52 Recently, data suggest that a 4-variable
model (end-diastolic ventricular septal and posterior
wall thickness, mitral medial e′, and mitral E/e′) or
4-variable model in addition to 15 speckle-tracking
echocardiography variables had promising results for
differentiating CP from RCM with area under the curve
of 0.94 and 0.96, respectively.52 This technology may
help less-experienced echocardiographers in diagnos-
ing less-frequently encountered diseases, such as CP.57
When noninvasive imaging is nondiagnostic, inva-
sive hemodynamics using the systolic area index (the
ratio of the RV-LV systolic pressure-time area during
inspiration to that during expiration) of >1.1 can be
useful with a sensitivity of 97% and a specificity of
100% for differentiating CP from RCM.58 The sys-
tolic area index >1.1 reflects RV-LV pressure discor-
Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878
dance with respiration, which is a characteristic of the
enhanced ventricular interaction in CP as opposed to
the concordant pattern in RCM. The data suggest that
the systolic area index is the most useful diagnostic
invasive hemodynamic finding when compared with
the other criteria: LV end-diastolic pressure minus RV
end-diastolic pressure ≤5 mm Hg, pulmonary artery
systolic pressure <55 mm Hg, RV end-diastolic pres-
sure-to-RV systolic pressure ratio >1/3, LV height of
rapid filling wave >7 mm Hg, or inspiratory decrease
in right atrial pressure <5 mm Hg.58 Occasionally,
despite all noninvasive imaging tools, the clinical pic-
ture may still be unclear, and endomyocardial biopsy
may be necessary.59
CONCLUSIONS
The diagnosis of CP is based on specific hemodynamic
characteristics, including respirophasic variation and
accentuated early diastolic filling in the absence of
myocardial disease. Echocardiography provides reli-
able hemodynamic data for this diagnosis. If needed,
CMR is complementary by reliably assessing ventricu-
lar interdependence. Importantly, the strength of CMR
is delineation of pericardial inflammation, which can
inform response to anti-inflammatory therapy and the
need for pericardiectomy. For the diagnosis of CP, CT
is limited because it primarily provides supportive ana-
tomic features, not diagnostic hemodynamic findings.
However, CT is helpful for procedural planning by out-
lining pericardial and aortic calcifications. In patients
with suspected CP, multimodality imaging, therefore,
typically provides a complete characterization of the
hemodynamic and anatomic features necessary for
optimal care.
ARTICLE INFORMATION
The Data Supplement is available at https://www.ahajournals.org/doi/
suppl/10.1161/CIRCIMAGING.118.007878.
Correspondence
Allan L. Klein, MD, Center for the Diagnosis and Treatment of Pericardial Dis-
eases, Section of Cardiovascular Imaging, Robert and Suzanne Tomsich Depart-
ment of Cardiovascular Medicine, Sydell and Arnold Miller Family Heart and
Vascular Institute, Cleveland Clinic, 9500 Euclid Ave, Desk J1–5, Cleveland, OH
44195. Email kleina@ccf.org
Affiliations
Department of Cardiovascular Medicine, Summa Health Heart and Vascular In-
stitute, Akron, OH (W.A.). Center for the Diagnosis and Treatment of Pericardial
Diseases, Heart and Vascular Institute (B.X., V.M., A.K., P.C.C., A.L.K.), Cardio-
vascular Section, Imaging Institute (A.S., M.A.B.), and Cleveland Clinic Alumni
Library (M.S.), Cleveland Clinic, OH. Division of Cardiology, American University
of Beirut, Lebanon (H.I.).
Disclosures
None.
November 2018 12
 Alajaji et al; Diagnosis of Constrictive Pericarditis
REFERENCES
1. Klein AL, Abbara S, Agler DA, Appleton CP, Asher CR, Hoit B, Hung J,
Garcia MJ, Kronzon I, Oh JK, Rodriguez ER, Schaff HV, Schoenhagen P, Tan
CD, White RD. American Society of Echocardiography clinical recommen-
dations for multimodality cardiovascular imaging of patients with pericar-
dial disease: endorsed by the Society for Cardiovascular Magnetic Reso-
nance and Society of Cardiovascular Computed Tomography. J Am Soc
Echocardiogr. 2013;26:965–1012.e15. doi: 10.1016/j.echo.2013.06.023
2. Nagueh SF, Smiseth OA, Appleton CP, Byrd BF 3rd, Dokainish H, Edvardsen
T, Flachskampf FA, Gillebert TC, Klein AL, Lancellotti P, Marino P, Oh JK,
Popescu BA, Waggoner AD. Recommendations for the evaluation of left
ventricular diastolic function by echocardiography: an update from the
American Society of Echocardiography and the European Association of
Cardiovascular Imaging. J Am Soc Echocardiogr. 2016;29:277–314. doi:
10.1016/j.echo.2016.01.011
3. Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J,
Brucato A, Gueret P, Klingel K, Lionis C, Maisch B, Mayosi B, Pavie A, Ristic
AD, Sabaté Tenas M, Seferovic P, Swedberg K, Tomkowski W; ESC Scien-
tific Document Group. 2015 ESC Guidelines for the diagnosis and man-
agement of pericardial diseases: the task force for the diagnosis and man-
agement of pericardial diseases of the European Society of Cardiology
(ESC)endorsed by: the European Association for Cardio-Thoracic Surgery
(EACTS). Eur Heart J. 2015;36:2921–2964. doi: 10.1093/eurheartj/ehv318
4. Cosyns B, Plein S, Nihoyanopoulos P, Smiseth O, Achenbach S, Andrade
MJ, Pepi M, Ristic A, Imazio M, Paelinck B, Lancellotti P; European As-
sociation of Cardiovascular Imaging (EACVI); European Society of Cardiol-
ogy Working Group (ESC WG) on Myocardial and Pericardial Diseases.
European Association of Cardiovascular Imaging (EACVI) position paper:
multimodality imaging in pericardial disease. Eur Heart J Cardiovasc Imag-
ing. 2015;16:12–31. doi: 10.1093/ehjci/jeu128
5. Miranda WR, Oh JK. Constrictive pericarditis: a practical clinical approach.
Prog Cardiovasc Dis. 2017;59:369–379. doi: 10.1016/j.pcad.2016.12.008
6. Boonyaratavej S, Oh JK, Tajik AJ, Appleton CP, Seward JB. Comparison of
mitral inflow and superior vena cava Doppler velocities in chronic obstruc-
tive pulmonary disease and constrictive pericarditis. J Am Coll Cardiol.
1998;32:2043–2048.
7. Syed FF, Schaff HV, Oh JK. Constrictive pericarditis–a curable dia-
Downloaded from http://ahajournals.org by on April 12, 2020
stolic heart failure. Nat Rev Cardiol. 2014;11:530–544. doi:
10.1038/nrcardio.2014.100
8. Cremer PC, Tariq MU, Karwa A, Alraies MC, Benatti R, Schuster A, Agar-
wal S, Flamm SD, Kwon DH, Klein AL. Quantitative assessment of pericar-
dial delayed hyperenhancement predicts clinical improvement in patients
with constrictive pericarditis treated with anti-inflammatory therapy. Circ
Cardiovasc Imaging. 2015;8. pii: e003125.
9. Feng D, Glockner J, Kim K, Martinez M, Syed IS, Araoz P, Breen J, Espinosa
RE, Sundt T, Schaff HV, Oh JK. Cardiac magnetic resonance imaging peri-
cardial late gadolinium enhancement and elevated inflammatory markers
can predict the reversibility of constrictive pericarditis after antiinflamma-
tory medical therapy: a pilot study. Circulation. 2011;124:1830–1837.
doi: 10.1161/CIRCULATIONAHA.111.026070
10. Zurick AO, Bolen MA, Kwon DH, Tan CD, Popovic ZB, Rajeswaran J, Rodri-
guez ER, Flamm SD, Klein AL. Pericardial delayed hyperenhancement with
CMR imaging in patients with constrictive pericarditis undergoing surgical
pericardiectomy: a case series with histopathological correlation. JACC Car-
diovasc Imaging. 2011;4:1180–1191. doi: 10.1016/j.jcmg.2011.08.011
11. Oh JK, Hatle LK, Seward JB, Danielson GK, Schaff HV, Reeder GS, Tajik AJ.
Diagnostic role of Doppler echocardiography in constrictive pericarditis. J
Am Coll Cardiol. 1994;23:154–162.
12. Nishimura RA. Constrictive pericarditis in the modern era: a diagnostic
dilemma. Heart. 2001;86:619–623.
13. Rajagopalan N, Garcia MJ, Rodriguez L, Murray RD, Apperson-Hansen C,
Stugaard M, Thomas JD, Klein AL. Comparison of new Doppler echocar-
diographic methods to differentiate constrictive pericardial heart disease
and restrictive cardiomyopathy. Am J Cardiol. 2001;87:86–94.
14. Kim KH, Miranda WR, Sinak LJ, Syed FF, Melduni RM, Espinosa RE, Kane
GC, Oh JK. Effusive-constrictive pericarditis after pericardiocentesis: inci-
dence, associated findings, and natural history. JACC Cardiovasc Imaging.
2018;11:534–541. doi: 10.1016/j.jcmg.2017.06.017
15. Talreja DR, Edwards WD, Danielson GK, Schaff HV, Tajik AJ, Tazelaar HD,
Breen JF, Oh JK. Constrictive pericarditis in 26 patients with histologi-
cally normal pericardial thickness. Circulation. 2003;108:1852–1857. doi:
10.1161/01.CIR.0000087606.18453.FD
16. Schnittger I, Bowden RE, Abrams J, Popp RL. Echocardiography: pericardial
thickening and constrictive pericarditis. Am J Cardiol. 1978;42:388–395.
Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878
17. Ling LH, Oh JK, Tei C, Click RL, Breen JF, Seward JB, Tajik AJ. Pericardial
thickness measured with transesophageal echocardiography: feasibility
and potential clinical usefulness. J Am Coll Cardiol. 1997;29:1317–1323.
18. Reuss CS, Wilansky SM, Lester SJ, Lusk JL, Grill DE, Oh JK, Tajik AJ. Using
mitral ‘annulus reversus’ to diagnose constrictive pericarditis. Eur J Echo-
cardiogr. 2009;10:372–375. doi: 10.1093/ejechocard/jen258
19. Veress G, Ling LH, Kim KH, Dal-Bianco JP, Schaff HV, Espinosa RE,
Melduni RM, Tajik JA, Sundt TM 3rd, Oh JK. Mitral and tricuspid annu-
lar velocities before and after pericardiectomy in patients with con-
strictive pericarditis. Circ Cardiovasc Imaging. 2011;4:399–407. doi:
10.1161/CIRCIMAGING.110.959619
20. Lu XF, Wang XF, Cheng TO, Xie MX, Lu Q. Diagnosis of constrictive pericar-
ditis by quantitative tissue Doppler imaging. Int J Cardiol. 2009;137:22–
28. doi: 10.1016/j.ijcard.2008.05.068
21. Kusunose K, Dahiya A, Popović ZB, Motoki H, Alraies MC, Zurick AO,
Bolen MA, Kwon DH, Flamm SD, Klein AL. Biventricular mechanics in con-
strictive pericarditis comparison with restrictive cardiomyopathy and im-
pact of pericardiectomy. Circ Cardiovasc Imaging. 2013;6:399–406. doi:
10.1161/CIRCIMAGING.112.000078
22. Liu S, Ma C, Ren W, Zhang J, Li N, Yang J, Zhang Y, Qiao W. Regional
left atrial function differentiation in patients with constrictive pericar-
ditis and restrictive cardiomyopathy: a study using speckle tracking
echocardiography. Int J Cardiovasc Imaging. 2015;31:1529–1536. doi:
10.1007/s10554-015-0726-7
23. Motoki H, Alraies MC, Dahiya A, Saraiva RM, Hanna M, Marwick TH,
Klein AL. Changes in left atrial mechanics following pericardiectomy for
pericardial constriction. J Am Soc Echocardiogr. 2013;26:640–648. doi:
10.1016/j.echo.2013.02.014
24. Engel PJ, Fowler NO, Tei CW, Shah PM, Driedger HJ, Shabetai R, Harbin
AD, Franch RH. M-mode echocardiography in constrictive pericarditis. J
Am Coll Cardiol. 1985;6:471–474.
25. Sengupta PP, Mohan JC, Mehta V, Arora R, Khandheria BK, Pandian NG.
Doppler tissue imaging improves assessment of abnormal interventricu-
lar septal and posterior wall motion in constrictive pericarditis. J Am Soc
Echocardiogr. 2005;18:226–230. doi: 10.1016/j.echo.2004.11.017
26. Sun JP, Abdalla IA, Yang XS, Rajagopalan N, Stewart WJ, Garcia MJ,
Thomas JD, Klein AL. Respiratory variation of mitral and pulmonary ve-
nous Doppler flow velocities in constrictive pericarditis before and after
pericardiectomy. J Am Soc Echocardiogr. 2001;14:1119–1126.
27. Ha JW, Oh JK, Ommen SR, Ling LH, Tajik AJ. Diagnostic value of mitral
annular velocity for constrictive pericarditis in the absence of respiratory
variation in mitral inflow velocity. J Am Soc Echocardiogr. 2002;15:1468–
1471. doi: 10.1067/mje.2002.127452
28. Welch TD, Ling LH, Espinosa RE, Anavekar NS, Wiste HJ, Lahr BD,
Schaff HV, Oh JK. Echocardiographic diagnosis of constrictive pericardi-
tis: mayo clinic criteria. Circ Cardiovasc Imaging. 2014;7:526–534. doi:
10.1161/CIRCIMAGING.113.001613
29. Oh JK, Tajik AJ, Appleton CP, Hatle LK, Nishimura RA, Seward JB. Preload
reduction to unmask the characteristic Doppler features of constrictive
pericarditis. A new observation. Circulation. 1997;95:796–799.
30. Sengupta PP, Mohan JC, Mehta V, Arora R, Pandian NG, Khandheria BK.
Accuracy and pitfalls of early diastolic motion of the mitral annulus for di-
agnosing constrictive pericarditis by tissue Doppler imaging. Am J Cardiol.
2004;93:886–890. doi: 10.1016/j.amjcard.2003.12.029
31. Choi JH, Choi JO, Ryu DR, Lee SC, Park SW, Choe YH, Oh JK. Mitral
and tricuspid annular velocities in constrictive pericarditis and restric-
tive cardiomyopathy: correlation with pericardial thickness on com-
puted tomography. JACC Cardiovasc Imaging. 2011;4:567–575. doi:
10.1016/j.jcmg.2011.01.018
32. Choi EY, Ha JW, Kim JM, Ahn JA, Seo HS, Lee JH, Rim SJ, Chung N. Incre-
mental value of combining systolic mitral annular velocity and time differ-
ence between mitral inflow and diastolic mitral annular velocity to early
diastolic annular velocity for differentiating constrictive pericarditis from
restrictive cardiomyopathy. J Am Soc Echocardiogr. 2007;20:738–743.
doi: 10.1016/j.echo.2006.11.005
33. Alraies MC, Kusunose K, Negishi K, Yarmohammadi H, Motoki H, AlJa-
roudi W, Popović ZB, Klein AL. Relation between echocardiographically
estimated and invasively measured filling pressures in constrictive peri-
carditis. Am J Cardiol. 2014;113:1911–1916. doi: 10.1016/j.amjcard.
2014.03.022
34. Ha JW, Oh JK, Ling LH, Nishimura RA, Seward JB, Tajik AJ. Annulus para-
doxus: transmitral flow velocity to mitral annular velocity ratio is inversely
proportional to pulmonary capillary wedge pressure in patients with con-
strictive pericarditis. Circulation. 2001;104:976–978.
November 2018 13
 Alajaji et al; Diagnosis of Constrictive Pericarditis
35. Kamdar AR, Meadows TA, Roselli EE, Gorodeski EZ, Curtin RJ, Sabik JF,
Schoenhagen P, White RD, Lytle BW, Flamm SD, Desai MY. Multidetec-
tor computed tomographic angiography in planning of reoperative
cardiothoracic surgery. Ann Thorac Surg. 2008;85:1239–1245. doi:
10.1016/j.athoracsur.2007.11.075
36. Johnson KT, Julsrud PR, Johnson CD. Constrictive pericarditis at abdominal
CT: a commonly overlooked diagnosis. Abdom Imaging. 2008;33:349–
352. doi: 10.1007/s00261-007-9246-9
37. Hanneman K, Thavendiranathan P, Nguyen ET, Moshonov H, Paul NS,
Wintersperger BJ, Crean AM. Cardiovascular CT in the diagnosis of
pericardial constriction: predictive value of inferior vena cava cross-
sectional area. J Cardiovasc Comput Tomogr. 2014;8:149–157. doi:
10.1016/j.jcct.2013.12.017
38. Ling LH, Oh JK, Schaff HV, Danielson GK, Mahoney DW, Seward JB,
Tajik AJ. Constrictive pericarditis in the modern era: evolving clinical
spectrum and impact on outcome after pericardiectomy. Circulation.
1999;100:1380–1386.
39. Rienmüller R, Doppman JL, Lissner J, Kemkes BM, Strauer BE. Con-
strictive pericardial disease: prognostic significance of a nonvisu-
alized left ventricular wall. Radiology. 1985;156:753–755. doi:
10.1148/radiology.156.3.4023238
40. Senapati A, Isma’eel HA, Kumar A, Ayache A, Ala CK, Phelan D,
Schoenhagen P, Johnston D, and Klein AL. Disparity in spatial distribu-
tion of pericardial calcifications in constrictive pericarditis. Open Heart.
2018;5:e000835.
41. Power JA, Thompson DV, Rayarao G, Doyle M, Biederman RW. Cardiac
magnetic resonance radiofrequency tissue tagging for diagnosis of con-
strictive pericarditis: a proof of concept study. J Thorac Cardiovasc Surg.
2016;151:1348–1355. doi: 10.1016/j.jtcvs.2015.12.035
42. Bolen MA, Rajiah P, Kusunose K, Collier P, Klein A, Popović ZB, Flamm
SD. Cardiac MR imaging in constrictive pericarditis: multiparametric as-
sessment in patients with surgically proven constriction. Int J Cardiovasc
Imaging. 2015;31:859–866. doi: 10.1007/s10554-015-0616-z
43. Francone M, Dymarkowski S, Kalantzi M, Rademakers FE, Bogaert J. As-
sessment of ventricular coupling with real-time cine MRI and its value to
differentiate constrictive pericarditis from restrictive cardiomyopathy. Eur
Radiol. 2006;16:944–951. doi: 10.1007/s00330-005-0009-0
44. Giorgi B, Mollet NR, Dymarkowski S, Rademakers FE, Bogaert J. Clinically
Downloaded from http://ahajournals.org by on April 12, 2020
suspected constrictive pericarditis: MR imaging assessment of ventricular
septal motion and configuration in patients and healthy subjects. Radiol-
ogy. 2003;228:417–424. doi: 10.1148/radiol.2282020345
45. Anavekar NS, Wong BF, Foley TA, Bishu K, Kolipaka A, Koo CW, Khan-
daker MH, Oh JK, Young PM. Index of biventricular interdependence cal-
culated using cardiac MRI: a proof of concept study in patients with and
without constrictive pericarditis. Int J Cardiovasc Imaging. 2013;29:363–
369. doi: 10.1007/s10554-012-0101-x
46. Cheng H, Zhao S, Jiang S, Lu M, Yan C, Ling J, Zhang Y, Liu Q, Ma N, Yin
G, Jerecic R, He Z. The relative atrial volume ratio and late gadolinium
enhancement provide additive information to differentiate constrictive
pericarditis from restrictive cardiomyopathy. J Cardiovasc Magn Reson.
2011;13:15. doi: 10.1186/1532-429X-13-15
47. Thavendiranathan P, Verhaert D, Walls MC, Bender JA, Rajagopalan S,
Chung YC, Simonetti OP, Raman SV. Simultaneous right and left heart
real-time, free-breathing CMR flow quantification identifies con-
strictive physiology. JACC Cardiovasc Imaging. 2012;5:15–24. doi:
10.1016/j.jcmg.2011.07.010
Circ Cardiovasc Imaging. 2018;11:e007878. DOI: 10.1161/CIRCIMAGING.118.007878
48. Bauner K, Horng A, Schmitz Ch, Reiser M, Huber A. New observations
from MR velocity-encoded flow measurements concerning diastolic func-
tion in constrictive pericarditis. Eur Radiol. 2010;20:1831–1840. doi:
10.1007/s00330-010-1741-7
49. Hanneman K, Thavendiranathan P, Nguyen ET, Moshonov H, Wald R, Con-
nelly KA, Paul NS, Wintersperger BJ, Crean AM. Use of cardiac magnetic
resonance imaging based measurements of inferior vena cava cross-sec-
tional area in the diagnosis of pericardial constriction. Can Assoc Radiol J.
2015;66:231–237. doi: 10.1016/j.carj.2014.12.007
50. Amaki M, Savino J, Ain DL, Sanz J, Pedrizzetti G, Kulkarni H, Narula J,
Sengupta PP. Diagnostic concordance of echocardiography and cardiac
magnetic resonance-based tissue tracking for differentiating constrictive
pericarditis from restrictive cardiomyopathy. Circ Cardiovasc Imaging.
2014;7:819–827. doi: 10.1161/CIRCIMAGING.114.002103
51. Fenstad ER, Dzyubak B, Oh JK, Williamson EE, F Glockner J, Young PM,
Anavekar NS, Leise MD, Ehman RL, Araoz PA, Venkatesh SK. Evaluation
of liver stiffness with magnetic resonance elastography in patients with
constrictive pericarditis: preliminary findings. J Magn Reson Imaging.
2016;44:81–88. doi: 10.1002/jmri.25126
52. Chang SA, Choi JY, Kim EK, Hyun SH, Jang SY, Choi JO, Park SJ, Lee SC,
Park SW, Oh JK. [18F]Fluorodeoxyglucose PET/CT predicts response to ste-
roid therapy in constrictive pericarditis. J Am Coll Cardiol. 2017;69:750–
752. doi: 10.1016/j.jacc.2016.11.059
53. Sengupta PP, Huang YM, Bansal M, Ashrafi A, Fisher M, Shameer K, Gall
W, Dudley JT. Cognitive machine-learning algorithm for cardiac imaging:
a pilot study for differentiating constrictive pericarditis from restrictive car-
diomyopathy. Circ Cardiovasc Imaging. 2016;9. pii: e004330
54. Sengupta PP, Krishnamoorthy VK, Abhayaratna WP, Korinek J, Belohlavek
M, Sundt TM 3rd, Chandrasekaran K, Mookadam F, Seward JB, Tajik AJ,
Khandheria BK. Disparate patterns of left ventricular mechanics differenti-
ate constrictive pericarditis from restrictive cardiomyopathy. JACC Cardio-
vasc Imaging. 2008;1:29–38. doi: 10.1016/j.jcmg.2007.10.006
55. Omar AM, Vallabhajosyula S, Sengupta PP. Left ventricular twist and tor-
sion: research observations and clinical applications. Circ Cardiovasc Imag-
ing. 2015;8. pii: e003029.
56. Kaga S, Mikami T, Takamatsu Y, Abe A, Okada K, Nakabachi M, Nishi-
no H, Yokoyama S, Nishida M, Shimizu C, Iwano H, Yamada S, Tsutsui
H. Quantitative and pattern analyses of continuous-wave Doppler-
derived pulmonary regurgitant flow velocity for the diagnosis of con-
strictive pericarditis. J Am Soc Echocardiogr. 2014;27:1223–1229. doi:
10.1016/j.echo.2014.07.002
57. Gilman G, Ommen SR, Hansen WH, Higano ST. Doppler echocardio-
graphic evaluation of pulmonary regurgitation facilitates the diagnosis of
constrictive pericarditis. J Am Soc Echocardiogr. 2005;18:892–895. doi:
10.1016/j.echo.2005.03.028
58. Mahmoud A, Bansal M, Sengupta PP. New cardiac imaging algorithms to
diagnose constrictive pericarditis versus restrictive cardiomyopathy. Curr
Cardiol Rep. 2017;19:43. doi: 10.1007/s11886-017-0851-0
59. Talreja DR, Nishimura RA, Oh JK, Holmes DR. Constrictive pericardi-
tis in the modern era: novel criteria for diagnosis in the cardiac cath-
eterization laboratory. J Am Coll Cardiol. 2008;51:315–319. doi:
10.1016/j.jacc.2007.09.039
60. Schoenfeld MH, Supple EW, Dec GW Jr, Fallon JT, Palacios IF. Restric-
tive cardiomyopathy versus constrictive pericarditis: role of endo-
myocardial biopsy in avoiding unnecessary thoracotomy. Circulation.
1987;75:1012–1017.
November 2018 14