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5 Clinical Challenges andDiagnostic Dilemma ofChronic Constrictive Pericarditis
rate and torsional myocardial deformation, in radial, longitudinal and circumferential planes. Additionally, speckle tracking, can assess septal-to-lateral rotation displacement (SLRD) which can quantify the rocking or swinging motion of the heart
[29–31, 36, 53–59, 80–91, 99–101, 105, 110–122].
Although American and European guidelines on the diagnosis and management
of pericardial diseases have been laid down, the role of multimodality imaging has
not been clearly laid down [1, 72]. Additionally, routine clinical application of the
above-mentioned guidelines may indeed be difcult because of (a) cost effectiveness, (b) exposure to iodinated contrast agent or ionizing radiation, (c) non—gated
CT limiting the evaluation of the pericardium because of motion artifacts, and (d)
imaging that can be challenging in patients with arrhythmia or poor breath holders
and in hemodynamically unstable patients.
Computed tomography and cardiac magnetic resonance are superior to echocardiography for detecting and distribution of thickness of the pericardium, calcication of the pericardium, pericardial mass, loculated pericardial effusion, and dening
the distribution of pericardial thickening. These imaging modalities are less operator dependent and are useful in determining the optimal surgical approach for pericardial resection including the redo pericardiectomy (Figs.5.5, 5.6, and 5.7) [17,
26–28, 62, 64, 100, 101, 112–116].
The normal pericardium is 1–2mm thick, where in constrictive pericarditis, the
pericardial thickness varies between 4 and 20mm. Computed tomography has the
advantage of detection of pericardial calcication but has the following limitations:
(i) inability to measure the exact pericardial thickness in the presence of minimal/
a
d
Fig. 5.5 Frontal chest radiograph (a) shows plaque-like calcication along the diaphragmatic
(white arrowhead) and left border (black arrowhead) areas of the heart. Note is made of right pleural effusion. Four-chamber (b), two-chamber (c) and short axis (d) reconstructions of CT angiography and volume rendered images (e and f) show extensive pericardial calcication along the
diaphragmatic surface and free walls of both ventricles. Note is made of biatrial dilatation and
tubular ventricles. [LA left atrium, LV left ventricle, RA right atrium, RV right ventricle]
b
e
c
f
cd
ac
5 Clinical Challenges andDiagnostic Dilemma ofChronic Constrictive Pericarditis
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a
Fig. 5.6 Volume rendered images (a–c) show extensive pericardial calcication predominantly
along the free wall and diaphragmatic surface of bilateral ventricles and the atrioventricular
groove. Volume rendered image (d) shows thick calcic spurs inltrating into the right ventricular
myocardium. [LA left atrium, LV left ventricle, RA right atrium; RV right ventricle]
b
b
Figs. 5.7 Four chamber MRI cine image (a) shows tubular ventricles with indentation (thick
white arrow) along the LV free wall. Short axis cine image (b) shows thin pericardial collection
with thickened pericardium (arrowheads) adherent along the inferolateral wall of LV.Short-axis
image from tagged cine sequence (c) shows adherence and immobility of the pericardialmyocardial interface
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5 Clinical Challenges andDiagnostic Dilemma ofChronic Constrictive Pericarditis
mild pericardial effusion (ii) unless gated, computed tomography cannot show functional changes associated with constriction [26–28, 102].
Since constrictive pericarditis is a hemodynamic diagnosis, the role of multimordality imaging is complimentary and at least two supportive diagnostic modalities are essential to conrm the diagnosis.
Several investigators including ourselves have demonstrated that a combination
of a thickened pericardium with or without calcication and a dilated inferior caval
vein is highly sensitive for conrmation of diagnosis of constrictive pericarditis. In
patients with symptoms suggestive of constrictive pericarditis, associated mediastinal lymphadenopathy i.e. enlargement >10mm with matting and hypodense centers
on abdominal computed tomography is also supportive of the diagnosis of constrictive pericarditis. The septal bounce in constrictive pericarditis may also be detected
by 4-dimensional computed tomography [1]. However, the limitations of computed
tomography include the use of intravenously administered iodinated contrast agents,
ionizing radiations, and inferior temporal resolution [1].
Cardiac magnetic resonance is a second-line imaging investigation of choice for
both structural and functional evaluation in chronic constrictive pericarditis. Unlike
non-gated computed tomography, which demonstrates only morphological changes,
Cardiac magnetic resonance has the ability to demonstrate both morphological
changes, namely dilation of the superior and inferior caval veins, left atrium, ventricular longation, myocardial atrophy and brosis and functional changes namely,
constriction, septal bounce, ventriculo-ventricular interaction with evidence of a
attened interventricular septum or its convexity towards left ventricle in enddiastole, suggesting high right ventricle pressure [26–28, 43–45, 101, 102].
As stated by Hurrell, “a thickened and calcied pericardium does not necessarily
cause constriction”. Similarly, patients with normal pericardial thickness on computed tomography and magnetic resonance imaging may still have constrictive
physiology [44, 131]. Therefore, clinical evidence of impaired diastolic lling along
with pericardial thickening and/or calcication and other associated morphological
ndings − such as dilated superior and inferior caval vein, dilated left atrium, attened interventricular septum, elongated ventricles with or without pleural effusion
on computed tomography/cardiac magnetic resonance imaging − should be used to
diagnose chronic constrictive pericarditis [26–28, 43–45, 101, 102, 132].
Since pericardial constriction can occur in patients with histologically normal
pericardial thickness, other ancillary ndings on multimordality imaging need documentation, including dilated superior and inferior caval vein, biatrial enlargement,
attened interventricular septum, elongated ventricles with or without pleural effusion [26–28, 43–45, 101, 102, 132].
Before the advent of Doppler era of hemodynamics, invasive cardiac catheterization data remained the standard method of diagnosis of constriction.Traditionally,
elevated atrial pressures, equalization of end-diastolic pressures in all cardiac chambers, and dip-and-plateau or square root sign of ventricular diastolic pressure have
been considered as the hallmark hemodynamic features of chronic constrictive pericarditis [43]. It is noteworthy that despite the difference in pathophysiologic mechanisms of constriction and restriction, considerable overlap exists in the parameters
of these entities.
5.1 Salient Hemodynamic Features ofChronic Constrictive Pericarditis
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Vaitkus and Kussmaul analyzed the predictive accuracy of three catheterization -derived hemodynamic criterions to diagnose constriction. A difference
between left- and right ventricular end-diastolic pressure of 5mmHg or less, a
right ventricular peak systolic pressure of 50mmHg or less, and a ratio of right
ventricular end- diastolic pressure to right ventricular systolic pressure of >1.3
carry 70%, 85% and 75% sensitivity respectively for diagnosis of constrictive
pericarditis [148]. Several investigators have demonstrated that pressure of all
three criterions is diagnostic or constrictive pericarditis in 90–95% of patients
[43, 136, 148].
Talreja and associates analysed an alternative method of demonstrating ventricular interdependence by measuring the ratio of right-to-left ventricular systolic area
during inspiration and expiration. This systolic area index had a sensitivity of 97%
and specicity of 100% for the identication of patients with surgically proven
constriction [134]. Presently, this is the most specic cardiac catheterization derived
nding for differentiating constrictive and restrictive physiologies.
Thus, patients with chronic constrictive pericarditis have symptoms and signs of
right heart failure disproportionate to left ventricular dysfunction or valvular heart
disease. The challenge remains to determine whether the symptomatology are secondary to pericardial restraint, myocardial restriction or both [44, 123, 126, 131,
137, 148].
If the diagnosis cannot be conrmed despite utilizing multimordality imaging
with invasive hemodynamic studies, endomyocardial biopsy may be performed for
diagnostic conrmation [21, 43, 105, 126–131, 137, 148].
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5.1 Salient Hemodynamic Features ofChronic
Constrictive Pericarditis
Prior to the advent of the Doppler era of haemodynamics, invasive haemodynamic
data remained the gold standard for conrmation of diagnosis of constriction. The
catheterization derived -criterions are as follows:
• Diastolic pressure plateau (equalization of end-diastolic pressure in all car-
diac chambers).
In constrictive pericarditis, there is failure of transmission of the intrathoracic
pressure variation into the ventricles. Hence, the diastolic pressures are the same
in the right and left ventricles within a 5mm range.
• Elevated right ventricular systolic pressure
As the diastolic pressures are elevated, the systolic pressure of the right ventricle
gets modestly elevated. In constrictive pericarditis, however, the right ventricular
systolic pressure mostly remains below 45–50mmHg.
• Right ventricular end-diastolic to right ventricular systolic pressure ratio
With severity of the disease progression, the right ventricular end-diastolic pres-
sure gets elevated. The right ventricular end-diastolic to systolic pressure ratio of
more than one-third in associated with 93% sensitivity.
• Left ventricular rapid lling wave
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5 Clinical Challenges andDiagnostic Dilemma ofChronic Constrictive Pericarditis
In constrictive pericarditis, there is rapid lling of the left ventricle in early dias-
tole. This is reected in the lling wave of 7mmHg or more.
• Lack of respiratory variation of right atrial pressure
In constrictive pericarditis, the right atrial pressure is elevated and does not vary
with respiration. The variation is less than 3mmHg.
• Left ventricular and right ventricular interdependence
With inspiration, the right ventricular systolic pressure increases and the left
ventricular systolic pressure decreases.
• The ratio of right ventricular to left ventricular systolic area index during
inspiration and expiration
This represents ventricular interdependence. As demonstrated by Talreja and
associates, this systolic area index is associated with a sensitivity of 97% and
specicity of 100% to diagnose constrictive pericarditis [134].
The diagnosis and management of pericardial diseases in general and chronic constrictive pericarditis in particular remain challenging because of the varied clinical
manifestations, inadequate number of patients and volume of clinical data, and the
absence of guidelines by the American heart association, American college of cardiology, Society Of Thoracic Surgeons, USA, and the European society of cardiology [1, 72].
Due to overlapping clinical manifestations, constrictive pericarditis and restrictive cardiomyopathy including endomyocardial brosis are difcult to diagnose
[25]. Doppler derived transmitral ow velocity is an useful parameter to differentiate the two disease entities [35, 36]. Patients with constrictive pericarditis exhibit
>25% respiratory variation of mitral inow velocity, whereas this phenomenon is
absent in restrictive cardiomyopathy [88–91]. In advanced cases of constrictive
pericarditis with elevated right atrial pressures, the respiratory variation is manifested by lling up the head.
On tissue Doppler imaging, the early diastolic mitral annular velocity (Ea) is
reduced to less than 8cm/s in restrictive cardiomyopathy, whereas it remains within
normal range in constrictive pericarditis [29–35, 37, 42, 100].
In constrictive pericarditis, rapid progression of early diastolic ow is preserved,
whereas in restrictive cardiomyopathy it is reduced on M-mode echocardiography.
A slope greater than 100 cm/s also distinguishes the two disease entities [88–
91, 100].
Restrictive cardiomyopathy is frequently associated with pulmonary hypertension (i.e. systolic pulmonary artery pressure more than 50mmHg), whereas it is less
than 50mmHg in cases of constrictive pericarditis. However, the above-mentioned
diagnostic criterions have specicity ranging between 24% and 57% in differentiating constrictive from restrictive physiology [43].
In constrictive pericarditis, during inspiration there is inspiratory rise of right
ventricular systolic pressure and fall of left ventricular systolic pressure. This phenomenon of dynamic respiratory variations indicating increased ventricular interdependence is associated with more than 90% sensitivity in cases of constrictive
physiology compared to restrictive physiology [43].
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61
Cardiac biomarkers, namely B-type natriuretic peptide more than 600pg/ml is
associated with restrictive cardiomyopathy whereas in constrictive pericarditis the
level is below 200pg/ml.
Clinically, constrictive pericarditis is suspected in a patient with signs and symptoms of right-sided cardiac failure disproportionate to left-sided heart diseases.
Analysis of the published series substantiates the notion that it is not possible to
diagnose cases of constrictive pericarditis using single approach. Additionally, at
least two studies are essential to distinguish the two disease entities in the majority
of cases. A combination of Doppler echocardiography with either computed tomography, Magnetic resonance imaging and/or hemodynamic studies are essential to
conclusively establish the diagnosis of constrictive pericarditis.
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