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20.2 Tuberculous Pericarditis
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Enlarged cardiothoracic ratio is seen in almost all cases of tuberculous pericardial effusion. In addition, features of active pulmonary tuberculosis is seen in 30%,
and pleural effusion in 40–60% of cases [36–39, 137, 167, 170–173, 175–177]. The
mediastinal node enlargement of tubercular pericardial effusion is not visible on a
routine chest radiograph but can be seen on computed tomography or magnetic
resonance imaging [20, 21, 112–115, 184]. Echocardiography is an accurate and
non-invasive method for diagnosis of pericardial effusion and constriction. [48, 49,
99, 100, 136, 137, 170–172, 181], Echocardiographic ndings of pericardial effu-
sion with brinous strands within the pericardial sac are commonly found in tuberculous pericardial effusion [48, 49, 106].
A computerized tomographic scan of the chest helps in diagnosis and evaluation of treatment. Pericardial effusion, thickened pericardium and enlarged mediastinal lymph nodes (i.e. enlargement >10 mm with matting and hypodense
centers) is in almost 100% of cases. Resolution of these features are evidences of
effective treatment [20, 21]. Magnetic resonance imaging reveals the extent of
pericardial inammation and myocardial involvement [38–43, 48–50, 58–67, 99,
100, 123, 150–152, 193],
“Denite” “diagnosis of tuberculous pericarditis is made when tubercle bacilli is
demonstrated in pericardial uid or on histological examination of pericardium. A
“probable” diagnosis is made when there is evidence of tuberculosis elsewhere in a
patient with unexplained pericarditis, a lymphocytic pericardial exudate with elevated ADA enzyme activity >40U/L, IFN-γ>50pg/dL or lysozyme level>6.5μg/
dL a positive gene expert test, and/or an appropriate response to antituberculosis
chemotherapy (Tables 20.2 and 20.3) [1, 6–9, 26, 55, 56, 79–93, 106, 108, 112–116,
119, 120, 144, 146–148, 153, 156, 182, 203–205].
20.2.8 Tuberculous Constrictive Pericarditis
Constrictive pericarditis is diagnosed on the basis of clinical features and conrmed
by investigations including electrocardiogram, chest X-ray, echocardiography,
computed tomographic scan and magnetic resonance imaging [3, 20–23, 29, 40–43,
Table 20.2 Diagnostic criteria for tuberculous pericarditis
Diagnostic category Criteria
“Denite or proven”
tuberculous pericarditis
“Probable or presumed”
tuberculous pericarditis
Tubercle bacilli are found in stained smear or culture of
pericardial uid; and/or
Tubercle bacilli or caseating granuloma are found on
histologic examination of pericardium
Evidence of pericarditis in a patient with tuberculosis
demonstrated elsewhere in the body; and/or
Lymphocytic pericardial exudate with elevated ADA activity,
IFN-γ, or lysozyme assay; and/or
Good response to antituberculosis chemotherapy
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Table 20.3
specicity of the indirect
biochemical methods for the
diagnosis of tuberculosis in
pericardial uid in
tuberculosis-endemic areas
Sensitivity and
Test Sensitivity Specicity
ADA enzyme activity ≥40U/L 87% 83%
IFN-γ ≥50pg/L 92% 100%
Lysozyme level>6.5μg/dL 100% 91%
ADA Adenosine DeAminase, IFN-γ Interferon Gamma
59, 65, 99, 151–153]. These investigative modalities have specic purposes while
evaluating for chronic constrictive pericarditis which are enumerated in Tables 20.1,
20.2, 20.3, and 20.4. If chronic constrictive pericarditis remains doubtful, endomyo-
cardial biopsy is useful [8, 111, 113–116, 121, 191].
20.3 Treatment
20.3.1 Tuberculous Pericardial Effusion
In tuberculosis-endemic regions, particularly in those patients with HIV infection, a
pericardial effusion is most likely to be tuberculous aetiology in the absence of an
alternative differential diagnosis [116, 117]. It is possible to achieve a denite diag-
nosis in approximately two-thirds of these patients after microbiological and histological examination [171, 172, 183, 184]. In rest of the patients, any other indirect
evidences of tuberculosis or an adequate response to empirical antituberculosis
therapy serve as support for the diagnosis. Even in the absence of a diagnosis of
tubercular pericarditis, considering the effectiveness of treatment, empirical antitubercular treatment should be started in patients from non-endemic areas [21–28,
48, 49, 55, 56, 113–119, 140, 144, 146, 148, 154, 167, 169–187, 209–213].
Symptoms and signs of acute pericarditis in this subset of patients may be sufcient
to prompt anti-tubercular therapy [11, 14, 117, 141].
Treatment of large pericardial effusion involves echo-guided pericardiocentesis
with extended intermittent drainage and early initiation of anti-tubercular chemotherapy [171, 172, 183–185, 203]. Timely institution of anti-tubercular chemotherapy has reduced mortality from 85% to 17–40% [10, 34, 66, 147]. However, the use
of adjuvant corticosteroids for the prevention of constriction and tuberculosisrelated mortality remains controversial [2, 55, 56, 61, 171, 172, 183, 184, 194].
20.3.2 Tuberculous Constrictive Pericarditis
The therapeutic strategy in patients with non-calcic constrictive pericarditis
involves a trial of anti-tubercular medication for 6–8 weeks. Patients with no
improvement and in cases of worsening symptoms, due to constrictive pericarditis,
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Table 20.4 Protocol for evaluation of suspected tuberculous pericardial effusion
Stage 1: Initial
noninvasive
Evaluation
Stage 2:
Pericardiocentesis
Stage 3:
Pericardial biopsy
Stage 4: Empiric
anti-TB
chemotherapy
Findings suggestive of pulmonary TB in Chest radiograph present in 30%
of cases.
Echocardiogram: when large pericardial effusion is present with frond-like
projections and thick “porridge-like” uid, it is suggestive of an exudate of
tubercular aetiology but not specic.
CT scan and MRI of chest are other imaging modalities: pericardial
effusion and thickening (>3mm), mediastinal and tracheobronchial
lymphadenopathy with features of tubercular aetiology (>10mm,
hypodense centers, matting) and sparing of hilar lymph nodes.
Culture of sputum, gastric aspirate and/or urine should be done to detect
mycobacterium infection. Biopsy of the right scalene lymph node should
be done if pericardial uid is not accessible and lymphadenopathy is
present.
Tuberculin skin test is not helpful in diagnosis.
Blood tests to detect predisposing conditions: HIV, white cell count, serum
globulin (if possible)
Cardiac tamponade is an absolute indication for therapeutic
pericardiocentesis.
Diagnostic pericardiocentesis should be performed in patients with
pericarditis of suspected tuberculous aetiology. Following tests are
performed on pericardial uid to diagnose tuberculosis:
Direct inoculation of pericardial uid into double-strength liquid
Kirchner culture medium (or equivalent medium), and culture for M
tuberculosis.
Tests according to Light’s criteria to differentiate between exudate and
transudate (uid and serum protein, uid, and serum LDH).
White cell count, and cytology: predominantly lymphocytic exudate
favours tubercular aetiology.
Indirect tests to detect tuberculous infection: ADA, IFN-γ, or lysozyme
assay.
Therapeutic biopsy is taken in patients in whom surgical drainage is
indicated due to clinical features of severe tamponade, recurrent tamponade
after pericardiocentesis or requiring open drainage of pericardial uid to
various other reasons.
Diagnostic biopsy is recommended in non-endemic areas, in patients with
>3weeks of illness and without aetiologic diagnosis having been reached
by other tests.
However, a diagnostic biopsy is not essential in endemic areas before
starting empiric anti-TB treatment.
Areas where TB is endemic: Empiric anti-tubercular chemotherapy is
recommended when (1) exudative pericardial effusion, after excluding
other causes such as post trauma, malignancy, and uremia and (2) score of
≥6in tuberculous pericarditis diagnostic index (see Table20.1) where
pericardiocentesis is not feasible.
Areas where TB is not endemic: There is no justication for empirical
anti-TB treatment when systematic investigation has failed to yield
evidence for tuberculous aetiology.
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as evidenced by structural and haemodynamic criteria are referred for surgical pericardiectomy [11, 22, 25, 27, 44, 61–63, 113–119, 124, 141, 171, 172, 183–185].
Calcic constrictive pericarditis is an absolute indication of pericardiectomy.
Calcic pericardium signies late presentation and can penetrate the myocardium,
causing left ventricular dysfunction that may limit surgical options [57, 68–72].
However, we have been able to remove the calcic spurs in all patients undergoing
pericardiectomy in our institution [22, 23, 27, 28].
20 Specic Disease Entities
20.3.3 Effusive-Constrictive Pericarditis
The treatment of effusive-constrictive pericarditis is not straight forward because
pericardiocentesis is not enough to relieve the impaired lling of the heart, and surgical stripping of brinous exudative coat off the visceral pericardium is difcult
and risky. In these patients, a better strategy is to give anti-tubercular drugs and
serially monitor pericardial thickness by echocardiography until it is amenable for
surgical stripping. The role of corticosteroids in such patients is not certain [9, 18].
20.3.4 Anti-Tubercular Drugs: Optimal Drug Regimen,
Dosing Frequency andTreatment Duration
There are no trials specically addressing therapeutic regimen of anti tubercular
chemotherapy for tuberculous pericarditis. Published literature and our own clinical
observations over three decades suggest that there is no evidence to administer antitubercular drugs for treatment of tuberculous pericarditis any longer than that for
extrapulmonary tuberculosis [21–27, 51, 112–119, 145, 154, 167, 173, 177, 178,
184, 187, 188, 209–212].
The guidelines for treatment of tuberculosis by WHO advocate a regimen consisting of rifampicin, isoniazid, pyrazinamide and ethambutol for at least two
months, followed by isoniazid and rifampicin for a period of 4 months (total
6months duration) [213].
According to WHO guidelines, the optimal dosing frequency for new patients
with tuberculous pericarditis is daily throughout the course of therapy (strong/high
grade of evidence of pulmonary TB). Thrice-weekly dosing [2(HRZE)3 4(HR)3]
may be an alternative to the above recommendation, provided that every dose is
directly observed, and the patient is not living with HIV or living in an HIV-prevalent
setting (conditional/high and moderate grade of evidence). Treatment regimes of
nine months or longer are not recommended as they do not give better results and
have the disadvantages of increased cost and poor compliance. Short-course chemotherapy is also effective in curing TB in HIV-infected patients [173, 184, 185, 213].
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20.3.5 Role ofCorticosteroids
Adjunctive steroids have benecial effects on mortality and morbidity in tuberculous pericardial effusion. However, published studies have failed to demonstrate any
signicant effect in prevention of reaccumulation of pericardial effusion or progression to constrictive pericarditis [2, 3, 21–28, 81, 83, 112, 113, 119, 120, 130, 131,
133, 146, 154, 164–179, 182–184].
Most guidelines recommend use of supplemental corticosteroids for treatment of
tuberculous pericarditis. However, there is no unied recommendation on the choice
of drug (prednisone, methylprednisolone, prednisolone), route (intravenous, oral,
intrapericardial) and dosage [2, 3, 21–28, 112, 113, 119, 133, 167, 170–177,
182–184].
A meta-analysis reported a signicant reduction in mortality when adjunctive
corticosteroids are used with rifampicin-containing drug regimes [119]. Despite
prompt anti-tubercular treatment and the use of corticosteroids, the disease progress
to chronic constrictive pericarditis in 30% to 60% of patients [21–29, 112, 113, 119,
133, 147, 154, 157, 167, 170–177, 182, 184].
A systematic meta-analysis by Critchley and associates in 2013 included 6 studies in patients with tuberculous pericarditis, demonstrating that corticosteroid use
was associated with a signicant reduction in mortality when trials using rifampicin- containing regimens only were analyzed [29].
In 2014, Mayosi and associates evaluated the effects of adjunctive corticosteroids and mycobacterium indicus pranii immunotherapy in patients with tuberculous pericarditis. There was no signicant difference in primary outcomes between
patients receiving either prednisolone or myocobacterium indicus pranii immunotherapy. Both prednisolone and mycobacterium indicus pranii immunotherapy were
associated with an increased incidence of HIV-associated cancer [122].
Overall, survival is dramatically increased by anti-tubercular chemotherapy in
tuberculous pericarditis. In the pre-antibiotic era, mortality was 80% to 90%. At
present the mortality rate ranges from 17% to 34% in HIV-infected individuals and
8% to 17% in rest of the patients [21–29, 48, 49, 55, 56, 112, 113, 119, 133–135,
167, 170–177, 182–184, 209–211].
20.3.6 Tuberculous Pericarditis withConcomitant HIV
The HIV epidemic has considerably altered the frequency and descriptive epidemiology of disseminated tuberculosis, which occurs more frequently and may be more
difcult to diagnose in HIV positive individuals [3, 11, 16, 25, 50–52, 129, 134,
141, 181, 186]. Due to multi-system involvement, in disseminated tuberculosis, the
clinical manifestations are protean. The presenting symptoms are fever, weight loss,
anorexia, and weakness [50, 52, 120, 142, 179, 181, 208], Approximately 25% of
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patients with tuberculous pericarditis have evidence of other organ involvement,
particularly pleuritis and lymphadenitis [10–12, 48, 64, 66].
The degree of immunodeciency, the risk of disseminated tuberculosis, other
opportunistic infections and death correlates with CD4 lymphocyte cell count [12,
122, 125]. The cornerstone of treatment of HIV infection is highly active antiretro-
viral therapy (HAART), which has been shown to reduce the mortality and morbidity of patients with advanced HIV disease [120–123, 139]. The goal of HAART is
maximal and durable viral suppression to enable preservation and restoration of the
immune system [125].
The concerns with HAART are complex drug interactions, adverse reactions,
non-adherence to treatment, and drug malabsorption [125]. Some investigators have
reported paradoxical deterioration with HAART therapy due to immune reconstruction inammatory syndrome in 11% to 36% of patients [133, 214]. Secondary preventive therapy with isoniazid reduces the recurrence of tuberculosis in HIV-infected
patients [30].
20 Specic Disease Entities
20.3.7 Effusive-Constrictive Pericarditis
Effusive-constrictive pericarditis is a unique clinical-haemodynamic syndrome of
multifactorial aetiology combining elements of pericardial effusion/tamponade and
constriction. This variety of constrictive pericarditis was mentioned by Wood,
Spodick and Kumar, and was emphasized by Hancock [31, 64–67, 71, 74, 195].
The clinical presentation may be secondary to pericardial effusion with cardiac
tamponade or pericardial constriction causing impaired diastolic lling [64, 71–74,
167, 177, 179, 186, 189–191]. In addition to pericardial thickening and diastolic
cardiac constriction, there is uid collection between the parietal and visceral pericardium. The effusive-constrictive pericarditis most likely represents an intermediate transition from acute pericarditis with pericardial effusion to pericardial
constriction [65].
The reported incidence of effusive-constrictive pericarditis in patients with pericardial effusion is approximately 4% to 5% but varies from 1% to 22% in different
series [3, 11, 16, 22–26, 50, 52, 120, 129, 134, 141, 142, 179, 181, 186, 190, 208],
The aetiologic spectrum is diverse, with the most common being idiopathic, neoplasia, radiation, tuberculosis, pericardiotomy, penetrating trauma, Lasa fever, salmonella and streptococcal infection [214, 215]. In developing countries, tuberculosis
accounts for 28%–70% cases of effusive-constrictive pericarditis [10, 11, 22–26,
34, 36, 38, 39, 57, 64, 65, 77, 83, 112, 113, 118, 125, 142, 149, 214–216]
The clinical, radiologic, haemodynamic, and echocardiographic ndings are
often mixtures of those associated with effusion and constriction [10, 11, 22–27].
The cardiopericardial silhouette may be larger on a chest roentgenogram than in
those with purely chronic constrictive pericarditis.
It has an insidious clinical course, ranging from months to years. An inammatory effusion typically dominates early, with constriction manifesting at a later
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stage. These patients are often identied when their haemodynamics fail to improve
following pericardiocentesis. The presence of additional constriction is frequently
overshadowed. In addition to physical signs of pericardial effusion, a diastolic
knock may be detected on palpation, and third heart sound [157] on auscultation.
Usually the visceral pericardium is maximally involved. An accepted denition
is failure of reduction of right atrial, right ventricular end-diastolic and pulmonary
capillary wedge pressures by at least 50% to a level below 10mmHg when intrapericardial pressure is reduced to almost zero by pericardiocentesis and/or all
detectable uid is removed [174, 191].
Initially the right atrial, pulmonary wedge, and intrapericardial pressures are
equally increased, and there is a prominent X descent with no prominent Y descent
in the right atrial pressure trace, and no prominent early diastolic dip in right ventricular pressure tracing. When all the pericardial uid is removed by pericardiocentesis, intrapericardial pressure falls to near zero, but the right atrial, right ventricular
diastolic, and pulmonary wedge pressures remain elevated. In addition, a prominent
Y descent appears in the right atrial pressure trace, and a large early diastolic dip
appears in the right ventricular pressure record. Effusive-constrictive pericarditis
may be missed if haemodynamics is not measured carefully after pericardiocentesis. Diagnosis is conrmed on pericardial uid biochemistry and histopathology.
Sagrista-Sauleda and associates reported on a series of more than 1000 patients
with pericarditis, 218 of whom had cardiac tamponade and underwent pericardiocentesis. In 15 of these patients, the right atrial and right ventricular end-diastolic
pressure remained elevated with dip-plateau morphology after pericardiocentesis,
thus establishing a new clinical entity: effusive-constrictive pericarditis [177–179].
In the Stanford series, there were 23 such cases with variable aetiology: radiotherapy (n=10), pericarditis (n=7), connective tissue disease (n=3), infections (n=2),
and neoplasia (n=1) [10, 11, 22–26, 31, 34, 36, 38, 39, 57, 64, 65, 77, 83, 112, 113,
118, 125, 142, 149, 215, 216],
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20.3.8 Management
The published literature does not narrate any guidelines on management of effusiveconstrictive pericarditis. The recent European Society of Cardiology guidelines on
management of pericardial diseases were also silent on the subset of patients with
effusive-constrictive pericarditis, presumably due to paucity of data on the subject
[3, 112].. The possible reasons are varied etiopathogenesis, diagnostic difculties,
patterns of evolution and lack of available data in the western world [3, 112, 126,
149, 186].
Generally, management is tailored to specic causes, if known. However, the
unresolved issues are falsely negative pericardial uid culture, and difculties in
establishing a bacteriological or histological diagnosis. One has, therefore, to rely
on pericardial tissue biopsy, microbiology or cytology [3, 22–26, 36, 37, 39, 47, 48,
55, 57, 103, 128, 132, 134, 156–160].
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20.3.9 Treatment Based onAetiology
The management of tubercular effusive-constrictive pericarditis has been elaborated
upon under tubercular pericarditis. In idiopathic cases, anti-inammatory treatment
may be used in an attempt to avoid pericardiectomy, but no guidance is available in
regard to the preferred approach. In idiopathic and post pericardiotomy cases with
tamponade and effusive-constrictive physiology, we favour a course of corticosteroids and colchicine, as outlined for the medical treatment of constriction.
Pericardiectomy is ultimately required in many of these patients [1, 3, 6, 8, 36, 37,
44, 103, 112, 113, 119, 149, 156–160, 167, 177, 179, 181, 186, 189–191, 205, 206].
20.3.10 Treatment Based onTiming ofPresentation
andResponse toMedication
Salami and colleagues proposed the following management algorithm [190]. Echo
guided pericardiocentesis is the rst step in patients with cardiac tamponade or
imminent tamponade. Then pericardiostomy and pericardial biopsy should be performed for bacteriological and histological examination. Next guiding point is the
duration of illness. Pericardiostomy and biopsy are advised in patients without tamponade of more than one year duration. These authors recommend pericardiectomy
only when there is persistent evidence of constriction even after a trial of medical
treatment for 6–8weeks. However, presence of constrictive pericardial thickening
with calcication is considered as an absolute indication for pericardiectomy [190].
These authors have recommended a more collaborative research for further
improvement of this management algorithm. The current ongoing multicentre study
on the role of steroids in prevention of constrictive pericarditis, involving centres in
South Africa, Nigeria and other African countries, is one such study [115, 116, 119].
20.3.11 Specic Surgical Manoeuvers
inEffusive-Constrictive Pericarditis
The importance of recognizing the haemodynamic syndrome of tamponade and
constriction characteristic of effusive-constrictive pericarditis lies in the contribution of the visceral layer of the pericardium to the pathogenesis of constriction and
its surgical removal, as highlighted by Harrington for a good clinical result [74].
However, due to risk of haemorrhage, it is sometimes surgically challenging to perform pericardiectomy in the presence of a imsy, brinous visceral pericardium. In
few cases considered as transient effusive-constrictive pericarditis, patients recover
with medical treatment alone [26, 138, 175, 176, 178, 186, 194, 196].
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20.3.12 Relapsing / Recurrent Pericarditis
The published literature uses both terminologies interchangeably, i.e. relapsing or
recurrent pericarditis [3, 99, 112, 193, 196–199]. Two types are recognized:
• Incessant type: There is a relapse on discontinuation of, or attempts to wean
patients from, anti-inammatory drugs (e.g. indomethacin, aspirin, ibuprofen) in
less than six weeks. The mean number of relapses has been demonstrated to be
much higher in those receiving adjunctive corticosteroids [3, 4, 32, 75, 80, 84,
85, 110, 126].
• Intermittent type: In this type, patients have symptom-free intervals of more than
six weeks without any treatment.
The precise frequency of relapsing pericarditis is unknown because of the inadequate number of patients experienced by investigators. The literature documents an
incidence between 8% and 80% with an average of 24%, suggesting non-uniformity
of diagnosis [4, 32, 196–199].
Viral infections, post-myocardial and post-pericardial injury syndromes, and
idiopathic aetiologies have been variously reported by different investigators. As
pointed out by Sagirsta and Galve, tuberculosis, bacterial/purulent, and neoplastic
pericarditis are not recognized causes of relapsing pericarditis [167, 177–179], An
autoimmune aetiology has been suggested by some investigators because of
response to corticosteroids and other immunosuppressants and the presence of autoantibodies [10, 53, 54, 112, 175, 190, 201].
The CORE trial suggested the following criteria for establishing the diagnosis of
relapsing pericarditis [75, 77, 78, 83–97]. A documented rst episode of acute pericarditis with evidence of recurrent pericardial chest pain plus one of the following
is required for establishing diagnosis of relapsing pericarditis: fever, pericardial
friction rub, electrocardiographic changes typical of acute pericarditis, pericardial
effusion on echocardiography, leucocytosis or raised erythrocyte sedimentation rate
or C-reactive protein concentration. Cardiac computed tomography may demonstrate a thickened pericardium and pericardial effusion [100, 101]. Delayed gadolinium enhancement of the pericardium by cardiac magnetic resonance imaging is a
reliable and objective method to detect pericardial inammation [100, 101, 123].
The rst symptom of recurrent pericarditis usually occurs within 18 to 20months
after the initial attack [83, 97]. Usually the initial attack of acute pericarditis is the
most severe when compared to subsequent episodes. It is associated with a sharp
and progressive chest pain which worsens on recumbency and is relieved by learning forward. Generally, patients do not have any symptoms between attacks.
However, some patients may experience a persistent or chronic course [112, 175,
190, 200].
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20.3.13 Treatment
The goal of treatment is restriction of physical activity, symptomatic relief and prevention of recurrences [54, 100]. Although tamponade, constrictive pericarditis and
myocardial dysfunction are not common in patients with relapsing pericarditis, frequent recurrences can severely impair the quality of life. Idiopathic and viral relapsing pericarditis have been treated with aspirin (650mg PO q 4–6 hours), other
NSAIDs (e.g. Ibuprofen 200–400mg q 4–6-hourly, Indomethacin 25–50mg q 6–8hourly, or acetaminophen (500–750mg q 4–6hours), alone or in combination [54,
196–199, 201].
The CORE trial demonstrated that colchicine was effective in preventing recurrent pericarditis if given after a rst episode of acute pericarditis or after a rst episode of recurrent pericarditis. It is recommended to start with a dose of 2–3mg/day
followed by a maintenance dose of 0.5–1.0mg/day for at least one year after the last
episode of pericarditis. The use of corticosteroids in the treatment of relapsing pericarditis is controversial. Although current guidelines recommend limited use of corticosteroids in treatment of relapsing pericarditis, they are administered in 60–90%
of patients in most clinical scenarios [75, 93–97].
The Mayo clinic group recommends corticosteroid treatment only to those
patients in whom colchicine and NSAIDs are contraindicated or in patients with
recurrent pericarditis of rheumatologic or autoimmune aetiology. Imazio etal. and
the Mayo Clinic Group have reported the benecial effects of low-dose corticosteroids with slow tapering in treatment of relapsing pericarditis [89–92]. Although
pericardiectomy is not always effective in prevention of recurrences, it should be
considered in patients with severe relapsing pericarditis that has not responded to
standard non surgical management [51, 102–104, 112].
20.3.14 Occult Constrictive Pericarditis
Bush and associates in 1977 rst observed that in some patients the physical and
haemodynamic features of constriction were not apparent in their baseline state but
were brought about by rapid volume loading. They labelled this syndrome as occult
constrictive pericarditis. The initial report was based on 19 patients with mostly
idiopathic pericarditis. Eleven patients had all pericardial adhesions removed surgically and showed improvement in fatigue and dyspnoea [13, 186, 202].
The sensitivity and specicity of response to volume loading and the role of
pericardiectomy in treating this condition are not well established. Sagrista-Souleda
advocated caution against volume loading as part of routine evaluation of patients
with suspected pericardial constriction [186, 202].
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