Diagnostic issues in the clinical management of pericarditis

Cardiology Department, Maria Vittoria Hospital, Torino, Italy.
International Journal of Clinical Practice (Impact Factor: 2.57). 09/2010; 64(10):1384-92. DOI: 10.1111/j.1742-1241.2009.02178.x
Source: PubMed
ABSTRACT
To review the current major diagnostic issues on the diagnosis of acute and recurrent pericarditis.
To review the current available evidence, we performed a through search of several evidence-based sources of information, including Cochrane Database of Systematic Reviews, Clinical Evidence, Evidence-based guidelines from National Guidelines Clearinghouse and a comprehensive Medline search with the MeSH terms 'pericarditis', 'etiology' and 'diagnosis'.
The diagnosis of pericarditis is based on clinical criteria including symptoms, presence of specific physical findings (rubs), electrocardiographical changes and pericardial effusion. Although the aetiology may be varied, most cases are idiopathic or viral, even after an extensive diagnostic evaluation. In such cases, the course is often benign following anti-inflammatory treatment, and management would be not affected by a more precise diagnostic evaluation. A triage of pericarditis can be safely performed on the basis of the clinical and echocardiographical presentation. Specific diagnostic tests are not warranted if no specific aetiologies are suspected on the basis of the epidemiological background, history and presentation. High-risk features associated with specific aetiologies or complications include: fever > 38 degrees C, subacute onset, large pericardial effusion, cardiac tamponade, lack of response to aspirin or a NSAID.
A targeted diagnostic evaluation is warranted in acute and recurrent pericarditis, with a specific aetiological search to rule out tuberculous, purulent or neoplastic pericarditis, as well as pericarditis related to a systemic disease, in selected patients according to the epidemiological background, presentation and clinical suspicion.

Full-text

Available from: Antonio Brucato, Jan 18, 2015
Diagnostic issues in the clinical management
of pericarditis
M. Imazio,
1
D. H. Spodick,
2,3
A. Brucato,
4
R. Trinchero,
1
G. Markel,
5
Y. Adler
5
Introduction
In clinical practice, the diagnosis of acute and recur-
rent pericarditis is easily made by clinical examina-
tion, ECG and echocardiography, while it is much
more complicated to reach a detailed aetiological
diagnosis (1,2). Many causes of pericarditis can be
listed (Table 1); however, in developed countries
most cases still remain idiopathic or viral (either pre-
sumed or finally diagnosed). In such cases with a
generally benign course, empiric anti-inflammatory
therapies are prescribed and a more precise diagnos-
tic evaluation does not affect the subsequent clinical
management (3–6). At presentation, specific features
have been associated with a higher risk of specific
aetiology and complications (5–7), and a probabilis-
tic approach has been suggested for the triage of
pericarditis.
Aim of this paper especially is to review critically
the major diagnostic issues in the clinical manage-
ment of acute and recurrent pericarditis.
how to perform the clinical diagnosis of pericarditis,
how to exclude concomitant myocardial involve-
ment,
how to identify the patient at risk of complications
or specific aetiology,
the aetiological search and the role of pericardio-
centesis and pericardial biopsy.
The clinical diagnosis of pericarditis
In clinical practice, the diagnosis of pericarditis is
based on clinical criteria: typical chest pain, pericar-
dial friction rub, widespread ST-segment elevation
and pericardial effusion. At least two of four should
be present for the diagnosis of acute pericarditis
1
Cardiology Department, Maria
Vittoria Hospital, Torino, Italy
2
Medical Services, St Vincent
Hospital, Worcester Medical
Center, Worcester, MA, USA
3
Department of Medicine,
St Vincent Hospital, University
of Massachusetts, Worcester,
MA, USA
4
Department of Internal
Medicine, Ospedali Riuniti,
Bergamo, Italy
5
Cardiac Rehabilitation
Institute, Chaim Sheba Medical
Center, Tel-Hashomer and
Sackler Faculty of Medicine,
Tel-Aviv, Israel
Correspondence to:
M. Imazio, MD, FESC,
Cardiology Department, Maria
Vittoria Hospital, Via Cibrario
72, 10141 Torino, Italy
Tel.: + 39 011 4393391
Fax: + 39 011 4393334
Email:
massimo_imazio@yahoo.it
Disclosures
None.
SUMMARY
Aims: To review the current major diagnostic issues on the diagnosis of acute and
recurrent pericarditis. Methods: To review the current available evidence, we per-
formed a through search of several evidence-based sources of information, includ-
ing Cochrane Database of Systematic Reviews, Clinical Evidence, Evidence-based
guidelines from National Guidelines Clearinghouse and a comprehensive Medline
search with the MeSH terms ‘pericarditis’, ‘etiology’ and ‘diagnosis’. Results: The
diagnosis of pericarditis is based on clinical criteria including symptoms, presence
of specific physical findings (rubs), electrocardiographical changes and pericardial
effusion. Although the aetiology may be varied, most cases are idiopathic or viral,
even after an extensive diagnostic evaluation. In such cases, the course is often
benign following anti-inflammatory treatment, and management would be not
affected by a more precise diagnostic evaluation. A triage of pericarditis can be
safely performed on the basis of the clinical and echocardiographical presentation.
Specific diagnostic tests are not warranted if no specific aetiologies are suspected
on the basis of the epidemiological background, history and presentation. High-risk
features associated with specific aetiologies or complications include: fever
>38C, subacute onset, large pericardial effusion, cardiac tamponade, lack of
response to aspirin or a NSAID. Conclusions: A targeted diagnostic evaluation is
warranted in acute and recurrent pericarditis, with a specific aetiological search to
rule out tuberculous, purulent or neoplastic pericarditis, as well as pericarditis
related to a systemic disease, in selected patients according to the epidemiological
background, presentation and clinical suspicion.
Review Criteria
To review the current available evidence in the
aetiological diagnosis of acute and recurrent
pericarditis, we performed a search of the following
evidence-based sources: Cochrane Database of
Systematic Reviews, Clinical Evidence, Evidence-
based guidelines from National Guidelines
Clearinghouse and a comprehensive Medline search
with the MeSH terms ‘pericarditis’, ‘etiology’ and
‘diagnosis’.
Message for the Clinic
A routine aetiological search is not warranted in all
cases. A targeted aetiological search should be
directed to the commonest aetiologies on the basis
of the epidemiological issues, clinical background or
specific presentations. Specific aetiologies are
generally associated with specific clinical features at
presentation that are also possible predictors of
complications during follow up. Clinicians should
rule out tuberculous, purulent or neoplastic
pericarditis, as well as pericarditis related to a
systemic disease.
REVIEW ARTICLE
ª 2010 Blackwell Publishing Ltd Int J Clin Pract, September 2010, 64, 10, 1384–1392
1384 doi: 10.1111/j.1742-1241.2009.02178.x
Page 1
(2–5,7–9). Evidence of elevated inflammatory mark-
ers (e.g. C-reactive protein) is confirmatory for the
diagnosis of pericarditis (Table 2) (2,9–11).
Diagnostic evaluation including physical ausculta-
tion, ECG, transthoracic echocardiography, markers
of inflammation (e.g. C-reactive protein) and myo-
cardial lesion (creatine-kinase, troponin) and chest
X-ray is mandatory in all cases of suspected pericar-
ditis (class I indication according to the 2004 guide-
lines of the European Society of Cardiology) (12).
Concomitant myocardial involvement (the
spectrum of myopericardial inflammatory
syndromes)
In the clinical setting, some cases of ‘pericarditis with
troponin elevation’ have been reported (13–15), being
the expression of concomitant myocardial involve-
ment. At the same time, widespread ST-segment ele-
vation has been considered the hallmark of acute
pericarditis (16–18) (Figure 1), but the pericardium is
electrically silent, being ST-elevation the expression of
subepicardial myocardial involvement. ST-segment
elevation has been reported from 60% to 90% of con-
secutive cases with acute pericarditis (7,15) and in a
higher number of cases with troponin elevation
(90–98%) (15,19). Thus, it is now clear that mixed
myocardial and pericardial involvement is probably
present in the majority of cases with pericarditis.
Myocarditis and pericarditis share common aetiologi-
cal agents, and thus a spectrum of myopericardial
inflammatory syndromes can be encountered in clini-
cal practice ranging from pure pericarditis towards
forms with increasing myocardial involvement: myo-
pericarditis (predominant pericarditis), perimyocard-
itis (predominant myocarditis) and pure myocarditis
(19–21). This is not an academic classification,
because forms with predominant pericarditis have a
good clinical prognosis without evolution towards
heart failure, constrictive pericarditis or increasing
recurrence rates (15,19–21). Subtle myocardial
involvement beyond ECG changes, troponin eleva-
tion, wall motion abnormalities on echocardiography
(usually discordant with ECG changes unlike acute
coronary syndromes) can be detected by cardiac mag-
netic resonance imaging (MRI) (19,20). On this basis,
a clinical diagnosis of myopericarditis can be made in
patients with diagnostic criteria for acute pericarditis
and elevation of markers of myocardial lesion and or
new abnormalities of the wall motion on echocardi-
ography. It is common that these wall motion abnor-
malities are discordant or poorly related with ECG
changes. A non-invasive diagnosis can be achieved by
Table 1 Aetiology of pericarditis: a simple basic classification is infectious (more than two of three cases) and not-
infectious forms (percentages refer to unselected cases)
Infectious pericarditis (2 3 of cases)
Viral
[most common: Echovirus and Coxsackievirus (usual), Influenza, EBV, CMV, Adenovirus, Varicella, Rubella, Mumps, HBV, HCV,
HIV, Parvovirus B19 and Human HerpesVirus 6 (increasing reports]
Bacterial
[most common: tuberculous (4–5%), Coxiella burnetii, other bacterial rare may include Pneumo-, Meningo-, Gonococcosis,
Haemophilus, Staphylococci, Chlamydia, Mycoplasma, Legionella, Leptospira, Listeria]
Fungal
(rare: Histoplasma more likely in immunocompetent patients, Aspergillosis, Blastomycosis, Candida more likely in
immunosuppressed host)
Parasitary
(very rare: Echinococcus, Toxoplasma)
Non-infectious pericarditis (1 3 of cases)
Autoimmune pericarditis
(< 10%)
Pericardial injury syndromes
(Postmyocardial infarction syndrome, Postpericardiotomy syndrome, Post-traumatic pericarditis)
Pericarditis in systemic autoimmune diseases
(more common in systemic lupus erythematosus, rheumathoid arthritis, Sjo
¨
gren
syndrome, systemic sclerosis, systemic vasculitides, Behc¸et syndrome, and familial Mediterranean fever)
Autoreactive pericarditis
Neoplastic pericarditis
(5–7%)
Primary tumours
(rare, above all pericardial mesothelioma)
Secondary metastatic tumours
(common, above all lung and breast cancer, lymphoma)
Metabolic pericarditis
(common:uremia, myxedema, other rare)
Traumatic pericarditis
(
rare
)
Direct injury
(penetrating thoracic injury, oesophageal perforation)
Indirect injury
(non-penetrating thoracic injury, radiation injury)
Drug-related pericarditis
(rare):
Procainamide, hydralazine, isoniazid and phenytoin
(lupus-like syndrome),
Penicillins
(hypersensitivity
pericarditis with eosinophilia),
Doxorubicin and daunorubicin
(often associated with a cardiomyopathy may cause a pericardiopathy).
Major causes of recurrences still remain idiopatic, other include viral, autoimmune forms, inadequate treatment of the index attack (in
relation to doses and or length of therapy) and neoplasia. EBV, Epstein-Barr virus; CMV, cytomegalo virus; HBV, hepatitis B virus;
HCV, hepatitis C virus; HIV, human immunodeficiency virus.
Diagnostic issues of pericarditis 1385
ª 2010 Blackwell Publishing Ltd Int J Clin Pract, September 2010, 64, 10, 1384–1392
Page 2
cardiac MRI with typical patterns of gadolinium late
enhancement (subepicardial or mid wall septal or lat-
eral) that can be differentiated by ischemic necrosis
(20). In some cases, exclusion of an acute coronary
syndrome is mandatory according to the clinical pre-
sentation, suspicion (age, coronary risk factor pro-
file), and coronary angiography and cardiac MRI are
useful diagnostic tests to rule out ST-segment acute
myocardial infarction and acute myocardial infarction
with ‘normal coronary arteries’.
Identification of high-risk patients: triage of
pericarditis
A number of clinical features have been related to an
increased risk of specific aetiology (non-idiopathic,
non-viral) or complications (recurrences, cardiac
tamponade and constrictive pericarditis) (2–
4,16,17,22–31). These clinical features may include
fever > 38 C (16,22,23), subacute onset (symptoms
developing during a period of several days or weeks)
(17,24,25), immunodepression (25,26), trauma
(16,23,25), oral anticoagulant therapy (16,27), myo-
pericarditis (pericarditis with clinical or serologic evi-
dence of myocardial involvement) (16,28), severe
pericardial effusion (a diastolic echo-free space of
more than 20 mm in width) (3,4,24) and cardiac
tamponade (18,24,29–31). In a prospective study on
more than 450 consecutive patients with acute peri-
carditis fever > 38 C (hazard ratio (HR) 3.6), sub-
acute course (HR 4.0), large pericardial effusion or
cardiac tamponade (HR 2.2) and failure of aspirin or
non-steroidal anti-inflammatory drugs (NSAID; HR
2.5) were identified as independent predictors of a
specific aetiology (non-viral or non-idiopathic aetiol-
ogy) (5). Large effusion and tamponade (HR 2.51),
as well as aspirin or NSAID failure (HR 5.50) identi-
fied also an increased risk of complications during
follow-up (5). Although a higher prevalence of con-
nective tissue diseases has been reported in women,
there are no recommended gender differences for the
clinical triage of pericarditis.
The presence of clinical poor prognostic predictors
including the lack of response to a trial of aspirin or
a NSAID identifies patients at high risk of a non-
idiopathic or non-viral aetiology (Table 3). For these
cases, hospitalisation and a full aetiological search are
warranted (Figure 2) (2,5–7,17,32).
Alternatively, when these negative predictors are not
present, the patients are at low risk of complications,
and specific aetiology and outpatient management
have also been proposed avoiding aetiological search.
In a prospective study of 300 consecutive patients with
acute pericarditis, 254 of all patients (85%) were at
Table 2 Diagnostic criteria for pericarditis (at least two
of four should be present)
Typical chest pain
Pericardial friction rub
Suggestive ECG changes (typically widespread ST segment ele-
vation, PR depression)
New or worsening pericardial effusion
Elevation of C-reactive protein is a confirmatory finding and is
required for the diagnosis of acute and recurrent pericarditis
by some authors (2,9–11).
Figure 1 Acute pericarditis: typical (quasi-diagnostic) stage 1 ECG. 53 year old man with apparently idiopathic/viral acute
pericarditis: Nearly ubiquitous J(ST) elevations with corresponding J(ST) depression in aVR. As is common in III and aVF
when the QRS axis is horizontal (or these leads are of small voltage), the J(ST) is not elevated. Height of J(ST) more than
25% of hieght of T-wave peak in V5 and V6. Most PR segments are slightly depressed with respect to the T-P baseline
(corresponding PR elevation in aVR)
1386 Diagnostic issues of pericarditis
ª 2010 Blackwell Publishing Ltd Int J Clin Pract, September 2010, 64, 10, 1384–1392
Page 3
low risk and were not admitted to hospital, but empir-
ically treated with aspirin 800 mg every 6 or 8 h for 7–
10 days without an aetiological search. The protocol
was safe (no cases of cardiac tamponade) and cost-
effective: 230 of 254 low-risk patients (90.6%) had a
final diagnosis of viral or idiopathic pericarditis also
after a long-term follow-up (mean 38 months) (7).
The same approach is useful also for recurrent
cases. In recurrent pericarditis, the clinical signs and
symptoms generally are fewer and less severe, and
the natural history of the disease is characterised by
an initial active phase of variable length followed by
a late dormant phase with less recurrences. A patient
with a recurrence may be generally treated as an out-
patient unless poor prognostic predictors are present,
or specific aetiology should be ruled out. If a clear
diagnosis of idiopathic aetiology is achieved, it is also
unnecessary to repeat a new aetiological search at
each recurrence, unless new clinical features become
evident. The commonest aetiologies of recurrences
are: idiopathic, viral, autoimmune (related to a con-
nective tissue disease), inadequate medical treatment
either of the index attack or the recurrence and less
commonly a neoplastic aetiology (8,33).
On this basis, a simple triage of pericarditis can be
performed following the initial clinical evaluation
and echocardiogram (Figure 2). If clinical diagnostic
criteria for pericarditis are not satisfied, an alterna-
tive diagnosis should be searched. Patients with a
definite diagnosis of pericarditis should be evalu-
ated for the possible presence of poor prognostic
predictors (high fever, subacute course, large pericar-
dial effusion, cardiac tamponade, lack of response to
aspirin or NSAID). Admission and aetiology search
are considered for patients with at least one poor
prognostic predictor, who are considered high-risk
patients (e.g. high risk of specific aetiologies or com-
plications). When no poor prognostic predictor is
Table 3 Clinical poor prognostic predictors* in acute
pericarditis (see text for details)
Major
Fever > 38 C
Subacute onset
Severe pericardial effusion
Cardiac tamponade
Lack of response to aspirin or NSAIDs after at least 1 week
of therapy
Minor
Myopericarditis
Immunodepression
Trauma
Oral anticoagulant therapy
*Major predictors have been validated in multivariable analy-
sis (5); for minor predictors: hospitalisation and monitoring
may be required although usually not associated with specific
aetiologies.
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Figure 2 In developed countries, a probabilistic approach is advisable in the immunocompetent patient. Aetiological
search should rule out the commonest aetiologies: bacterial (generally tuberculous, rarely purulent), neoplastic pericarditis
and pericarditis related to a systemic disease. CRP, C-reactive protein
Diagnostic issues of pericarditis 1387
ª 2010 Blackwell Publishing Ltd Int J Clin Pract, September 2010, 64, 10, 1384–1392
Page 4
present, the patient is considered to be at low to
moderate risk, and outpatient treatment can be con-
sidered with a close follow-up within 7–10 days.
Patients who do not respond to outpatient empiric
medical therapy after 7–10 days (at least showing a
response with reduction in symptoms, inflammatory
markers and pericardial effusion) should be consid-
ered for admission and at least aetiology search.
Aetiological search and the role of
pericardiocentesis and pericardial biopsy
Despite several possible causes of pericardial diseases
(34), the clinician should particularly identify those
patients with aetiologies that require targeted thera-
pies. In developed countries, about 85% of cases with
acute pericarditis are viral or idiopathic in the
immunocompetent patient (see Table 4) (3–5,35).
Acute viral or idiopathic pericarditis typically follows
a brief and benign course after empiric treatment
with salicylates or other NSAID (1,2,6,17,18,24,32),
and thus may not require a full diagnostic search for
specific viral aetiologies that do not have demon-
strated effective therapeutic options beyond anti-
inflammatory treatments, at least in the immuno-
competent patients. Although nothing is really idio-
pathic (34), and this diagnostic label is often a
statement of diagnostic ignorance, this diagnosis may
be still useful for pericarditis in clinical practice if it
means that specific aetiologies have been excluded.
In fact, these patients have an overall good prognosis
without a significant risk of important complications
such as constriction (< 1% following viral and idio-
pathic pericarditis, 0% in idiopathic recurrent peri-
carditis). The risk of constriction following
pericarditis is more related to the aetiology rather
than the number of recurrences (7,9,33). Obviously,
this diagnostic approach may be different for
research purposes.
Alternatively, the aetiology of acute pericarditis is
completely different in developing countries, with a
high prevalence of specific forms related to tubercu-
losis (for instance, 70–80% of patients in Sub-Saha-
ran Africa, and even up to more than 90% when
pericarditis is associated with HIV-infection). The
incidence of tuberculous pericarditis is increasing in
Africa as a result of the HIV epidemic (35,36). How-
ever, increasing cases with tuberculous pericarditis
can be expected and may be found in immigrants or
immunodepressed patients.
For clinical purposes, the major specific aetiologies
to be ruled out in developed countries include tuber-
culous pericarditis, neoplastic pericarditis and peri-
carditis associated to a systemic disease (generally a
connective tissue disease). Each of these specific aeti-
ologies has a frequency of about 5% of all unselected
cases. It is evident that the knowledge of the epidemi-
ological background is essential to develop a rational,
cost-effective management programme for acute and
recurrent pericarditis, and that different diagnostic
approaches are warranted according to the epidemio-
logical issue and the clinical or research setting.
When a significant pericardial effusion is present, a
diagnostic pericardiocentesis is mandatory if a specific
aetiology such as bacterial or neoplastic pericarditis is
highly suspected. In current European guidelines (12),
pericardiocentesis is indicated for cardiac tamponade,
high suspicion of tuberculous, purulent or neoplastic
pericarditis. Pericardiocentesis may be considered also
for large or symptomatic effusions refractory to medi-
cal treatment. The rationale for this diagnostic use of
pericardiocentesis is that the definite diagnosis of bac-
terial (tuberculous or purulent) and neoplastic peri-
carditis is the demonstration of the infectious agent
or neoplastic cells in pericardial fluid or tissue. Peri-
cardiocentesis may be guided by fluoroscopy or echo-
cardiography or both. If haemorrhagic fluid is
Table 4 Final aetiological diagnosis in major published series of acute pericarditis (unselected patients)
Permanyer-Miralda
et al. (3)
(n = 231)
1977–83
Zayas et al. (4)
(n = 100)
1991–3
Imazio et al. (5)
(n = 453)
1996–2004
Reuter et al. (35)*
(n = 233)
1995–2001
Setting Western Europe Western Europe Western Europe Africa
Idiopathic 199 (86.0%) 78 (78.0%) 377 (83.2%) 32 (13.7%)
Specific aetiology: 32 (14.0%) 22 (22.0%) 76 (16.8%) 201 (86.3%)
Neoplastic 13 (5.6%) 7 (7.0%) 23 (5.1%) 22 (9.4%)
Tuberculosis 9 (3.9%) 4 (4.0%) 17 (3.8%) 161 (69.5%)
Autoimmune 4 (1.7%) 3 (3.0%) 33 (7.3%) 12 (5.2%)
Purulent 2 (0.9%) 1 (1.0%) 3 (0.7%) 5 (2.1%)
*Including pericardial effusions.
1388 Diagnostic issues of pericarditis
ª 2010 Blackwell Publishing Ltd Int J Clin Pract, September 2010, 64, 10, 1384–1392
Page 5
aspirated, a practical aid is to remember that blood
stained pericardial fluid does not clot, because fibri-
nolytic activity in the pericardium prevents blood
clotting in subacute and chronic effusion, while clot-
ting is easily observed when blood is collected from a
cardiac chamber. If the answer is not clear, contrast
medium may be injected under fluoroscopic observa-
tion as well as agitated saline under echocardiographi-
cal observation to exclude cardiac puncture (37).
Echo-guided pericardiocentesis is safe and convenient
and may be performed in a large number of medical
settings allowing different approaches to the effusion
beyond the standard ‘subxiphoid’ route. Clinicians
may choose the best puncture site closest to the larg-
est amount of pericardial fluid identified by the echo-
cardiogram also without a cath-lab facility. However,
the hemodynamic evaluation may allow more precise
detection of effusive-constrictive pericarditis.
In previous studies, pericardial biopsy was gener-
ally performed as a part of a therapeutic procedure
(surgical drainage) in patients with cardiac tampon-
ade relapsing after pericardiocentesis (therapeutic
biopsy) and as a diagnostic procedure in patients
with an illness lasting more than 3 weeks without a
definite diagnosis (3).
Technical advances in instrumentation with intro-
duction of pericardioscopy, and in contemporary
pathology, virology and molecular biology have
improved the diagnostic value of epicardial pericar-
dial biopsy (12,38,39). Targeted biopsy during pericar-
dioscopy was particularly useful in the diagnosis of
neoplastic pericarditis (38). Nevertheless, the use of
pericardioscopy is not generally available outside ter-
tiary referral centres for pericardial diseases, and
advanced diagnostic methods seem warranted in
refractory cases to full conventional therapy, suspected
tuberculous, purulent or neoplastic pericarditis when
the diagnosis cannot be reached by other means.
In patients with pericardial effusion, a systematic
approach to diagnostic testing has been proposed by
French authors (40–42). Polymerase chain reaction
(PCR) techniques may represent a useful adjunct to
conventional laboratory studies in the investigation
of pericardial fluid, permitting the rapid identifica-
tion of microorganisms otherwise not easily found
(42,43). However, other authors have underlined the
need of a careful selection of patients, because the
use of molecular methods led to an absolute increase
in specific useful diagnoses in about 4% of patients
in an already selected population. Moreover,
although potentially useful, if indicated without clini-
cal judgement, molecular diagnostic techniques could
lead to irrelevant findings, such as viral infections for
which specific drug treatments are not available or
necessary in most cases (44).
In many clinical settings, a simple screening is to
perform a thorax and abdominal CT scan to rule out
the presence of lymphoadenopathies and masses. A
normal CT scan almost excludes a tuberculous or
neoplastic origin of pericarditis. CT scan is per-
formed after diagnostic pericardiocentesis when peri-
cardial fluid analysis is available to achieve better
visualisation of the pericardium. If concomitant
pleural effusion is present, thoracentesis is indicated
and the same analyses applied to pleural fluid. Addi-
tional investigations should be addressed according
to the clinical suspicion.
Aetiological search in ‘high risk’ patients and
when a specific aetiology is suspected
Viral pericarditis is often overlooked in clinical prac-
tice. Most cases of acute pericarditis and up to one-
third of recurrent cases are because of viral infections
(2,8,33). A definite diagnosis would require analysis
of pericardial fluid or tissue, while serology and other
cultural studies (i.e. throat and rectal swabs) are not
reliable and diagnostic; even a fourfold rise in serum
antibody levels or evidence of specific antiviral IgM is
suggestive of a recent systemic infection, but not spe-
cifically diagnostic for pericarditis (33). A definite
diagnosis is often missing, but fortunately these cases
are generally self-limiting and can be treated with
aspirin or a non-steroidal anti-inflammatory drug. As
a precise diagnostic definition is not necessary and
does not alter management, most cases are not inves-
tigated and thus are labelled as idiopathic in clinical
practice. Obviously, a comprehensive and invasive
approach including systematic evaluation of pericar-
dial fluid and tissue may be able to reduce these ‘idio-
pathic’ cases, but this approach is usually not
warranted or available in routine clinical practice,
and more sophisticated diagnostic techniques includ-
ing PCR for the detection of viral genome may be
considered especially for research purposes.
Bacterial pericarditis is one of the most important
specific diagnoses to rule out in selected patients.
Purulent pericarditis is nowadays less common than
in the past (£ 1% of unselected cases of acute peri-
carditis in developed countries), and the clinical
presentation is usually acute and highly suggestive.
The only way to diagnose purulent pericarditis is to
obtain pericardial fluid for culture and direct micros-
copy. Cultures with antibiograms are useful to select
targeted antibiotic therapy. Echocardiography will
detect pericardial effusion virtually in all patients
with purulent pericarditis, and cardiac tamponade is
frequent in this setting (22,45).
Tuberculous pericarditis represents about 5% of
unselected patients with acute pericarditis from devel-
oped countries, but more than 60% of patients from
Diagnostic issues of pericarditis 1389
ª 2010 Blackwell Publishing Ltd Int J Clin Pract, September 2010, 64, 10, 1384–1392
Page 6
developing countries (35,36). It usually develops by
retrograde lymphatic spread from peritracheal, peri-
bronchial or mediastinal lymph nodes or by haemat-
ogenous spread from a primary tuberculous infection.
Chest radiograph may be useful to detect features
of active pulmonary tuberculosis (about one-third of
patients), concomitant pleural effusion (40–60% of
patients) and enlarged cardiac shadow when a large
pericardial effusion is present. Chest CT scan may
show typical changes in mediastinal lymph nodes
(i.e. enlargement > 10 mm with matting and hypo-
dense centres) and sparing of hilar lymph nodes.
The early lymphatic involvement is the reason for
the common presence of pericardial effusion. Echo-
cardiographical findings are non-specific, but the
effusion is usually moderate to large, moreover car-
diac tamponade, fibrinous strands, echo dense exu-
dates and pericardial thickening are commoner than
in viral or ‘idiopathic’ cases (35,46).
A definite diagnosis of tuberculous pericarditis is
based on the demonstration of tubercle bacilli in
pericardial fluid or biopsy (46), thus pericardiocente-
sis is recommended if tuberculous pericarditis is sus-
pected (12). Direct methods for the diagnosis of
tuberculous pericarditis include the study of pericar-
dial fluid and tissue. The pericardial fluid is usually
bloodstained, with high protein content and a pre-
dominance of lymphocytes and monocytes. Addi-
tional testing includes search for acid-fast bacilli and
culture from sputum and pericardial fluid, consider-
ing also gastric washing, urine according to the indi-
vidual case. Biopsy specimen may be considered
from the pericardium, and right scalene lymph node
in specific cases when pericardial fluid is not avail-
able and lymphadenopathy is present. However, the
sensitivity of pericardial biopsy is low (10–64%) and
a negative biopsy does not exclude tuberculous peri-
carditis. PCR for the detection of Micobacterium
tuberculosis DNA has been suggested either in the
pericardial fluid or biopsy. The sensitivity is higher
with tissue rather than pericardial fluid, and the
technique is less sensitive than other methods and
may be prone to contamination and false-positive
results (35). Indirect methods for the diagnosis of
tuberculous pericarditis include the evaluation of
biochemical markers in the pericardial fluid. Differ-
ent studies have demonstrated that elevated levels of
adenosine deaminase (ADA) can be found in tuber-
culous pericarditis. Different cut-off levels have been
suggested for the diagnosis. With a cut-off level for
ADA activity of 30 U l, sensitivity was 94%, specific-
ity was 68% and positive predictive value was 80%,
while a cut-off level for ADA of 40 U l shows better
diagnostic accuracy (87% sensitivity, 89% specificity,
positive predictive value 95%) (46,47). High levels of
ADA are also correlated with a higher risk of devel-
oping constrictive pericarditis. Additional tests to be
considered include pericardial lysozyme with a cut-
off level of 6.5 lg dl (sensitivity 100%, specificity
92%), interferon-c (IFN-c) with a cut-off level
> 200 pg l (100% sensitivity and specificity) (46,47).
Serology is less useful than other conventional diag-
nostic methods (35). A response to a trial of antitu-
berculous drugs makes also the diagnosis probable,
but should be avoided in developed countries with a
low prevalence of the disease (46).
Neoplastic pericarditis is also an important specific
diagnosis to rule out in patients with pericarditis.
Despite a higher frequency in selected patients, neo-
plastic pericarditis is responsible of about 5% of
unselected patients of acute pericarditis in Western
Europe and North America and may be sometimes
the cause of recurrences. Virtually, any malignant
tumour can metastasise to the pericardium, with the
most common being lung and breast cancer and
lymphomas. Lung cancer is the commonest malig-
nancy giving early invasion of lymphatic nodes and
thus being easily responsible for pericardial effusion.
Primary tumours of the pericardium are less com-
mon. Important among them is the highly malignant
mesothelioma, which can be extensive.
In a report of 450 consecutive patients, neoplastic
aetiology was found in 33 of 450 patients with acute
pericardial disease (7.3%). Acute pericardial disease
(acute pericarditis and cardiac tamponade) was the
first manifestation of previously unknown malignan-
cies in 18 of 450 patients (4.0%), and lung cancer was
the most common malignancy (72.2%). Risk factors
for a neoplastic aetiology were a history of malignancy
[odds ratio (OR) 19.8], cardiac tamponade at presen-
tation (OR 7.0), a lack of response to non-steroidal
anti-inflammatory drugs and recurrent or incessant
pericarditis (OR 10.0). A similar prognosis was found
in patients with or without a known malignancy (30).
Thus, a detailed evaluation, including a search for
occult malignancy, should generally be reserved for
patients who have persistent or recurrent pericarditis
that is unresponsive to anti-inflammatory therapy,
and those who present with a new large pericardial
effusion or cardiac tamponade.
Even in large case series, only 40–55% of patients
with known malignancy and pericardial effusion
could be confirmed (by cytology or histology) to
have malignant pericarditis (48). The remaining
causes included radiation, infection, haemorrhage
and idiopathic. When neoplastic pericarditis is sus-
pected, pericardiocentesis is recommended for cytol-
ogy. A positive cytology that results in pericardial
fluid is the gold standard for recognition of malig-
nant pericardial effusion. The reported sensitivity of
1390 Diagnostic issues of pericarditis
ª 2010 Blackwell Publishing Ltd Int J Clin Pract, September 2010, 64, 10, 1384–1392
Page 7
cytology is between 67% and 92% and is the lowest
for mesothelioma and lymphoma (48–50). However,
negative cytology should not be used alone to
exclude the diagnosis of malignancy, particularly if
the index of suspicion is high. Unfortunately, cyto-
logical examination of the pericardial fluid is nega-
tive in 30–50% of patients with malignant pericardial
effusion. Tumour marker assessment in pericardial
fluid may help to recognise malignant pericardial
effusion. With a cut-off value for carcinoembryonic
antigen (CEA) level of 5 ng ml, sensitivity was 75%
and specificity 100% in the diagnosis of malignant
pericarditis (51). CYFRA 21-1 > 100 ng ml or CEA
>5ng ml was found in 14 15 patients with malig-
nant pericardial effusion and negative pericardial
fluid cytology (52).
A pericardial biopsy may be required and can be
performed via a subxiphoid or transthoracic pericar-
diostomy (window) or by pericardioscopy. Pericar-
dioscopy allows direct visualisation of the pericardial
space; the reported sensitivity for the diagnosis of
malignancy is as high as 97%. If available flexible
pericardioscopy may allow inspection and targeted
epicardial or pericardial biopsy. In contrast, the sen-
sitivity for blind pericardial biopsy is lower (56–
65%), presumably because of sampling error (12,38).
Additional testing should be directed towards the
identification of the primary malignancy, generally
lung, breast cancer or lymphomas.
Systemic autoimmune diseases have been found
responsible for acute pericarditis in 2–7% of patients,
and in many cases, the diagnosis of a connective tis-
sue disease was already known at the time of the
diagnosis of pericarditis (3–5,17). Systemic autoim-
mune diseases may be also responsible for recurrent
pericarditis with a higher prevalence (53). A number
of rheumatic diseases can involve the pericardium.
This is most likely to occur in patients with a known
systemic lupus erythematosus and rheumatoid arthri-
tis, but can also occur in progressive systemic sclero-
sis, mixed connective tissue disease, Sjo
¨
gren’s
Syndrome, polyarteritis, giant cell arteritis, other sys-
temic vasculitides and familial Mediterranean fever.
Symptomatic pericarditis can occur with all of these
disorders, during the active phase of the systemic
disease. In other cases, pericardial involvement may
be subclinical with a pericardial effusion clinically
silent. Although antinuclear antibodies are often used
as a screening test, they may be equally distributed
in patients with or without a final rheumatological
diagnosis (53). Also in this setting, it should be
recognised that rheumatological diagnoses are not
based on a single test but require a combination of
symptoms, signs and laboratory findings. Thus, at
presentation, suggestive symptoms and signs for a sys-
temic autoimmune disease may be present during an
acute attack of pericarditis, including fatigue, fever,
weight loss, joint symptoms, skin abnormalities above
all if appear after exposure to sun, photosensitivity,
Raynaud phenomenon, alopecia, muco-cutaneous
ulcers, dryness of the eyes. Thus, consultation with an
expert and a careful history and physical examination
are mandatory before an extensive and ‘blind’ use
of diagnostic tests.
Conclusions
The aetiology of pericarditis is varied and complex.
In the clinical setting, diagnostic efforts are worthy if
they may affect subsequent treatments and prognosis.
Basic diagnostic evaluation for all patients with peri-
carditis includes physical auscultation, ECG, trans-
thoracic echocardiography, markers of inflammation
(e.g. C-reactive protein) and myocardial lesion (crea-
tine-kinase, troponin) and chest X-ray. Additional
diagnostic tests are not warranted if no specific aeti-
ologies are suspected on the basis of the epidemio-
logical background, history and presentation. A
triage of pericarditis can be safely performed on the
basis of the clinical and echocardiographical presen-
tation. Specific aetiologies are generally associated
with specific clinical features at presentation that are
also possible predictors of complications during fol-
low-up. High-risk features associated with specific
aetiologies or complications include: fever > 38 C,
subacute onset, large pericardial effusion, cardiac
tamponade, lack of response to aspirin or a NSAID.
On this basis, a routine aetiological search is not
warranted in all cases. Clinicians should rule out
tuberculous, purulent, neoplastic pericarditis, as well
as pericarditis related to a systemic disease. A differ-
ent approach with an extensive aetiological search
may be considered for research purposes.
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Supporting information
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ment of pericarditis.
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corresponding author for the article.
Paper received February 2009, accepted June 2009
1392 Diagnostic issues of pericarditis
ª 2010 Blackwell Publishing Ltd Int J Clin Pract, September 2010, 64, 10, 1384–1392
Page 9
  • Source
    • "Mycobacterium tuberculosis is the most frequently diagnosed bacterial agent and usually occurs in developing countries or immune-compromised hosts [1,2]. In Western countries, the large majority of acute pericarditis cases are viral, and echovirus, coxsackievirus, influenza, Epstein-Barr virus, cytomegalovirus, adenovirus, varicella, rubella, mumps, hepatitis B, hepatitis C, human immunodeficiency virus, parvovirus B19 and human herpesvirus 6 are the principal infectious agents123. Determination of pericarditis etiology is difficult, and a large number of cases remain unexplained. Indeed, idiopathic pericarditis represents between 40% and 85% of pericarditis cases, and most of them are suspected to be of viral origin [2,4]. "
    [Show abstract] [Hide abstract] ABSTRACT: Pericarditis is a common human disease defined by inflammation of the pericardium. Currently, 40% to 85% of pericarditis cases have no identified etiology. Most of these cases are thought to be caused by an infection of undetected, unsuspected or unknown viruses. In this work, we used a culture- and sequence-independent approach to investigate the viral DNA communities present in human pericardial fluids. Seven viral metagenomes were generated from the pericardial fluid of patients affected by pericarditis of unknown etiology and one metagenome was generated from the pericardial fluid of a sudden infant death case. As a positive control we generated one metagenome from the pericardial fluid of a patient affected by pericarditis caused by herpesvirus type 3. Furthermore, we used as negative controls a total of 6 pericardial fluids from 6 different individuals affected by pericarditis of non-infectious origin: 5 of them were sequenced as a unique pool and the remaining one was sequenced separately. The results showed a significant presence of torque teno viruses especially in one patient, while herpesviruses and papillomaviruses were present in the positive control. Co-infections by different genotypes of the same viral type (torque teno viruses) or different viruses (herpesviruses and papillomaviruses) were observed. Sequences related to bacteriophages infecting Staphylococcus, Enterobacteria, Streptococcus, Burkholderia and Pseudomonas were also detected in three patients. This study detected torque teno viruses and papillomaviruses, for the first time, in human pericardial fluids.
    Full-text · Article · Apr 2014 · PLoS ONE
  • [Show abstract] [Hide abstract] ABSTRACT: Pericarditis, the most common disease of the pericardium, may be isolated or a manifestation of a systemic disease. The etiology of pericarditis is varied and includes infectious (especially viral and tuberculosis) and noninfectious causes (autoimmune and autoinflammatory diseases, pericardial injury syndromes, and cancer [especially lung cancer, breast cancer, and lymphomas]). Most cases remain idiopathic with a conventional diagnostic evaluation. A targeted etiologic search should be directed to the most common cause on the basis of the patient's clinical background, epidemiologic issues, specific presentations, and high-risk features associated with specific etiologies or complications (fever higher than 38°C, subacute onset, large pericardial effusion, cardiac tamponade, lack of response to NSAIDs). The management of pericardial diseases is largely empiric because of the relative lack of randomized trials. NSAIDs are the mainstay of empiric anti-inflammatory therapy, with the possible addition of colchicine to prevent recurrences.
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  • [Show abstract] [Hide abstract] ABSTRACT: Pericarditis may be caused by infectious or noninfectious noxa. Most cases are labeled as 'idiopathic' because the traditional diagnostic approach often fails to identify the etiology. Most important causes are presumed to be viruses in countries with a low prevalence of tuberculosis and tuberculosis in developing countries. Noninfectious pericarditis mainly includes autoimmune systemic diseases, post-pericardiotomy syndromes and neoplastic pericardial disease. Treatment should be targeted to the cause, but remains empirical with NSAIDs and the possible adjunct of colchicine in idiopathic cases. Corticosteroids use should be limited to patients with NSAID contraindications/intolerance or failure, and rarely for specific conditions (i.e., pregnancy and systemic autoimmune diseases). Recurrences are the most common complication, but the overall prognosis is related to the etiology, usually benign in idiopathic pericarditis.
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