Pericarditi

PERICARDITIS
Summaries
-Introduction ( Key words)
-Definition?
-Frequency?
-Risk factors?
-Clinical signs?
-Etiology?
-Non specific diagnosis?
-Etiological diagnosis?
-Treatment?
-Evolution?
-Complications?
-Prevention?
-State of the art?
-Publication from IFR on subject ?
-More information on subject?
-Correspondent from l'IFR48
Key words
Pericardial effusion – Tamponade – Constrictive pericarditis-
Hypothyroidism - Q fever

Definition of the syndrome
Acute pericarditis is a syndrome caused by the inflammation of
the pericardium, a sac composed of visceral and parietal layers
separated by the pericardial cavity. Acute pericarditis can be
dry, fibrinous or effusive, independent from its etiology, and may
occur as an isolated entity or as a result of a systemic disease
Detection and treatment of pericarditis remains a challenging
problem and the aetiology is unknown in 40 to 85% of the
cases. We have previously developed [1] a diagnostic strategy
that recommends the systematic use of a combination of non
invasive tests for the diagnosis of benign pericardial effusions.
In addition, it allowed identifying two frequently under
diagnosed causes in our area, Q fever [2,3] and
hypothyroidism, both of which are easily treated. This strategy
lead to a reduction in the number of pericarditis classified as
idiopathic compared to a prescription based on selecting
laboratory tests intuitively [4,5].
For some patients pericardiocentesis is necessary. We perform
a systematic analysis of pericardial fluid and biopsy specimens,
using cultures and molecular analyses for identification of
bacteriological, fungal, and viral agents, as well as
histopathological examination [6].
1/ Levy PY, Corey R, Berger P, et al. Etiologic diagnosis of 204
pericardial effusions. Medicine (Baltimore) 2003; 82: 385-91.
2/ Levy PY, Raoult D. Coxiella burnetii pericarditis : a report of
15 cases and review. Clin Infect Dis. 1999;29:393-397.

3/ Levy PY, Thuny F, Habib G, Bonnet JL, Djiane P, Raoult D:
Diagnosis of Coxiella burnetii pericarditis by using a
systematic prescription kit in case of pericardial effusion. N Y
Acad Sci. (in press 2006)
4/ Levy PY, Moatti J.P, Gauduchon V, Vandenesch F, Habib G,
Raoult D. comparison of intuitive versus systematic strategies
for etiological diagnosis of pericardial effusion.. Scand J Infect
Dis 2005; 37, 216-20.
5/ Levy PY, Kahn M, Raoult D. Acute pericarditis. N Engl J
Med 2005; 352:1154-5;
6/ Levy PY, Fournier PE, Charrel R, Habib G, Metras, Raoult
D: Molecular analysis of pericardial fluid: a 7 year experience.
Eur Heart J. 2006;16:1942-46.

Frequency?
It represents 2.5% of hospitalized patients in Cardiology. In
Marseilles we can estimated the frequency around 30/100.000
inhabitants. However, the true incidence and prevalence of
pericarditis remains difficult to measure. The incidence of
pericarditis in postmortem studies ranges from 1-6% , whereas
it is diagnosed ante mortem in only 0.1% of hospitalized
patients, and in 5% of emergency room patients that present
with chest pain in the absence of myocardial infarction. In Africa,
the incidence of tuberculous pericarditis is rising as direct result
of HIV where 40-75% of patients with large pericardial effusion
are infected with HIV. Pericardial effusion occurs in up to onethird
of patients with myxoedema and it is detected clinically in
up to 20% of uremic patients who require chronic dialysis. [1].
1.Maisch B, Seferovic PM Ristic AD, and al. Guidelines on the
diagnosis and management of pericardial diseases. The
Taskforce on diagnosis and management of pericardial
diseases of the European Society of cardiology. Eur Heart
J. 2004 ;25:587-610.

Risk factors?
The diminution of steroidal treatment or anticoagulant treatment
can be responsible of exacerbation of pericardial effusion.
Radiation injury to the heart is a significant complication of
radiation therapy used in the treatment of breast carcinoma,
Hodgkin’s disease and non-Hodgkin lymphoma [1],. It is
dependent on the radiation dosage, the duration of therapy, the
volume of heart included in the radiation field and anterior
weighting of the radiation dose
It has been reported following cardiac perforation by catheter
and epicardial pacemaker implantation Cardiac tamponade is
more frequent following valve surgery than coronary bypass
grafting[2].
1. Brosius FC, Waller BF, Roberts WC. Radiation heart
disease. Analyses of 16 young (aged 15 to 33 years)
necropsy patients who received over 3,500 rads to the
heart. Am J Med. 1981;70:519-530
2. Tsang TS, Enriquez-Sarano M, Freeman WK, and al.
Consecutive 1127 therapeutic echocardiographically
quided pericardiocenteses: clinical profile, practice
patterns and outcomes spanning 21 years. Mayo Clin Proc
2002; 77: 429-36

Clinical diagnosis?Clinical signs.
• Progressive, frequently severe chest pain, generally worse
when lying supine, relieved by sitting and might radiate to the
neck, arms. Since the phrenic nerve crosses the pericardium,
pericarditis is often responsible of pain to the trapezius
muscle ridges.
• Dyspnea worsened with decubitus dorsal.
• Additional symptoms can be observed, particularly fever,
cough, sputum production, and weight loss, but are generally
related to underlying diseases.
Physical examination
•A pericardial friction rub is pathognomonic. The intensity vary
quickly and it is best heard at the left sternal border at end of
expiration with the patient leaning forward. It is audible
throughout the respiratory cycle which makes the difference
from pleural rub.
TO LISTEN
•http://www-sante.ujf-grenoble.fr/sante/CardioCD/cardio/
chapitre/405.htm
•Clinical signs in favor of tamponade (pulsus paradoxus)
should be searched.

Etiology?
Etiology
Bacterial , fungal and
parasites Infections
Coxiella burnetii
Incidence Western
countries
Etiological
Diagnostic tools
(material)
Depend on country7% of Serology (serum)
infectious pericarditis]
Tuberculosis 4% (7% of tamponade) Culture, Molecular
Biology (PE,PB)
Gram negative rods, Staphylococci, S.pneumoniae Rare

Pericardial perforation (penetrating injury,
oesophageal perforation), cardiac injury (surgery,
percutaneous procedures)
Diseases in adjacent
structures
Myocardial infarction, and postmyocardial
syndrome
aortic dissection, pneumonia, pulmonary
embolism, empyema
Association with other
syndromes
Inflammatory bowel disease, Loffler,
syndrome, Stevens-Johnson syndrome,
giant-cell aortitis, hypereosinophilic
syndromes, acute pancreatitis
1-3%
5-10% cases
Rare

Stade IV: Reversion of T wave to normal.
In addition to this features, are frequently associated,
depression of PR segment, sinus tachycardia and microvoltage.
• Echocardiography
The advent of echocardiography, an accurate noninvasive
method for the detection of effusion, has clarified the definition
and led standardizing effusion as a clear entity. It reveals the
size: small (echo free space in diastole10mm posterior); or large (>20mm eventually with
compression of the heart).
Pericardial biopsy

•
Pericardiocentesis is a life-saving procedure in decompensate
cardiac tamponade and is indicated for effusions of greater than
20 mm in diastole visualized by echocardiography, in urgency
in case of tamponnade.
Percutaneous pericardiocentesis can be guided by fluoroscopy,
echocardiography, or a surgical approach and, in most cases,
can be done safely and rapidly. Puncture of pericardial fluid
should be proposed as a second line of investigation when
serological tests are negative (including antinuclear antibodies
and serum thyroid-stimulating hormone), except in the case of
urgent drainage for tamponade. It can be also proposed when a
neoplasm, tuberculosis, or infection are suspected. [2].
1/ Feigenbaum H. Pericardial disease. In: Feigenbaum H,
ed. Echocardioraphy. 5th ed. Lea & Febiger;
1994:556-588
2/ Gibbs CR, Watson RD, Singh SP, Lip GYH. Management
of pericardial effusion by drainage: a survey of 10 year’s
experience in a city centre general hospital serving a
multiracial population. Postgrad Med J 2000;76:809-13
Etiological diagnosis?

1/ Constitution of the kit (specific strategy of the IFR)
• As soon as the diagnosis is made :
o Blood cultures set aero and anaerobic
o Sterile swabs for viral culture of pharynx
o Viral serology : HIV, Hepatitis C, CMV, EBV,
Enterovirus, Adenovirus
o Bacterial serology : Coxiella, Bartonella, Rickettsia,
Legionella, Mycoplasma, Chlamydia, Brucella
o Toxoplasma
o Thyroid Stimulating Hormone, Waaler –Rose,
Antinuclear antibodies
• H+1 Blood cultures set aero and anaerobic
• J+3 Sterile swabs for viral culture of pharynx
• J+15 2 ème same serological tests as J0
• [link to FICHE DE RENSEIGNEMENTS ] :
2/ Analyse des liquides (stratégie spécifique de l’IFR)
• Culture:
o Standard agar and shell vials
o Mycobacteria
• Viral culture :
o Shell vials: BGM, Vero, MDCK,cellules diploïdes MRC5
• Molecular analysis :
o Bacteria 16S RNA ; 18S RNA ; Mycobacterium
o Virus : Herpes consensus ; Enterovirus ; Parvovirus B19
• Histological examination :
Stained with May-Grünwald-Giemsa hematoxylin-eosinsaffron.
Special stains were used for detection of fungi and
bacteria, which included periodic acid-Schiff, Giemsa, Brown-
Hopps tissue Gram, Grocott-Gomori methenamine silver, and
Warthin-Starry stains.
3/ Suggested decisional algorithm)
•

Circumstances of diagnosis
Systematic
Acute
Chronic
Tamponade
Echocardiography
Pericardial
Obvious cause
Non obvious cause
Volume>200cc or
CT scanner
Diagnosis
compatible
Levy PY, Lepidi H, Habib G, Collard F, Raoult D: Etiological
diagnosis of pericardial effusion. Future Microbiology.
STOP
2006;1:229-39
Systematic non invasive
exploration: Serological tests,
TSH ACAN, Viral cultures.
No
diagnosis or
inefficacy of
treatment
Tumors markers
Research of primitive
cancer
Pericardiocentesis
- Standard Culture
- Viral culture
- Mycobacteria
- Molecular biology
(16SRNA, 18SRNA,
Enterovirus, Herpes
consensus)

Treatment?Symptomatic treatment with aspirin (up to 650
mg every 4 hours) or nonsteroidal anti-inflammatory drugs
are the mainstay treatment. Ibuprofen is generally preferred for
its rare side-effects, favourable impact on the coronary flow, and
the large dose range 300-800mg every 6-8 hours. It can be
continued for days or weeks. Colchicine (0.5mgbid) added or
as monotherapy also appears to be effective for the initial attack
and the prevention of recurrences. Systemic corticosteroid
therapy should be restricted to connective tissues, uremic
pericarditis. It is contraindicated in case of infectious pericarditis
except in patients with secondary tuberculous pericarditis as an
adjunct to tuberculostatic treatment.
Quelle est l’évolution du syndrome?
Evolution depends from etiology: acute benign pericarditis
generally resolves with 3 weeks. Tuberculosis and radiation
therapy tends to be responsible of constrictive pericarditis.
Possible complications?
Possible complications of pericarditis include cardiac
tamponade, in which the accumulation of fluids can cause
severe compression, recurrent pericarditis with a symptom free
interval, and pericardial constriction, in which an adherent
pericardium restricts the diastolic filling of the heart. Chronic (>3

months) pericarditis includes effusive, adhesive and constrictive
forms
• Myopericarditis
It is characterized frequently by atrial arrhythmias and elevation
of cardiac biological markers. Pejorative evolution toward
cardiac insufficiency can be noted.
• Tamponnade
It is the decompensate phase of cardiac compression caused
by effusion accumulation and the increased intrapericardial
pressure. It can be an surgical urgency.
Clinically, heard sounds are distant, orthopnoea, cough,
dysphagia with episodes of unconsciousness are observed.
Arterial hypotension with pulsus paradoxus (decreased of
systolic pressure with breath inspiration) is noted. In half of the
cases, it is from neoplasm origin and need surgical drainage.
• Constrictive pericarditis
It is a rare but severe disabling consequence of the chronic
inflammation.

The calcification is responsible of the diminution of the diastolic
filling which can be diagnose in front of right cardiac
insufficiency signs, and micro voltage on l’EKG. On
echocardiography is note pericardial thickness with
sometimes small pericardial effusion, and expansion of the right
atrial.
• Recurrent pericarditis.
Recurrent pericarditis with a symptom free interval are noted in
20 to 30% of cases. It is generally due to a common mistake
with the use of too low dose of non steroidal anti-inflammatory
doses to be effective or a dose to rapidly decreased. Correct
NSAID regimens usually improve the symptomatology.
How to prevent infections?

Since the etiologies are multiple, it is not possible to prevent
pericardial effusion.
State of research in pericarditis field?
The remaining idiopathic pericarditis still represents a high
percentage and may be due to uncultivable agents or to
unknown immune mechanisms. Potential underlying genetic
disorders have been also reported. Electron microscopy is not
very developed yet because it is still expensive but it will be a
very interesting tool for the diagnosis of viral pericarditis. In
Africa, the impact of HIV infection on outcome in tuberculous
pericarditis is the crucial point and will have to be studied in
long-term works. Improving therapeutical management to
avoided recurrence is also a very important objective for the
next few years. The indications for intrapericardial
administration of drugs will probably increase.
Main publications from l’IFR on pericardial effusion
1.Levy PY, Raoult D. Coxiella burnetii pericarditis : a report of
15 cases and review. Clin Infect Dis. 1999;29:393-397.

2.Levy PY, Corey R, Berger P, et al. Etiologic diagnosis of
204 pericardial effusions. Medicine (Baltimore) 2003; 82:
385-91.
3.Levy PY,. Fournier PE, Carta M, Raoult D. Pericardial
effusion due to Bartonella Quintana in homeless man. J
Clin Microbiol 2003;41:5291-93.
4.Levy PY, Moatti J.P, Gauduchon V, Vandenesch F, Habib G,
Raoult D. comparison of intuitive versus systematic
strategies for etiological diagnosis of pericardial effusion..
Scand J Infect Dis 2005; 37, 216-20.
5.Levy PY, Kahn M, Raoult D. Acute pericarditis. N Engl J
Med 2005; 352:1154-5;
6.Levy PY, Fournier PE, Charrel R, Habib G, Metras, Raoult
D: Molecular analysis of pericardial fluid: a 7 year
experience. Eur Heart J. 2006;16:1942-46.
7.Levy PY, Lepidi H, Habib G, Collard F, Raoult D: Etiological
diagnosis of pericardial effusion. Future Microbiology.
2006;1:229-39.
8.Levy PY, Thuny F, Habib G, Bonnet JL, Djiane P, Raoult D:
Diagnosis of Coxiella burnetii pericarditis by using a
systematic prescription kit in case of pericardial effusion. N
Y Acad Sci. (in press 2006).
More information on the subject?
• Savoia MC, Oxman MN. Myocarditis and pericarditis. In:
Mandell GL, Bennet JE, Dolin R, Eds. Principles and

Practice of Infectious Diseases, 6th Edition ed. Philadelphia:
Churchill Livingstone, 2004, p.1052-70.
• Permanyer-Miralda G, Sagrista-Sauleda J, Soler-Soler J.
Primary acute pericardial disease: a prospective series of
231 consecutive patients. Am J Cardiol. 1985; 56: 623-30.
• Corey GR, Campbell PT, Van Trigt P, et al. Etiology of large
pericardial effusions. Am J Med. 1993; 95: 209-13.
• Troughton R.W, Asher C.R, Klein A.L. Pericarditis.Lancet
2004; 363:717-27.
•Tsang TS, Enriquez-Sarano M, Freeman WK, and al.
Consecutive 1127 therapeutic echocardiographically quided
pericardiocenteses: clinical profile, practice patterns and
outcomes spanning 21 years. Mayo Clin Proc 2002; 77:
429-36.
•Nugue O, Millaire A, Porte H and al. Pericardioscopy in the
etiologic diagnosis of pericardial effusion in 141 consecutive
patients. Circulation 1996; 94: 1635-41.
•Lange RA, Hillis LD. Acute pericarditis. N Engl J Med
2004;351:2195-202 .
Who to call at IFR48
Dr Pierre –Yves LEVY
Associated professor
04 91 38 55 14
PLEVY@mail.ap-hm.fr

Consultations :
Sur rendez vous Vendredi matin
Hôpital la Timone Laboratoire de microbiologie 1 er Etage
Sur rendez vous mercredi matin
Hôpital la Timone Département de cardiologie 10 ème Etage

FICHE DE RENSEIGNEMENT IFR48
Conformément à la Loi Bioéthique 2004, les patients
ont été informés que sauf avis contraire de leur
part, leurs prélèvements ou les résultats biologiques
obtenus pourront être utilisés de manière anonyme à
des fins scientifiques.
NOM : .....................................................NOM
D’EPOUSE................................................
PRENOM : ........................................
SEXE M F
DATE DE NAISSANCE : ....../......./...... LIEU DE
NAISSANCE : ..............……………………
HABITAT : Urbain Rural Lieu de
résidence : ..........................................…………………
PROFESSION : ...................................…….
HOPITAL : ...................................................
SERVICE : .........................................………….
Date d'entrée…………Date de sortie du service……………
Journées d'Hospitalisation………………
EPIDEMIOLOGIE
VOYAGES depuis 6 mois OUI NON
Date : .......................: Lieu
CONTACT AVEC DES ANIMAUX OUI NON
Animaux de compagnie : Rongeurs :
Bétail : Arthropodes :
Produits laitiers non pasteurisés
TERRAIN
Immunodépression : Hémopathie
Transplantation Chimiothérapie SIDA
Corticothérapie Radiothérapie Diabète
Alcoolisme Toxicomanie Sans domicile
fixe Grossesse
Maladie auto-immune, préciser : .........................
ANTECEDENTS
Symptômes identiques à l’épisode actuel

Tuberculose Dysthyroïdie Cancer Exposition
aux toxiques :
CLINIQUE
DATE DE DEBUT DES
SYMPTOMES : ..................................
CADRE NOSOLOGIQUE
Péricardite aiguë Péricardite récidivante
Myopéricardite Tamponnade
Découverte échographique fortuite
SYMPTOMES
Fièvre Céphalées Syndrome pseudo-grippal
Diarrhée Conjonctivite Pharyngite Uréthrite
Arthrite Toux Adénopathies
Eruption cutanée : Maculo-papuleuse
Vésiculeuse Purpurique Erythème
noueux
Antibiothérapie préalable
Frottement Douleurs rétro sternales
Anomalies ECG
Préciser : .............................................................................
......
Anomalies échocardiographiques
Préciser : .........................................................................
Anomalies radiologiques
Préciser : .........................................................................
BIOLOGIE
Anomalies des leucocytes
Hyperleucocytose à polynucléaires neutrophiles (>
10G/L)
Hyperéosinophilie (> 500/mL)
Leucopénie (< 1000/mL)
Thrombopénie (< 150G/L)
Elévation de la vitesse de sédimentation (> 20)
Elévation des transaminases (> 1,5 N)
Elévation de la créatinine (> 1,5 N)
Elévation de la troponine (> 1,5 N)