Acute Pericarditis

LESLIE E. TINGLE, MD; DANIEL MOLINA, MD; and CHARLES W. CALVERT, DO

Baylor Family Medicine Residency at Garland, Garland, Texas

Although acute pericarditis is most often associated with viral infection, it may also be caused
by many diseases, drugs, invasive cardiothoracic procedures, and chest trauma. Diagnosing
acute pericarditis is often a process of exclusion. A history of abrupt-onset chest pain, the pres-
ence of a pericardial friction rub, and changes on electrocardiography suggest acute pericardi-
tis, as do PR-segment depression and upwardly concave ST-segment elevation. Although highly
specific for pericarditis, the pericardial friction rub is often absent or transient. Auscultation
during end expiration with the patient sitting up and leaning forward increases the likelihood
of observing this physical finding. Echocardiography is recommended for most patients to con-
firm the diagnosis and to exclude tamponade. Outpatient management of select patients with
acute pericarditis is an option. Complications may include pericardial effusion with tampon-
ade, recurrence, and chronic constrictive pericarditis. Use of colchicine as an adjunct to con-
ventional nonsteroidal anti-inflammatory drug therapy for acute viral pericarditis may hasten
symptom resolution and reduce recurrences. (Am Fam Physician 2007;76:1509-14. Copyright
© 2007 American Academy of Family Physicians.)

A
cute pericarditis is a common Etiology
disease that must be considered Although viral infection is the most com-
in the differential diagnosis of mon identifiable cause of acute pericardi-
chest pain in adults.1 The clinical tis, the condition may be associated with
syndrome of pericarditis results from inflam- many diseases.4 Nonviral causes of pericar-
mation of the pericardium, a fibrous sac that ditis include bacterial infection, MI, chest
envelops the heart and the base of the great trauma, and neoplasm. Causes of pericardi-
vessels. The pericardium has a visceral and a tis are listed in Table 1.5-7
parietal layer, between which up to 50 mL of Pericardial disease is the most common
serous fluid is found in healthy patients.2 Peri- cardiovascular manifestation of AIDS,
carditis may present as an indolent process occurring in up to 20 percent of patients
with no significant pain, as seen in patients with human immunodeficiency virus infec-
with tuberculosis, or it may be heralded by tion/AIDS. Although the incidence of bac-
the sudden onset of severe substernal chest terial pericarditis is declining in developed
pain in acute idiopathic or viral pericarditis. countries, it has increased among patients
Although the incidence of acute pericarditis with AIDS.8,9 Patients with AIDS and other
is unknown, up to 5 percent of visits to emer- immunocompromised persons are also
gency departments for nonacute myocardial at high risk for tuberculous and fungal
infarction (MI) chest pain may be related to pericarditis.
pericarditis.3 Recognition of the clinical syn- The mortality rate for untreated tuber-
drome is important because it must be distin- culous pericarditis approaches 85 percent.
guished from acute coronary syndromes and Tuberculous pericarditis often presents
pulmonary embolism. Further, the syndrome with subacute illness that includes fever, a
may lead to cardiac tamponade large pericardial effusion, and tamponade.
or constrictive pericarditis, or The diagnosis is confirmed by identification
Nonviral causes of pericardi- may be associated with under- of Mycobacterium tuberculosis in pericar-
tis include bacterial infec- lying conditions (e.g., acquired dial fluid or tissue. Other diagnostic tools
tion, myocardial infarction, immunodeficiency syndrome include polymerase chain reaction for DNA
chest trauma, and neoplasm. [AIDS], malignancy, MI, colla- of mycobacteria, adenosine deaminase, and
gen vascular disease). interferon-γ in pericardial fluid.10


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 SORT: KEY RECOMMENDATIONS FOR PRACTICE

Evidence
Clinical recommendation rating References

Echocardiography is recommended for patients with suspected pericardial disease, including C 10, 25
effusion, constriction, or effusive-constrictive process.
Pericardiocentesis should be reserved to treat cardiac tamponade and suspected purulent pericarditis. C 10, 25
Colchicine should be considered as an adjunct to nonsteroidal anti-inflammatory drug therapy in B 28, 29
patients with acute viral or idiopathic pericarditis.
Corticosteroid therapy alone should be avoided in patients with acute or idiopathic pericarditis. B 29

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-
oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 1435 or http://
www.aafp.org/afpsort.xml.

Pericarditis also can arise as a compli-

Table 1. Causes of Pericarditis cation of MI. Post–MI pericarditis may
develop two to four days after an acute
Idiopathic (nonspecific, probably viral) infarction and results from a reaction
Infectious causes between the pericardium and the damaged
Viruses: coxsackievirus A and B, hepatitis viruses, human immunodeficiency adjacent myocardium. Dressler’s syndrome
virus, influenza, measles virus, mumps virus, varicella virus is a post–MI phenomenon in which peri-
Bacteria: gram-positive and gram-negative organisms; rarely, carditis develops weeks to months after an
Mycobacterium tuberculosis
acute infarction; this syndrome is thought
Fungi (most common in immunocompromised patients): Blastomyces
dermatitidis, Candida species, Histoplasma capsulatum
to reflect a late autoimmune reaction medi-
Echinococcus granulosus
ated by antibodies to circulating myocardial
Noninfectious causes
antigens.2
Acute myocardial infarction*
Pathophysiology
Aortic dissection
Renal failure†
The acute inflammatory response in pericar-
Malignancy: breast cancer, lung cancer, Hodgkin’s disease, leukemia,
ditis can produce either serous or purulent
lymphoma by local invasion fluid, or a dense fibrinous material. In viral
Radiation therapy (usually for breast or lung cancer) pericarditis, the pericardial fluid is most
Chest trauma commonly serous, is of low volume, and
Postpericardiotomy resolves spontaneously. Neoplastic, tuber-
Cardiac procedures: catheterization, pacemaker placement, ablation culous, and purulent pericarditis may be
Autoimmune disorders: mixed connective tissue disorder, associated with large effusions that are exu-
hypothyroidism, inflammatory bowel disease, rheumatoid arthritis, dative, hemorrhagic, and leukocyte filled.2,11
scleroderma, spondyloarthropathies, systemic lupus erythematosus, Gradual accumulation of large fluid volumes
Wegener’s granulomatosis
in the pericardium, even up to 250 mL, may
Sarcoidosis
not result in significant clinical signs.12
Medications
Although pericardial effusion may be absent
Dantrolene (Dantrium), doxorubicin (Adriamycin), hydralazine
in 60 percent of patients, large pericardial
(Apresoline; brand not available in the United States), isoniazid (INH),
mesalamine (Rowasa), methysergide (Sansert; brand not available effusions may accumulate rapidly and impede
in United States), penicillin, phenytoin (Dilantin), procainamide diastolic filling of the right heart, resulting in
(Procanbid), rifampin (Rifadin) cardiac tamponade and death.1,3,11 Cardiac
tamponade associated with acute pericardial
*—Pericardial effusion may occur on the second to fourth day after acute myocardial
infarction as a reaction to underlying necrotic myocardium in up to 25 percent of disease is more common in patients with neo-
patients. It can also develop weeks to months after myocardial infarction in patients plastic, tuberculous, and purulent pericarditis
with post–myocardial infarction syndrome (i.e., Dressler’s syndrome); in this situation, (60 percent) than in patients with acute viral
pericarditis occurs because of a late autoimmune reaction stimulated by the entry of
necrotic myocardial tissue into the circulation, where it acts as an antigen. pericarditis (14 percent).11,13
†—Pericarditis in uremia indicates a need for dialysis; pericarditis may also be associ- Prolonged pericarditis may result in
ated with hemodialysis. persistent accumulation of pericardial
Information from references 5 through 7. fluid. In this case, the fluid constitutes to
form a thick coating that surrounds the

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 Table 2. Differentiation of Acute Pericarditis from
Myocardial Ischemia or Infarction

Myocardial ischemia
myocardium. The ultimate manifestation Clinical finding Acute pericarditis or infarction
may be constrictive pericarditis.4 Chest pain
Character Sharp, stabbing Pressure-like, heavy,
Diagnosis squeezing
history and physical examination
Duration Hours to days Minutes to hours
Patients with acute pericarditis commonly Change with position Worse when supine; No
report a prodrome of fever, malaise, and improved when
myalgias. The cardinal features of acute peri- sitting up or leaning
carditis are chest pain, pericardial friction forward
rub, and gradual repolarization changes on Change with Worse with inspiration No
respiration
electrocardiography (ECG).4,14,15 In patients
Response to No change Improved
with acute pericarditis, chest pain is abrupt nitroglycerin
in onset, pleuritic, and substernal or left Electrocardiography
precordial in location. It may radiate to the PR-segment Frequent (early) Rare
trapezius ridge, neck, arms, or jaw. The pain depression
is relieved by leaning forward and is made Q waves Absent May be present
worse by lying supine. The classic triphasic Ratio of ST-segment Greater than 0.25 Less than 0.25
pericardial rub is best heard along the left elevation to T-wave
sternal border with the patient sitting up and amplitude in V6
leaning forward (Table 2).7 ST-segment elevation Widespread concave Localized convex
Although auscultation of a pericardial T waves Inverted after ST Inverted when ST
friction rub has high specificity (approach- segments have segments are still
normalized elevated
ing 100 percent) for acute pericarditis, it has
Friction rub Present in 85 percent Absent
low sensitivity that varies with the frequency on physical of patients
of auscultation.15,16 The pericardial rub is examination
best auscultated with the diaphragm of the
stethoscope over the left lower sternal border Adapted with permission from Lange RA, Hillis LD. Clinical practice. Acute pericarditis.
N Engl J Med 2004;351:2197.
in end expiration with the patient leaning
forward. It has a rasping or creaking sound
similar to leather rubbing against leather.
The classic pericardial rub is triphasic but collapse of the right atrium, right ventricle,
occurs in only one half of patients with a or both serves to confirm tamponade.4
rub, whereas the remainder of patients have Tuberculous pericarditis presents differ-
a biphasic or monophasic rub. The three ently. A study of 233 patients found that fever,
phases of the pericardial rub correspond to night sweats, weight loss, elevated serum
the movement of the heart against the peri- globulin, and normal peripheral white blood
cardial sac during atrial systole, ventricular cell count were independent predictors of
systole, and rapid ventricular filling. The tuberculous pericarditis and could be used
rub of pericarditis may be transient, mak- in a clinical decision tool for making an
ing it important for physicians to auscul- accurate diagnosis.17
tate the heart repeatedly.4,5,15 The presence
diagnostic tests
of a monophasic rub occurring with the
respiratory cycle in the absence of diag- Superficial myocardial inflammation is
nostic changes on ECG or elevated cardiac believed to explain the four stages of ECG
enzymes should alert physicians to the pos- changes visible during acute pericarditis.18
sibility of pleuritis.3 These stages involve diffuse, upwardly con-
Physical findings that suggest acute cardiac cave ST-segment elevation; T-wave inver-
tamponade include tachypnea, tachycardia, sion; and PR-segment depression.19,20 The
neck vein distention, hypotension, and inspi- evolution of these ECG changes helps distin-
ratory fall in arterial blood pressure. Echo- guish pericarditis from early repolarization
cardiographic evidence of diastolic chamber and acute MI19 (Table 27).

November 15, 2007 ◆ Volume 76, Number 10 www.aafp.org/afp American Family Physician  1511
Acute Pericarditis

In stage I, which can last a few hours to pericarditis, the diagnosis is confirmed.
several days, ST segments elevate, T waves However, results of echocardiography may
remain upright, and PR segments are iso- be normal in patients with the clinical syn-
electric or become depressed. After a few drome of pericarditis.10 Computed tomog-
days, the ST and PR segments normalize, raphy (Figure 1) and magnetic resonance
typifying stage II. In stage III, diffuse T-wave imaging are useful if the initial work-up for
inversions remain after the ST segments have pericarditis is inconclusive.10
normalized. The ECG returns to normal in
recommended diagnostic strategy
stage IV unless chronic pericarditis develops,
leading to persistence of T-wave inversion.20 Most cases of acute pericarditis are idiopathic,
No reciprocal changes or Q waves are found and initial work-up should be limited to a his-
in the 12-lead ECG during acute pericarditis, tory and physical examination, complete blood
which is an important feature in distinguish- count, erythrocyte sedimentation rate, tropo-
ing acute pericarditis from acute MI.13,21,22 nin I, serum chemistry, ECG, chest radiogra-
The changes in stage I may be confused phy, and echocardiography. For patients with
with findings of MI or early repolarization; tamponade, those with no known associated
old ECGs help differentiate among these illness (Table 1),5-7 and those in whom pericar-
conditions. It is important to remember that dial disease does not improve within one week,
no PR-segment depression occurs in MI. The antinuclear antibodies, rheumatoid factor, and
absence of PR-segment depression, however, mycobacterial studies (i.e., cultures of sputa
does not rule out acute pericarditis because it and gastric aspirate) should be obtained.13
may be found in about 25 percent of cases. In If the patient also has a pleural effusion,
addition, the ST-segment elevation in acute thoracentesis is recommended. The pleu-
infarction is upwardly convex in concordant ral fluid should be assessed for adenosine
leads, and Q waves often appear. The most deaminase, cytology, and mycobacteria.13,25
reliable differential finding in the ECG is the Pericardiocentesis is only indicated to treat
ratio of the magnitude of the ST-segment cardiac tamponade or when purulent peri-
elevation to the T-wave amplitude in the V6 carditis is suspected.
lead; acute pericarditis is more likely when If pericardiocentesis is ineffective or tam-
the ratio is greater than 0.25.19,23 ponade recurs, subxiphoid pericardial drain-
Acute pericarditis is often associated with age and biopsy with histology and cultures
elevated markers of acute inflammation, are recommended.13 The diagnostic yield for
including C-reactive protein, erythrocyte pericardiocentesis and pericardial biopsy
sedimentation rate, and leukocyte count.
Markers of myocardial injury such as the
MB isoenzyme of creatine kinase and car-
diac troponins are often elevated. Troponin I
elevation occurs in patients with ST-segment
elevation and likely corresponds to epicar-
dial cell damage. This type of cell damage
in patients with acute pericarditis is seen in
especially young patients and in those with
recent infection. Family physicians should
consider consultation with a cardiologist for
patients with an atypical pericarditis presen-
tation and elevated troponin I.24
In patients with suspected pericarditis,
echocardiography helps detect pericardial Figure 1. Computed tomography of a peri-
cardial effusion in a 54-year-old man with
effusion, cardiac tamponade, and underly- chest pain and shortness of breath. The peri­
ing myocardial disease.10,25 When pericardial cardium (long arrow) and the epicardium
effusion is found in the setting of clinical (short arrow) are shown.

1512  American Family Physician www.aafp.org/afp Volume 76, Number 10 ◆ November 15, 2007
 Acute Pericarditis

is about the same (19 percent).14 The yield

increases to 34 percent when either proce- Table 3. Indications for
dure is performed therapeutically, as for Hospitalization of Patients with
patients with symptomatic cardiac tampon- Acute Pericarditis
ade. Some experts recommend that pericar-
diocentesis not be performed exclusively for Anticoagulation therapy
diagnostic purposes unless purulent pericar- Body temperature greater than 100.4° F (38° C)
ditis is strongly suspected.14,26 Echocardiographic findings of a large
pericardial effusion
Treatment Findings of cardiac tamponade (i.e.,
hypotension and neck vein distention)
The goal of treating acute viral pericarditis is
History of trauma and compromised immune
to relieve pain and to prevent complications system
such as recurrence, tamponade, and chronic Myopericarditis
restrictive pericarditis. Because most episodes Troponin I elevation
of acute pericarditis are uncomplicated, many
patients may be managed in the outpatient Information from reference 26.
setting.26,27 Indications for hospitalization of
patients with acute pericarditis are listed in
Table 3.26 When tamponade is identified, peri- treat [NNT] = 5). Addition of colchicine also
cardiocentesis is the intervention of choice.13 decreased symptom persistence at 72 hours
If the patient has no poor prognostic indica- (11.7 percent versus 36.7 percent for aspirin
tors (e.g., body temperature > 100.4° F [38° C], or prednisone alone; P  = .003; NNT = 4).29
findings of tamponade, history of immuno- Results were similar for patients with recur-
compromise or trauma) and the basic labora- rent pericarditis.28
tory studies discussed earlier are reassuring, Use of corticosteroids alone was an inde-
outpatient management is an option.24 pendent risk factor for the subsequent
Nonsteroidal anti-inflammatory drugs, recurrence of pericarditis in this study,29
including aspirin and ibuprofen (Motrin), although corticosteroids may be useful in
have been used to relieve chest pain, fever, refractory acute pericarditis. Side effects in
and friction rub in patients with acute peri- the colchicine and noncolchicine groups
carditis.10,24-26 Aspirin (up to 800 mg every six were similar. This study was limited by an
hours) and ibuprofen (300 to 800 mg every open-label design and the use of the subjec-
six hours) are conventional therapies.10 tive end points of symptom recurrence, but
The authors of two recent randomized the results29 provide some evidence that col-
controlled trials examined the value of col- chicine should be considered as an adjunct
chicine in the treatment of acute and recur- to anti-inflammatory drugs, and that corti-
rent pericarditis.28,29 Participants in each study costeroids should be used with caution.
received either conventional treatment with
aspirin (800 mg orally every six or eight hours Prognosis
for seven to 10 days with gradual tapering Generally, acute pericarditis is benign and self-
over three to four weeks) or aspirin at the limiting. Occasionally, acute pericarditis will
same dose combined with colchicine (1.0 to be complicated by tamponade, constriction,
2.0 mg for the first day, then 0.5 to 1.0 mg or recurrence. Nearly 24 percent of patients
daily for three months). Patients intolerant with acute pericarditis will have recurrence.
of aspirin were given a tapering dose of pred- Most of these patients will have a single recur-
nisone over one month.29 rence within the first weeks after the initial
The addition of colchicine reduced the episode, and a minority may have repeated
recurrence rate of pericarditis at 18 months episodes for months or years. The first episode
(32.3 percent for aspirin or prednisone of viral pericarditis is usually the most severe,
alone, 10.7 percent for an anti-inflammatory whereas recurrences are less severe and may
plus colchicine; P = .004; number needed to present only with chest pain.16

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Acute Pericarditis

11. Permanyer-Miralda G, Sagrista-Sauleda J, Soler-Soler J.

The Authors Primary acute pericardial disease: a prospective series of
231 consecutive patients. Am J Cardiol 1985;56:623-30.
LESLIE E. TINGLE, MD, is a faculty member and the pro-
12. Sagrista-Sauleda J, Angel J, Permanyer-Miralda G,
gram director of the Baylor Family Medicine Residency Soler-Soler J. Long-term follow-up of idiopathic chronic
at Garland, Tex. He received his medical degree from pericardial effusion. N Engl J Med 1999;341:2054-9.
the University of Texas Medical Branch at Galveston and
13. Permanyer-Miralda G. Acute pericardial disease:
completed his residency in family medicine at the Univer-
approach to the aetiologic diagnosis. Heart 2004;
sity of Arkansas for Medical Sciences College of Medicine, 90:252-4.
Little Rock.
14. Soler-Soler J, Permanyer-Miralda G, Sagrista-Sauleda J.
DANIEL MOLINA, MD, is a chief resident in the Baylor Fam- A systematic diagnostic approach to primary acute peri-
ily Medicine Residency at Garland. He received his medi- cardial disease. The Barcelona experience. Cardiol Clin
cal degree from the Uniformed Services University of the 1990;8:609-20.
Health Sciences, Bethesda, Md. and is a Lieutenant in the 15. Spodick DH. Pericardial rub. Prospective, multiple
United States Public Health Service. observer investigation of pericardial friction in 100
patients. Am J Cardiol 1975;35:357-62.
CHARLES W. CALVERT, DO, is a second-year resident in 16. Sagrista-Sauleda J, Permanyer-Miralda G, Soler-Soler
the Baylor Family Medicine Residency at Garland. He J. Diagnosis and management of acute pericardial syn-
received his medical degree from the University of North dromes. [Spanish] Rev Esp Cardiol 2005;58:830-41.
Texas Health Science Center, Texas College of Osteopathic 17. Reuter H, Burgess L, van Vuuren W, Doubell A. Diagnos-
Medicine, Fort Worth. ing tuberculous pericarditis. Q J Med 2006;99:827-39.
Address correspondence to Leslie E. Tingle, MD, 601 Clara 18. Marinella MA. Electrocardiographic manifestations and
Barton Blvd., Suite 340, Garland, TX 75042 (e-mail: lest@ differential diagnosis of acute pericarditis. Am Fam Phy-
baylorhealth.edu). Reprints are not available from the sician 1998;57:699-704.
authors. 19. Spodick DH. Electrocardiogram in acute pericardi-
tis. Distribution of morphologic and axial changes by
The authors thank Debra Faber; Rajasree Nair, MD; John stages. Am J Cardiol 1974;33:470-4.
Bret, MD; and Shannon Moss, PhD, for their assistance 20. Baljepally R, Spodick DH. PR-segment deviation as the
with the preparation of the manuscript. initial electrocardiographic response in acute pericardi-
tis. Am J Cardiol 1998;81:1505-6.
Author disclosure: Nothing to disclose.
21. Aikat S, Ghaffari S. A review of pericardial diseases:
clinical, ECG and hemodynamic features and manage-
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