The new england journal of medicine

clinical practice

Acute Pericarditis
Richard A. Lange, M.D., and L. David Hillis, M.D.
This Journal feature begins with a case vignette highlighting a common clinical problem.
Evidence supporting various strategies is then presented, followed by a review of formal guidelines,
when they exist. The article ends with the authors’ clinical recommendations.

A 35-year-old woman who is otherwise healthy has had constant retrosternal chest pain
for two days. The pain becomes worse when she lies down and improves when she sits
up and leans forward. On physical examination, the patient is afebrile and has a friction
rub. The 12-lead electrocardiogram shows widespread ST-segment elevation and con-
comitant PR-segment depression. How should the patient be evaluated and treated?

the clinical problem

The fibrous pericardium surrounding the heart is composed of visceral and parietal From the Department of Internal Medicine,
layers separated by the pericardial cavity, which normally contains 15 to 50 ml of straw- Cardiology Division, Johns Hopkins Medi-
cal Institutions, Baltimore (R.A.L.); and the
colored fluid. Acute pericarditis may occur as an isolated entity or as the result of a sys- University of Texas Southwestern Medical
temic disease. The incidence of pericarditis in postmortem studies ranges from 1 percent Center, Dallas (L.D.H.). Address reprint
to 6 percent, whereas it is diagnosed ante mortem in only 0.1 percent of hospitalized requests to Dr. Hillis at Rm. G5.232, Uni-
versity of Texas Southwestern Medical Cen-
patients and in 5 percent of patients seen in emergency rooms with chest pain but with- ter, 5323 Harry Hines Blvd., Dallas, TX
out myocardial infarction.1,2 The possible sequelae of pericarditis include cardiac tam- 75390-9030, or at dhilli@parknet.pmh.org.
ponade,3,4 recurrent pericarditis,5,6 and pericardial constriction.7-11
N Engl J Med 2004;351:2195-202.
Copyright © 2004 Massachusetts Medical Society.

strategies and evidence

causes
In 9 of 10 patients with acute pericarditis, the cause of the disease is either viral or un-
known (idiopathic).3,4 In the remainder of patients, pericarditis occurs after a transmu-
ral myocardial infarction, in association with other infectious agents, in conjunction with
a dissecting aortic aneurysm (in which blood leaks into the pericardial space), after
blunt or sharp trauma to the chest, as a result of neoplastic invasion of the pericardium,
after chest irradiation, in association with uremia, after cardiac or other thoracic surgery,
in association with an inflammatory or autoimmune disorder, or as a result of taking
certain pharmacologic agents (Table 1).

evaluation
A diagnosis of acute pericarditis should be reserved for patients with an audible peri-
cardial friction rub or chest pain with typical electrocardiographic findings, most nota-
bly widespread ST-segment elevation. Subsequent testing is performed to assess the
cause of the disease, to corroborate the diagnosis, and to direct therapy. Important
conditions that may cause chest pain similar to that of pericarditis include myocardial
infarction and pulmonary embolism (Table 2).

History
The chest pain of acute pericarditis typically is retrosternal in location, sudden in onset,
and pleuritic in nature, in that it is exacerbated by inspiration. It is often worse when the

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 The new england journal of medicine

Table 1. Tests and Treatments for Various Causes of Acute Pericarditis.*

Condition Estimated Incidence† Clinical Indications and Tests Usual Treatment

Idiopathic 85–90% Aspirin, NSAIDs
Infectious
Viral 1–2% Acute and convalescent viral titers, Aspirin, NSAIDs
viral cultures, serologic test for HIV
Bacterial 1–2% Fever, elevated white-cell count; exam- Antibiotics, drainage of
ination of pericardial fluid pericardial fluid
Tuberculous 4% Chest radiography, tuberculin skin Multidrug antitubercu-
test, histologic examination, cul- lous therapy and
tures, and measurement of adeno- prednisone
sine deaminase level in pericardial
fluid and tissue
Acute myocardial NA (occurs in 5–10% of Electrocardiography, serum troponin Aspirin (avoid NSAIDs)
infarction patients with myocar- or creatine kinase, echocardio-
dial infarction) gram
Aortic dissection Rare (<1%) Magnetic resonance imaging, com- Urgent surgery
puted tomography, transesopha-
geal echocardiography
Trauma NA Clinical history NSAIDs (avoid aspirin)
Neoplasm 7% Constitutional symptoms, lymphade- NSAIDs, glucocorti-
nopathy; chest radiography, coids (by intraperi-
examination of pericardial fluid cardial instillation)
Chest-wall irradiation Rare (<1%) Clinical history NSAIDs
Uremia NA (occurs in approxi- Serum blood urea nitrogen and creati- Initiate or intensify
mately 5% of patients nine levels dialysis
with chronic renal dis-
ease before initiation of
dialysis and 13% after
initiation of dialysis)
Cardiotomy or thoracic Rare (<1%) Clinical history, evidence of poly- Aspirin, NSAIDs
surgery serositis; chest radiography,
erythrocyte sedimentation rate
Autoimmune or inflam- 3–5% Rheumatoid factor, complement Aspirin, NSAIDs,
matory disease levels, antinuclear antibodies glucocorticoids
Adverse drug reaction‡ Rare (<1%) Clinical history; eosinophil count Discontinue drug;
aspirin, NSAIDs

* NSAID denotes nonsteroidal antiinflammatory drug, HIV human immunodeficiency virus, and NA not applicable.
† Estimated incidence is derived from studies that excluded patients with pericarditis associated with renal failure, known
neoplastic disease, trauma, or radiation. Data are adapted from Zayas et al.3 and Permanyer-Miralda et al.4
‡ Commonly implicated drugs include dantrolene, doxorubicin, hydralazine, isoniazid, methysergide, pergolide, phenyl-
butazone, phenytoin, and procainamide.

patient is supine and improves when he or she sits ease.3 Typically, the rub is a high-pitched scratchy
upright and leans forward. As in myocardial infarc- or squeaky sound best heard at the left sternal bor-
tion, the pain often radiates to the neck, arms, or leftder at end expiration with the patient leaning for-
shoulder. If the pain radiates to one or both trape- ward. Since pericardial friction rubs often vary in
zius muscle ridges, it is probably due to pericardi- intensity from minute to minute, patients who
tis, since the phrenic nerve (which innervates these have suspected pericarditis should be examined re-
muscles) traverses the pericardium. peatedly.
The friction rub corresponds temporally to
Physical Examination movement of the heart within the pericardial sac.
About 85 percent of patients with pericarditis have Although it is thought to be caused by the rubbing
an audible friction rub during the course of their dis- together of the inflamed, adjacent visceral and pa-

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 clinical practice

Table 2. Features That Differentiate Pericarditis from Myocardial Ischemia or Infarction and Pulmonary Embolism.

Symptom and Clinical Myocardial Ischemia

Finding or Infarction Pericarditis Pulmonary Embolism
Chest pain
Location Retrosternal Retrosternal Anterior, posterior, or lateral
Onset Sudden, often waxing Sudden Sudden
and waning
Character Pressure-like, heavy, Sharp, stabbing, occasionally dull Sharp, stabbing
squeezing
Change with respiration No Worsened with inspiration In phase with respiration (absent
when the patient is apneic)
Change with position No Worse when patient is supine; No
improved when sitting up
or leaning forward
Radiation Jaw, neck, shoulder, Jaw, neck, shoulder, one or both Shoulder
one or both arms arms, trapezius ridge
Duration Minutes (ischemia); Hours to days Hours to days
hours (infarction)
Response to nitroglycerin Improved No change No change
Physical examination
Friction rub Absent (unless peri- Present (in 85% of patients) Rare; a pleural friction rub is
carditis is present) present in 3% of patients
S3 sound, pulmonary May be present Absent Absent
congestion
Electrocardiogram
ST-segment elevation Convex and localized Concave and widespread Limited to lead III, aVF, and V1
PR-segment depression Rare Frequent None
Q waves May be present Absent May be present in lead III or aVF
or both
T waves Inverted when ST Inverted after ST segments have Inverted in lead II, aVF, or V1
segments are still normalized to V4 while ST segments are
elevated elevated
Atrioventricular block, Common Absent Absent
ventricular arrhythmias
Atrial fibrillation May be present May be present May be present

rietal pericardial surfaces, it is present even when a The presence of systemic arterial hypotension,
large effusion separates these surfaces, and it often tachycardia, elevated jugular venous pressure, and
disappears when the effusion is evacuated, a find- pulsus paradoxus (a decrease in systolic arterial
ing that casts doubt on this explanation. The friction pressure of more than 10 mm Hg with inspiration)
rub is classically described as having three compo- suggests cardiac tamponade; the presence of pul-
nents, which correspond to atrial systole (in patients sus paradoxus is most sensitive, although not spe-
with sinus rhythm), ventricular systole, and rapid cific, for the diagnosis. Tamponade, a potentially
ventricular filling during early diastole. However, lethal complication of pericarditis, is reported in
in reality, the rub is reported to be triphasic in about about 15 percent of patients with idiopathic peri-
half the patients, biphasic in a third, and monopha- carditis but in as many as 60 percent of those with
sic in the remainder.12 A pericardial friction rub neoplastic, tuberculous, or purulent pericarditis.13
should not be confused with a pleural rub; the With tamponade, the accumulation of pericardial
former is audible throughout the respiratory cycle, fluid increases the intrapericardial pressure so that
whereas the latter is absent when respirations are it equals or exceeds the pressure in the right heart
suspended. chambers, leading to impaired filling, with result-

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ant collapse of the right atrium and ventricle during ST-segment elevations are often convex (dome-
diastole and diminished cardiac output. These find- shaped) rather than concave in configuration, and
ings should prompt immediate echocardiographic they are regional rather than widespread; Q-wave
evaluation, including pulsed-wave Doppler analysis. formation and loss of R-wave voltage often occur;
A body temperature greater than 38°C is uncom- T-wave inversions appear before the ST segments
mon and may indicate purulent pericarditis. Pa- return to baseline; PR-segment depression is un-
tients who are febrile should undergo prompt echo- common; and atrioventricular block or ventricular
cardiography, and the physician should consider arrhythmias are common (Table 2). The most reli-
obtaining pericardial fluid for analysis. able distinguishing feature may be the ratio of ST-
segment elevation (in millimeters) to T-wave am-
Electrocardiography plitude (height in millimeters) in lead V6. When
The 12-lead electrocardiogram in patients with this ratio exceeds 0.24, acute pericarditis is almost
acute pericarditis classically shows widespread up- always present.14
ward concave ST-segment elevation and PR-seg-
ment depression (Fig. 1).14-17 The electrocardio- Chest Radiography
graphic abnormalities may evolve through four Chest radiography is performed primarily to rule out
phases: diffuse ST-segment elevation and PR-seg- abnormalities in the mediastinum or lung fields that
ment depression (stage I); normalization of the may be responsible for the pericarditis. The appear-
ST and PR segments (stage II); widespread T-wave ance of cardiomegaly indicates a substantial peri-
inversions (stage III); and normalization of the cardial effusion (more than 250 ml).
T waves (stage IV).15 Although the prompt institu-
tion of therapy may prevent the appearance of all Serologic and Other Testing
four stages,18 the changes in stage I are observed in Data assessing the cost-effectiveness of various
more than 80 percent of patients with pericarditis.19 testing strategies are lacking. Although the white-
ST-segment elevation also occurs in patients with cell count, erythrocyte sedimentation rate, and se-
myocardial infarction, but several features may help rum C-reactive protein concentration usually are el-
to distinguish these entities. With infarction, the evated in patients with acute pericarditis, these tests

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

II

Figure 1. A 12-Lead Electrocardiogram from a Patient with Acute Pericarditis, Demonstrating Widespread ST-Segment
Elevation and PR-Segment Depression.

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 clinical practice

usually provide little, if any, insight into the cause patients with acute pericarditis in whom the cause
of the disease or indications regarding which ther- was unknown after routine clinical and laboratory
apy is called for. A markedly elevated white-cell evaluation, pericardiocentesis and pericardial biop-
count suggests the presence of purulent pericardi- sy provided a diagnosis in only 6 percent and 5 per-
tis; therefore, it is reasonable to obtain a complete cent of cases, respectively. In subjects with tam-
blood count in all patients. The clinical presentation ponade of unknown cause, pericardiocentesis and
should guide the ordering of additional tests (i.e., pericardial biopsy provided a diagnosis in 29 per-
serologic testing for antinuclear antibody or infec- cent and 54 percent of cases, respectively.4
tion with the human immunodeficiency virus). Rou- When pericardiocentesis is performed, the fluid
tine serologic testing, including testing for anti- should be analyzed for red-cell and white-cell
nuclear antibody and rheumatoid factor, reveals a counts, cytologic evidence of cancer, and triglycer-
source for the pericarditis in only 10 to 15 percent ides (a fluid that is milky in color and consistency
of patients, and in these cases other evidence typi- suggests a chylous effusion). Although the pH and
cally suggests the underlying disease. Many patients levels of glucose, lactic dehydrogenase, and protein
with idiopathic pericarditis probably have a viral in- often are measured, no accepted criteria link such
fection, but viral cultures and antibody titers are not measures to specific causes of pericarditis. The fluid
useful clinically,3,4,13 and the documentation of a should be examined microscopically for organisms,
recent viral infection does not alter management. and it should be cultured. The results of polymer-
Plasma troponin concentrations are elevated in ase-chain-reaction assays or high concentrations of
35 to 50 percent of patients with pericarditis, a adenosine deaminase activity (greater than 30 U per
finding that is thought to be caused by epicardial liter) are helpful in identifying Mycobacterium tuber-
inflammation rather than myocyte necrosis.6,20,21 culosis.24-27 Pericardial biopsy should be considered
The magnitude of elevation in the serum troponin for patients who have recurrent tamponade despite
concentration appears to correlate with the magni- treatment.13
tude of the ST-segment elevation, and the concen-
tration usually returns to normal within one to two treatment
weeks after diagnosis. An elevated troponin con- If a specific cause of pericarditis is identified, treat-
centration does not predict an adverse outcome,5,6 ment should be directed accordingly. A detailed
although a prolonged elevation (lasting longer than discussion of therapies directed to specific causes
two weeks) suggests associated myocarditis, which is beyond the scope of this review, but the treat-
has a worse prognosis. Although the concentrations ments are summarized in Table 1.
of serum creatine kinase and its MB fraction may For patients with idiopathic pericarditis, therapy
also be elevated with pericarditis, they are abnormal is aimed at the relief of chest pain and inflammation.
less often than is the troponin concentration. However, such treatment does nothing to prevent
tamponade, constriction, or recurrent pericarditis.
Echocardiography Nonsteroidal antiinflammatory agents (NSAIDs) are
Transthoracic echocardiography22,23 is often rec- the mainstay of therapy; in observational studies,
ommended in patients with suspected pericarditis, these drugs are effective in relieving chest pain in
since the presence of an effusion helps to confirm 85 to 90 percent of patients,3,4,20 and limited obser-
the diagnosis, and clinical or echocardiographic ev- vational data suggest that the various agents have
idence of tamponade indicates the need for pericar- similar efficacy.28-30 Aspirin (2 to 4 g daily), in-
diocentesis. The test is unnecessary in patients with domethacin (75 to 225 mg daily), and ibuprofen
unequivocal evidence of pericarditis and no poor (1600 to 3200 mg daily) are prescribed most often,
prognostic indicators. with ibuprofen preferred, since it has a lower inci-
dence of adverse effects than the others. Aspirin is
Pericardiocentesis and Biopsy preferable for patients who have had a recent myo-
Pericardiocentesis is indicated in patients with peri- cardial infarction, since other NSAIDs impair scar
cardial tamponade and in those with known or sus- formation in studies in animals.28,31-33 Indometha-
pected purulent or neoplastic pericarditis. In pa- cin should be avoided in patients with coronary
tients with a small or midsize effusion of unknown artery disease, since it diminishes coronary blood
cause, neither pericardiocentesis nor pericardial bi- flow.28
opsy usually yields a diagnosis. In 231 consecutive Colchicine (administered at a dose of 0.6 mg

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twice daily) appears to be effective alone or in com- ministration of NSAIDs. If a small or midsize effu-
bination with ibuprofen in treating acute pericardi- sion is present, it usually resolves within weeks. As
tis, although it has not been tested in randomized a result, hospitalization for evaluation or treatment
trials; it is preferred for patients who have recur- is unnecessary in most cases, and follow-up evalu-
rent pericarditis.34,35 In a multicenter trial of 51 pa- ation is not required unless symptoms recur or new
tients who had recurrent pericarditis despite treat- symptoms appear. Several indicators of a poor prog-
ment with nonsteroidal antiinflammatory agents, nosis are recognized, however. These include a tem-
glucocorticoids, pericardiocentesis, or some com- perature above 38°C, a subacute onset (symptoms
bination thereof, only 7 of the patients who were developing during a period of several weeks), an im-
treated with colchicine (14 percent) had a recur- munosuppressed state, pericarditis associated with
rence during 1004 patient-months of follow-up.34 trauma, a history of oral anticoagulant therapy, my-
Typically, patients’ symptoms improve within opericarditis (pericarditis with clinical or serologic
days of the initiation of antiinflammatory therapy. evidence of myocardial involvement), a large peri-
If chest pain persists after two weeks of treatment cardial effusion (an echo-free space of more than
with an NSAID, a different NSAID should be given 20 mm in width) (Fig. 2), or cardiac tamponade.
or colchicine should be added to provide combina- Although serologic criteria for associated myocardi-
tion therapy. If the patient continues to have chest tis are not well defined, historically concern has fo-
pain despite combination therapy, glucocorticoids cused on elevated levels of creatine kinase, particu-
should be considered. A lack of response to gluco- larly if the elevation is sustained for more than a
corticoids often reflects the use of an inadequate week. Patients with one or more of these symptoms
dose or too-rapid tapering. Patients with a relapse of are at increased risk for serious complications, in-
pericarditis after a short-term course of low-dose cluding death from tamponade and purulent peri-
glucocorticoid therapy often obtain symptomatic carditis. In a report describing 253 patients who had
relief when higher-dose prednisone therapy (1 to none of these poor prognostic indicators and were
1.5 mg per kilogram of body weight daily) is ad- treated without admission to the hospital,20 none of
ministered for four weeks.36 the patients had serious complications during an
Concern has been raised that treating acute peri- average follow-up of 39 months.
carditis with prednisone may increase the risk of
recurrence.37-39 In observational studies, patients guidelines
who received glucocorticoids early in the course of
the disease appeared to be more likely to develop There are no specific guidelines for evaluating or
recurrent pericarditis than patients who did not re- treating pericarditis. A joint task force of the Amer-
ceive glucocorticoids. Data from animal studies have ican College of Cardiology, the American Heart
shown that glucocorticoids exacerbated pericardial Association, and the American Society of Echocar-
injury that was virally induced.40 These data argue diography recommends that echocardiography be
against the routine administration of glucocorti- performed in all patients with known or suspect-
coids during a first episode of pericarditis.35,39,41,42 ed pericardial disease. (Guidelines are available on-
In general, systemic glucocorticoid treatment line at www.acc.org, www.americanheart.org, and
(prednisone, 1 to 1.5 mg per kilogram daily) should www.asecho.org.) Subsequent echocardiography
be restricted to patients with connective-tissue dis- is not recommended in patients who are stable and
eases or severely symptomatic recurrent pericarditis whose pericardial effusions are small, but this pro-
that is unresponsive to NSAIDs and colchicine. Al- cedure may be performed if a recurrence of effu-
ternatively, the intrapericardial instillation of a non- sion or early constriction is suspected.22,23
absorbable steroid has appeared highly effective in
a case series of patients with refractory or recurrent areas of uncertainty
pericarditis and has averted the adverse effects of
these agents.43 Randomized trials are lacking to guide the evalua-
tion and management of acute pericarditis. Strate-
hospitalization gies to prevent recurrent pericarditis, which occurs
In most patients, acute pericarditis has a brief and in 15 to 30 percent of patients with idiopathic peri-
benign course, with symptoms lasting less than two carditis, require further study. It remains uncertain,
weeks, and the condition responds well to the ad- but of concern, whether the early use of glucocorti-

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 clinical practice

coids increases the risk of recurrent pericarditis.

When there is a recurrence, pericardiectomy can be
performed, but the procedure is rarely successful in
resolving symptoms, perhaps because of an auto-
immunologic reaction to persistent antigens in the
epicardium. Observational data suggest that phys-
ical invasion of the pericardium (with pericardioto-
my or the creation of a window) promotes recurrenc-
es, a finding similar to that regarding glucocorticoid
therapy. In most patients, then, treatment of recur-
rent pericarditis is largely supportive. Observational
data suggest that colchicine offers the best prophy-
laxis against recurrent episodes. Although recur-
rences are often accompanied by a pericardial effu-
sion, tamponade and constriction rarely occur; thus,
these effusions do not require drainage.

Figure 2. Large Pericardial Effusion.

conclusions A parasternal long-axis view from a transthoracic echocardiogram shows the
and recommendations heart surrounded by a large pericardial effusion, seen as an echo-free space
more than 20 mm in width (arrow).
In patients with acute pericarditis, such as the wom-
an described in the vignette, the cause is most often
either idiopathic or viral. The diagnosis is based on
clinical criteria (i.e., a pericardial friction rub or
chest pain with typical electrocardiographic find- above 38°C, a subacute onset, an immunosup-
ings), and laboratory testing is not routinely re- pressed state, a history of trauma, a history of oral
quired. Since simple pericardiocentesis with sub- anticoagulant therapy, myopericarditis, a large peri-
sequent analysis of the pericardial fluid is unlikely cardial effusion, or evidence of tamponade. In most
to provide valuable diagnostic information in the patients, acute pericarditis has a brief and benign
absence of cardiac tamponade or suspected puru- course and an excellent response to NSAIDs, alone
lent or neoplastic pericarditis, the procedure should or in combination with colchicine. Therapy with
generally be reserved for patients in whom such glucocorticoids should be reserved for the patient
conditions are suspected. with pericarditis that is unresponsive to combina-
The evaluation and treatment of patients with tion therapy, since some studies suggest that the
acute pericarditis can be performed in the ambula- early use of these drugs may increase the risk of re-
tory setting unless the patient has a temperature currence.

references
1. Lorell BH. Pericardial diseases. In: 5. Imazio M, Demichelis B, Cecchi E, et al. JH. Transient effusive-constrictive pericar-
Braunwald E, ed. Heart disease: a textbook Cardiac troponin I in acute pericarditis. ditis due to chemotherapy. Clin Cardiol
of cardiovascular medicine. 5th ed. Phila- J Am Coll Cardiol 2003;42:2144-8. 1999;22:316-8.
delphia: W.B. Saunders, 1997:1478-534. 6. Bonnefoy E, Godon P, Kirkorian G, 10. Haley JH, Tajik AJ, Danielson GK, Schaff
2. Launbjerg J, Fruergaard P, Hesse B, Jor- Fatemi M, Chevalier P, Touboul P. Serum HV, Mulvagh SL, Oh JK. Transient constric-
gensen F, Elsborg L, Petri A. Long-term risk cardiac troponin I and ST-segment elevation tive pericarditis: causes and natural history.
of death, cardiac events and recurrent chest in patients with acute pericarditis. Eur Heart J Am Coll Cardiol 2004;43:271-5.
pain in patients with acute chest pain of dif- J 2000;21:832-6. 11. Sagrista-Sauleda J, Permanyer-Miralda
ferent origin. Cardiology 1996;87:60-6. 7. Allaria A, Michelli D, Capelli H, Berri G, G, Candell-Riera J, Angel J, Soler-Soler J.
3. Zayas R, Anguita M, Torres F, et al. Inci- Gutierrez D. Transient cardiac constriction Transient cardiac constriction: an unrecog-
dence of specific etiology and role of meth- following purulent pericarditis. Eur J Pediatr nized pattern of evolution in effusive acute
ods for specific etiologic diagnosis of pri- 1992;151:250-1. idiopathic pericarditis. Am J Cardiol 1987;
mary acute pericarditis. Am J Cardiol 1995; 8. Oh JK, Hatle LK, Mulvagh SL, Tajik AJ. 59:961-6.
75:378-82. Transient constrictive pericarditis: diagno- 12. Spodick DH. Pericardial rub: prospec-
4. Permanyer-Miralda G, Sagrista-Saule- sis by two-dimensional Doppler echocar- tive, multiple observer investigation of peri-
da J, Soler-Soler J. Primary acute pericardial diography. Mayo Clin Proc 1993;68:1158- cardial friction in 100 patients. Am J Cardiol
disease: a prospective series of 231 consecu- 64. 1975;35:357-62.
tive patients. Am J Cardiol 1985;56:623-30. 9. Woods T, Vidarsson B, Mosher D, Stein 13. Permanyer-Miralda G. Acute pericardial

n engl j med 351;21 www.nejm.org november 18, 2004 2201

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Downloaded from nejm.org at UNIVERSIDAD TECNOLOGICA DE PEREIRA on November 9, 2021. For personal use only. No other uses without permission.
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 clinical practice

disease: approach to the aetiologic diagno- tice Guidelines (ACC/AHA/ASE Committee Brown EJ Jr, Hale S, Braunwald E. In-
sis. Heart 2004;90:252-4. to Update the 1997 Guidelines for the Clini- domethacin-induced scar thinning after ex-
14. Ginzton LE, Laks MM. The differential cal Application of Echocardiography). Cir- perimental myocardial infarction. Circula-
diagnosis of acute pericarditis from the nor- culation 2003;108:1146-62. tion 1983;67:1290-5.
mal variant: new electrocardiographic crite- 24. Aggeli C, Pitsavos C, Brili S, et al. Rele- 34. Adler Y, Finkelstein Y, Guindo J, et al.
ria. Circulation 1982;65:1004-9. vance of adenosine deaminase and lysozyme Colchicine treatment for recurrent peri-
15. Spodick DH. Diagnostic electrocardio- measurements in the diagnosis of tubercu- carditis: a decade of experience. Circulation
graphic sequences in acute pericarditis: sig- lous pericarditis. Cardiology 2000;94:81-5. 1998;97:2183-5.
nificance of PR segment and PR vector 25. Burgess LJ, Reuter H, Carstens ME, Tal- 35. Millaire A, de Groote P, Decoulx E,
changes. Circulation 1973;48:575-80. jaard JJ, Doubell AF. The use of adenosine Goullard L, Ducloux G. Treatment of recur-
16. Surawicz B, Lasseter KC. Electrocardio- deaminase and interferon-gamma as diag- rent pericarditis with colchicine. Eur Heart J
gram in pericarditis. Am J Cardiol 1970;26: nostic tools for tuberculous pericarditis. 1994;15:120-4.
471-4. Chest 2002;122:900-5. 36. Marcolongo R, Russo R, Laveder F, No-
17. Wang K, Asinger RW, Marriott HJL. ST- 26. Cegielski JP, Devlin BH, Morris AJ, et al. venta F, Agostini C. Immunosuppressive
segment elevation in conditions other than Comparison of PCR, culture, and histopa- therapy prevents recurrent pericarditis. J Am
acute myocardial infarction. N Engl J Med thology for diagnosis of tuberculous peri- Coll Cardiol 1995;26:1276-9.
2003;349:2128-35. carditis. J Clin Microbiol 1997;35:3254-7. 37. Stubbs DF. Post-acute myocardial in-
18. Spodick DH. Acute pericarditis: current 27. Dogan R, Demircin M, Sarigul A, Ciliv farction symptomatic pericarditis (PAMISP):
concepts and practice. JAMA 2003;289: G, Bozer AY. Diagnostic value of adenosine report on a large series and the effect of
1150-3. deaminase activity in pericardial fluids. methylprednisolone therapy. J Int Med Res
19. Bruce MA, Spodick DH. Atypical elec- J Cardiovasc Surg (Torino) 1999;40:501-4. 1986;14:Suppl 1:25-9.
trocardiogram in acute pericarditis: charac- 28. Schifferdecker B, Spodick DH. Nonste- 38. Spodick DH. Intrapericardial treatment
teristics and prevalence. J Electrocardiol roidal anti-inflammatory drugs in the treat- of persistent autoreactive pericarditis/myo-
1980;13:61-6. ment of pericarditis. Cardiol Rev 2003;11: pericarditis and pericardial effusion. Eur
20. Imazio M, Demichelis B, Parrini I, et al. 211-7. Heart J 2002;23:1481-2.
Day-hospital treatment of acute pericarditis: 29. Arunasalam S, Siegel RJ. Rapid resolu- 39. Godeau P, Derrida JP, Bletry O, Herre-
a management program for outpatient ther- tion of symptomatic acute pericarditis with man G. Recurrent acute pericarditis and
apy. J Am Coll Cardiol 2004;43:1042-6. ketorolac tromethamine: a parenteral non- corticoid dependence: apropos of 10 cases.
21. Newby LK, Ohman EM. Troponins in steroidal antiinflammatory agent. Am Heart Sem Hop 1975;51:2393-400. (In French.)
pericarditis: implications for diagnosis and J 1993;125:1455-8. 40. Kilbourne ED, Wilson CB, Perrier D.
management of chest pains patients. Eur 30. Berman J, Haffajee CI, Alpert JS. Thera- The induction of gross myocardial lesions
Heart J 2000;21:798-800. py of symptomatic pericarditis after myocar- by a Coxsackie (pleurodynia) virus and corti-
22. Cheitlin MD, Alpert JS, Armstrong WF, dial infarction: retrospective and prospec- sone. J Clin Invest 1956;35:362-70.
et al. ACC/AHA guidelines for the clinical tive studies of aspirin, indomethacin, 41. Clementy J, Jambert H, Dallocchio M.
application of echocardiography: a report of prednisone, and spontaneous resolution. Recurrent acute pericarditis: 20 cases. Arch
the American College of Cardiology/Ameri- Am Heart J 1981;101:750-3. Mal Coeur Vaiss 1979;72:857-61. (In French.)
can Heart Association Task Force on Prac- 31. Brown EJ Jr, Kloner RA, Schoen FJ, 42. Raatikka M, Pelkonen PM, Karjalainen
tice Guidelines (Committee on Clinical Ap- Hammerman H, Hale S, Braunwald E. Scar J, Jokinen EV. Recurrent pericarditis in chil-
plication of Echocardiography): developed thinning due to ibuprofen administration dren and adolescents: report of 15 cases.
in collaboration with the American Society after experimental myocardial infarction. J Am Coll Cardiol 2003;42:759-64.
of Echocardiography. Circulation 1997;95: Am J Cardiol 1983;51:877-83. 43. Maisch B, Ristic AD, Pankuweit S. Intra-
1686-744. 32. Jugdutt BI, Basualdo CA. Myocardial in- pericardial treatment of autoreactive peri-
23. Cheitlin MD, Armstrong WF, Aurigem- farct expansion during indomethacin or cardial effusion with triamcinolone: the
ma GP, et al. ACC/AHA/ASE 2003 guideline ibuprofen therapy for symptomatic post in- way to avoid side effects of systemic corti-
update for the clinical application of echo- farction pericarditis: influence of other phar- costeroid therapy. Eur Heart J 2002;23:
cardiography: summary article: a report of macologic agents during early remodelling. 1503-8.
the American College of Cardiology/Ameri- Can J Cardiol 1989;5:211-21. Copyright © 2004 Massachusetts Medical Society.
can Heart Association Task Force on Prac- 33. Hammerman H, Kloner RA, Schoen FJ,

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