Acute Pericarditis - Treatment and Prognosis - UpToDate

23/2/24, 14:11 Acute pericarditis: Treatment and prognosis - UpToDate
Official reprint from UpToDate®

www.uptodate.com © 2024 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
Acute pericarditis: Treatment and prognosis

AUTHOR: Massimo Imazio, MD, FESC, FHFA
SECTION EDITOR: Martin M LeWinter, MD
DEPUTY EDITOR: Susan B Yeon, MD, JD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2024.

This topic last updated: Nov 10, 2023.
INTRODUCTION
The pericardium is a fibroelastic sac made up of visceral and parietal layers separated by a
(potential) space, the pericardial cavity. In healthy individuals, the pericardial cavity contains
15 to 50 mL of an ultrafiltrate of plasma.
Diseases of the pericardium present clinically in one of several ways:
● Acute and recurrent pericarditis

● Pericardial effusion without major hemodynamic compromise
● Cardiac tamponade
● Constrictive pericarditis
● Effusive-constrictive pericarditis
Acute pericarditis refers to inflammation of the pericardial sac. The term myopericarditis, or
perimyocarditis, is used for cases of acute pericarditis that also demonstrate myocardial
inflammation; myopericarditis is used for cases with predominant pericarditis and normal
ventricular function, and perimyocarditis is used for cases with predominant myocarditis
and/or ventricular dysfunction (ie, new wall motion abnormalities or reduced left ventricular
ejection fraction). (See "Myopericarditis".)
The treatment and prognosis of acute pericarditis will be reviewed here. The etiology, clinical
presentation, and diagnostic evaluation of acute pericarditis and other pericardial disease
processes are discussed separately. (See "Etiology of pericardial disease" and "Acute
pericarditis: Clinical presentation and diagnosis" and "Recurrent pericarditis" and
https://www-uptodate-com.bibliotecavirtual.udla.edu.ec/contents/acute-pericarditis-treatment-and-prognosis/print?search=pericarditis&source=s… 1/23
"Myopericarditis" and "Cardiac tamponade" and "Constrictive pericarditis: Diagnostic

evaluation" and "Pericardial effusion: Approach to diagnosis".)
TREATMENT
The therapy of acute pericarditis should be targeted as much as possible to the underlying
etiology ( table 1) [1-5]. However, in resource-abundant countries, most cases of acute
pericarditis in immunocompetent patients are due to viral infection or are idiopathic; it is
generally assumed that most cases of "idiopathic" pericarditis are viral in etiology. Because
of the relatively benign course associated with the most common causes of pericarditis (>80
percent of cases), it is not necessary to search for the etiology in all patients. As such, most
patients are treated for a presumptive viral cause with nonsteroidal antiinflammatory drugs
(NSAIDs) and colchicine. (See "Pericardial disease associated with cancer: Clinical
presentation and diagnosis" and "Tuberculous pericarditis" and "Purulent pericarditis".)
In acute viral or idiopathic pericarditis, no therapy has been rigorously proven to prevent
serious sequelae, such as cardiac tamponade and constrictive pericarditis. Fortunately,
however, these complications are rare [6,7]. (See "Constrictive pericarditis: Diagnostic
evaluation" and "Cardiac tamponade".)
General approach to treatment — In the treatment of acute pericarditis, the goals of

therapy are the relief of pain, resolution of inflammation (and, if present, pericardial
effusion), and the prevention of recurrence. Our general approach to treatment is as follows
( algorithm 1):
● Ambulatory versus inpatient treatment – Most low-risk patients with acute

pericarditis can be managed effectively in an ambulatory setting, while high-risk
patients should be admitted to initiate treatment and continue the diagnostic
evaluation. (See 'Which patients require hospitalization?' below.)
● Activity restriction – Patients should be instructed to restrict strenuous physical

activity until symptoms have resolved and biomarkers have normalized. (See 'Activity
restriction' below.)
● Initial treatment
• For nearly all patients with acute idiopathic or viral pericarditis, we recommend
combination therapy with colchicine plus NSAIDs. (See 'Nonsteroidal
antiinflammatory drugs' below and 'Colchicine' below.)
• For patients with an identified cause other than viral infection, specific therapy
appropriate to the underlying disorder is indicated.
• Glucocorticoids should be used for initial treatment of acute pericarditis only in

patients with contraindications to NSAIDs (eg, renal failure or pregnancy at ≥20
weeks gestation), or for specific indications (eg, systemic inflammatory diseases),
and should be used at the lowest effective dose. (See 'Glucocorticoids' below.)
● Tapering treatment – Following the resolution of symptoms, we taper the dose of the
antiinflammatory agent weekly in an attempt to reduce the subsequent recurrence
rate. Colchicine is continued for a total duration of three months. (See 'NSAID dosing'
below and 'Glucocorticoid dosing' below and 'Colchicine dosing' below.)
● Refractory or recurrent symptoms – Most patients whose symptoms worsen or recur

following the initial course of therapy can still be managed effectively with medical
therapy alone, and outpatient management remains feasible in almost all cases. (See
"Recurrent pericarditis".)
Which patients require hospitalization? — High-risk patients with acute pericarditis

( algorithm 1) should be admitted to the hospital in order to initiate appropriate therapy
and expedite a thorough initial evaluation. Conversely, patients with uncomplicated (ie, low-
risk) acute pericarditis can usually be evaluated and sent home, with outpatient follow-up to
assess the efficacy of treatment.
Features of acute pericarditis associated with a higher risk include [8,9]:
● Fever (>38°C [100.4°F])

● Subacute course (without acute onset of chest pain)
● Evidence suggesting cardiac tamponade (eg, hemodynamic compromise) (see "Cardiac
tamponade")
● A large pericardial effusion (ie, an end-diastolic echo-free space of more than 20 mm)
● Immunosuppression and immunodepressed patients
● Anticoagulant use (eg, vitamin K antagonists [eg, warfarin] or novel oral anticoagulants)
● Acute trauma
● Failure to show clinical improvement following seven days of appropriately dosed
NSAID and colchicine therapy
● Elevated cardiac troponin, which suggests myopericarditis/perimyocarditis
Patients with none of these high-risk features can be safely treated on an outpatient basis
( algorithm 1). A full discussion of risk assessment and determining the need for
hospitalization is presented separately. (See "Acute pericarditis: Clinical presentation and
diagnosis", section on 'Assessment of risk and need for hospitalization'.)
Activity restriction — Strenuous physical activity may trigger recurrence of symptoms;

therefore, such activity should be avoided until symptom resolution and normalization of
biomarkers. While there are little systematic data to guide recommendations on activity
restriction, our experts' approach to activity restriction is consistent with the advice of
professional societies [10]:
● Noncompetitive athletes should restrict activity until the resolution of symptoms and
normalization of biomarkers (this approach has been endorsed by the 2015 ESC
guidelines) [11].
● Competitive athletes should not participate in competitive sports for at least three
months following the resolution of symptoms and normalization of biomarkers, and
should be re-evaluated by a clinician prior to resuming training and competition. In
patients with milder symptoms which promptly resolve with treatment, a shorter period
or activity restriction (a minimum of one month) may be reasonable on a case-by-case
basis.
● In cases of myopericarditis or perimyocarditis, we recommend withdrawal from

competitive sports for six months and return to play only after normalization of
laboratory data (eg, markers of inflammation, electrocardiogram [ECG], and
echocardiogram). (See "Myopericarditis", section on 'Treatment'.)
Medical therapies
Nonsteroidal antiinflammatory drugs — For nearly all patients with acute idiopathic or
viral pericarditis, we recommend NSAIDs (in combination with colchicine) as the initial
treatment ( algorithm 1). There are two approaches to determine the duration of NSAID
therapy and the proper time to begin tapering treatment; long-term data demonstrating
superiority of one method over the other are not available.
● Duration of treatment is based upon the resolution of symptoms, which usually occurs
in two weeks or less, with tapering once the patient is symptom-free for at least 24
hours.
● Duration of treatment is based upon the resolution of symptoms and normalization of

C-reactive protein (CRP). In this approach, CRP is assessed at presentation and then
weekly, using the antiinflammatory dose of NSAIDs until complete resolution of
symptoms (for at least 24 hours) and normalization of CRP, at which point tapering
begins [12].
Failure to respond to aspirin or NSAID therapy within one week (defined as persistence of
fever, pleuritic chest pain, a new pericardial effusion, or worsening of general illness)
suggests that a cause other than idiopathic or viral pericarditis is present. In such instances,
a thorough search for the etiology should be performed. To expedite the diagnostic
evaluation and for symptom control, some patients may require admission to the hospital.
The main causes to be ruled out include tuberculous or other bacterial forms of pericarditis,
cancer (especially lung cancer, breast cancer, and lymphomas and leukemias), post-cardiac
injury syndromes, and systemic inflammatory diseases. (See "Acute pericarditis: Clinical
presentation and diagnosis", section on 'Establishing a definite etiology'.)
Based on the results of multiple cohort studies and one randomized study, treatment with an
antiinflammatory dose of NSAIDs alone appears to be effective in approximately 70 to 80
percent of pericarditis cases presumed to be of viral or idiopathic origin [7,8,13]. Primary
therapy has been the administration of oral NSAIDs, particularly ibuprofen or aspirin;
ketorolac, a parenteral NSAID, is also effective ( table 2) [14]. NSAIDs (including aspirin)
function to both reduce inflammation and relieve pain in most patients [7,8,13,15-17].
Despite these benefits, however, there is no evidence that NSAIDs alter the natural history of
acute pericarditis.
In a series of 254 patients deemed to be at low risk who were treated with aspirin as
outpatients, 98 percent of patients who responded to aspirin were presumed to have
idiopathic or viral disease, while 2 percent of the patients who responded to aspirin were
subsequently diagnosed with an autoimmune disorder [8]. By contrast, among the patients
who did not respond to aspirin after seven days, only 39 percent were deemed idiopathic,
while 43 percent were diagnosed with an autoimmune disorder and 18 percent with
tuberculous pericarditis. At follow-up, aspirin resistance was associated with significant
increases in the rates of recurrent pericarditis (61 versus 10 percent) and constrictive
pericarditis (9 versus 1 percent).
A theoretical concern is that the antiplatelet activity of aspirin (or another NSAID) might
promote the development of a hemorrhagic pericardial effusion. However, such a
relationship has never been convincingly established, and the risk-benefit ratio seems to
favor the use of these drugs. (See 'Bleeding risk of NSAIDs combined with other
antithrombotics' below.)
NSAID dosing — We agree with the 2015 ESC guidelines, which recommended the use
of an NSAID for the treatment of acute pericarditis [11]. One of the following NSAID
regimens is commonly used ( table 2):
● Ibuprofen – The ibuprofen dose is 600 to 800 mg three times per day ( table 2).
Following the resolution of symptoms, we taper the ibuprofen dose weekly in an
attempt to reduce the subsequent recurrence rate [8,18].
● Aspirin – The aspirin dose is 650 to 1000 mg three times per day ( table 2). Following
the resolution of symptoms, we taper the aspirin dose weekly in an attempt to reduce
the subsequent recurrence rate [8].
● Indomethacin – The indomethacin dose is 25 to 50 mg three times per day ( table 2).
Following the resolution of symptoms, we taper the indomethacin dose weekly in an
attempt to reduce the subsequent recurrence rate [8,18]. Indomethacin is associated

with more side effects, and it is usually considered for recurrences. (See "Recurrent
pericarditis", section on 'NSAID or aspirin'.)
Any of the listed NSAIDs can be continued for days or weeks, if necessary, for recurrent or
incessant attacks. (See "Recurrent pericarditis", section on 'NSAID or aspirin'.)
In symptomatic pericarditis occurring within days after an acute myocardial infarction, we

suggest aspirin plus colchicine rather than another NSAID plus colchicine. The use of NSAIDs
other than aspirin should be avoided, since antiinflammatory therapy may impair scar
formation [19]. Aspirin may also be the first choice in patients who require concomitant
antiplatelet therapy for any reason. With either regimen, gastrointestinal protection should
be provided. (See "Pericardial complications of myocardial infarction" and "NSAIDs (including
aspirin): Primary prevention of gastroduodenal toxicity" and 'Gastrointestinal protection'
below.)
Gastrointestinal protection — NSAIDs can lead to gastrointestinal toxicity (ie,

gastritis, ulcers, etc), particularly when used in high doses or for prolonged periods of time.
In addition to high doses or prolonged periods of treatment, patient-related factors
associated with a higher risk of gastrointestinal toxicity include:
● History of peptic ulcer disease

● Age greater than 65 years
● Concurrent use of aspirin, corticosteroids, or anticoagulants
Patients considered at risk of gastrointestinal toxicity related to NSAID treatment should be

treated with NSAIDs for the shortest interval possible and receive concomitant
gastroprotective therapy while taking NSAIDs. Proton pump inhibitors (eg, omeprazole,
pantoprazole) are generally preferred for prevention of gastrointestinal toxicity due to their
efficacy and favorable safety profile. (See "NSAIDs (including aspirin): Primary prevention of
gastroduodenal toxicity".)
Bleeding risk of NSAIDs combined with other antithrombotics — In patients who

require more than one antiplatelet or anticoagulant as therapy for an underlying condition,
there is a greater risk of bleeding complications. On occasion, patients with acute pericarditis
treated with NSAIDs may also have an indication for an additional antiplatelet or
anticoagulant, in which case the overall risk of bleeding should be assessed. Because NSAIDs
(especially aspirin) can impact the metabolism of vitamin K antagonists, patients will typically
require close monitoring and dose adjustments for the duration of treatment for acute
pericarditis. (See "Management of warfarin-associated bleeding or supratherapeutic INR",
section on 'Mitigating bleeding risk' and "Biology of warfarin and modulators of INR control",
section on 'Aspirin/NSAIDs'.)
In patients who require antiplatelet therapy for another indication (eg, following coronary
stenting), there are no specific contraindications or additional risks of bleeding when NSAIDs
are used during acute pericarditis. In this setting, however, aspirin is generally the first
choice to treat pericarditis, but doses should be increased to reach antiinflammatory effects
(from 100 to 300 mg to up to 650 to 1000 mg three times per day). (See 'NSAID dosing'
above.)
Concomitant use of heparin and anticoagulant therapies is often perceived as a possible risk
factor for the development of a worsening or hemorrhagic pericardial effusion that may
result in cardiac tamponade, but the available evidence does not support this [20].
● An analysis of 453 consecutive cases of acute pericarditis did not show a higher risk of
hemorrhagic effusion in patients on antithrombotics [9].
● In another study of 274 patients with acute pericarditis or myopericarditis, the use of
heparin or other anticoagulants was not associated with an increased risk of cardiac
tamponade (odds ratio [OR] 1.1, 95% CI 0.3-3.5) [21].
NSAIDs (including aspirin) alter the metabolism of vitamin K antagonists (eg, warfarin), thus
enhancing the anticoagulant effect. Consequently, careful monitoring and frequent dose
adjustment are needed. Additionally, consideration should be given to using alternative
antiinflammatory options, such as glucocorticoids. Although glucocorticoids have the
potential for fewer bleeding-related drug interactions in patients requiring both
antiinflammatory drugs and chronic anticoagulation therapy, the potential benefits of
reduced risk of bleeding should be weighed against potential side effects and a higher rate
of recurrent pericarditis associated with glucocorticoids. Because of these glucocorticoid
concerns, we generally prefer therapy with NSAIDs, with additional monitoring for drug
interactions and bleeding complications. (See "Major adverse effects of systemic
glucocorticoids".)
There are no significant reported interactions between NSAIDs or other antiplatelet

therapies and colchicine [22].
Colchicine — For all patients with acute idiopathic or viral pericarditis ( algorithm 1), we
recommend that colchicine be added to antiinflammatory therapy (either NSAIDs or
glucocorticoids) ( table 2) [11,23]. Additionally, colchicine is generally efficacious for
pericarditis caused by systemic inflammatory diseases and post-cardiac injury syndromes.
However, for patients with diagnosed bacterial pericarditis, colchicine has not been proven
efficacious and, on the contrary, may theoretically impair the clearance of the infectious
agent. Colchicine is also not proven to be efficacious in malignancy-related pericarditis and
pericardial effusion.
Colchicine, when used as an adjunct to NSAID therapy, reduces symptoms, decreases the
rate of recurrent pericarditis, and is generally well tolerated. The 2015 ESC guidelines
concluded that the weight of evidence supported the efficacy of colchicine, alone or in
combination with NSAIDs, in the treatment of acute pericarditis [11]. Of note, colchicine is
not approved for the prevention of recurrent pericarditis in North America and most
European countries (as of 2019, it is approved for this indication in Italy and Austria), as such
its use is off-label. (See "Recurrent pericarditis", section on 'Colchicine'.)
The efficacy of colchicine in the primary management of acute pericarditis has been
evaluated in randomized trials:
● In the ICAP trial, a randomized, double-blind study of colchicine versus placebo in

addition to standard antiinflammatory therapy for treatment of a first episode of acute
pericarditis (77 percent idiopathic) in 240 patients, colchicine added to standard
antiinflammatory therapy significantly reduced the risk of recurrence (17 versus 38
percent with antiinflammatory therapy alone; relative risk reduction 0.56, 95% CI 0.30-
0.72) [24]. In addition, colchicine added to antiinflammatory treatment resulted in
significantly better rates of remission and fewer hospitalizations compared with
antiinflammatory treatment alone. No serious adverse events were observed.
● In the open label COPE trial of 120 patients with a first episode of acute pericarditis (84
percent idiopathic), the recurrence rate of pericarditis within 18 months was
significantly lower in the colchicine plus aspirin group (11 versus 32 percent with aspirin
alone; number needed to treat to prevent one recurrence equals five) [13].
● In a later open-label trial in 110 patients with a first episode of acute idiopathic
pericarditis, the addition of colchicine to conventional antiinflammatory treatment did
not reduce the recurrence rate [25]. However, the study has important limitations to be
acknowledged (eg, probably underpowered to test colchicine efficacy, diagnostic
criteria for pericarditis not consistent with 2015 ESC guidelines, and possible significant
delay in the administration of colchicine from symptoms onset) that may limit its clinical
applicability [26].
In the COPE and ICAP studies, adult patients were excluded if they had elevated levels of
aminotransferases, creatinine, or troponin and liver diseases, myopathy, blood dyscrasias, or
inflammatory bowel disease. Pregnant or lactating women were also excluded as well as
patients with bacterial or neoplastic pericarditis.
The efficacy of colchicine in the treatment of pericarditis has also been assessed in several
systematic reviews and meta-analyses (which include patients with both acute and recurrent
pericarditis) [27-30]. In a 2014 systematic review and meta-analysis, which included four
randomized, double-blind trials (564 patients) of colchicine for both initial and recurrent
episodes of pericarditis, colchicine use was associated with a reduced risk of recurrent
pericarditis at 18 months in patients being treated for acute (hazard ratio [HR] 0.40, 95% CI
0.27-0.61) or recurrent (HR 0.37, 95% CI 0.24-0.58) pericarditis [28]. There was no significant
increase in adverse effects related to colchicine therapy [29]. (See "Recurrent pericarditis",
section on 'Colchicine'.)
Colchicine dosing — The 0.5 mg dose of colchicine is not available in many countries,
including the United States and Canada where 0.6 mg tablets are used empirically in place of
0.5 mg tablets.
Colchicine may be given with or without a loading dose. When a loading dose is chosen, the
loading dose is typically 0.5 to 1 mg (or 0.6 to 1.2 mg) twice daily on day 1, depending upon
the patient’s body weight.
The daily maintenance dose of colchicine is weight-based:
● Patients weighing ≥70 kg should receive 0.5 to 0.6 mg twice daily

● Patients weighing <70 kg should receive 0.5 to 0.6 mg once daily
Colchicine should be administered for a total of three months for patients with an initial
episode of acute pericarditis. In ICAP, colchicine was given without a loading dose as 0.5 mg
twice daily for three months for patients weighing >70 kg or 0.5 mg once daily for patients
weighing ≤70 kg.
Colchicine side effects — Colchicine is typically well tolerated. Side effects, most
commonly gastrointestinal (eg, diarrhea, nausea, vomiting), are uncommon at low doses (0.5
to 1.2 mg per day), even when given continuously over years. Less common (<1 percent) side
effects include bone marrow suppression, hepatotoxicity, and myotoxicity. Chronic renal
insufficiency leading to increased colchicine levels appears to be the major risk factor for side
effects and other possible negative interactions. In addition, colchicine has drug interactions
and altered metabolism in certain patient populations.
Glucocorticoids — Glucocorticoids should be used for initial treatment of acute pericarditis

only in patients with contraindications to NSAIDs (eg, renal failure or pregnancy at ≥20 weeks
gestation), or for specific indications (eg, systemic inflammatory diseases), and should be
used at the lowest effective dose. The number of such patients requiring glucocorticoids
should be quite low (10 percent or less), as illustrated in two studies by an almost 90 percent
response rate to aspirin alone within seven days, with most of the nonresponders having an
autoimmune disease or tuberculosis [8,13]. Glucocorticoids may also be used in the event of
failed initial therapy with aspirin/NSAID plus colchicine, suggesting recurrent or refractory
pericarditis. (See "Recurrent pericarditis".)
Limited data are available on the efficacy of glucocorticoid therapy for acute pericarditis, as
such therapy is generally limited to patients with nonresponse or contraindications to NSAID
use [25]. Observational studies suggest that glucocorticoid therapy early in the course of the
disease is more likely to be associated with recurrent episodes [13,31-33]. The best data
come from the COPE trial of colchicine therapy in which glucocorticoids were given only
when aspirin was contraindicated or not tolerated [13]. Glucocorticoid use was a significant
predictor of recurrence (OR 4.30, 95% CI 1.21-15.25). The same effect has been reported for
patients with the first recurrence or multiple recurrences and may be due to promotion of
viral replication [31,34-36]. In a subsequent systematic review which included two
randomized trials comparing steroid therapy with standard NSAID therapy and one trial of
low-dose versus high-dose steroid therapy (with or without other therapy with NSAIDs or
colchicine), the administration of steroids was associated with a trend toward a higher rate of
recurrent pericarditis (OR 7.50, 95% CI 0.62-90.65) [37].
In addition to concerns about the efficacy of glucocorticoid therapy as initial treatment of

acute pericarditis, chronic use of systemic glucocorticoids is associated with a number of
potentially significant side effects. As such, when glucocorticoids are required, they should
be given at the lowest appropriate and effective dose. (See "Major adverse effects of
systemic glucocorticoids".)
Glucocorticoid dosing — While NSAIDs and colchicine remain the preferred treatment
options for acute pericarditis, a minority of patients will have refractory symptoms requiring
treatment with systemic steroid therapy. There are conflicting data, mostly derived from
observational studies, regarding the optimal dosing and tapering of steroid therapy when
used to treat pericarditis.
Our approach to glucocorticoid dosing — For patients who require glucocorticoid

therapy for acute pericarditis, we suggest the use of moderate initial dosing (eg, 0.2 to 0.5
mg/kg/day of prednisone) followed by a slow taper ( table 2) rather than high doses with a
rapid taper. We add colchicine during glucocorticoid therapy and continue colchicine for
three months for initial cases of acute pericarditis and six months in recurrent cases. We
introduce aspirin or another NSAID toward the end of tapering or in case of recurrences
instead of increasing the dose of the glucocorticoids. (See "Recurrent pericarditis".)
Results from a study of patients with recurrent pericarditis suggest that lower glucocorticoid
doses may also be feasible in acute pericarditis, although these populations differ. In an
observational study, 100 patients with recurrent pericarditis were treated with
glucocorticoids (51 with prednisone 1 mg/kg/day and 49 with prednisone 0.2 to 0.5
mg/kg/day) [38]. After adjustment for potential confounders, only high doses of prednisone
were associated with more side effects, recurrences, and hospitalizations (HR 3.61, 95% CI
1.96-6.63). In a systematic review of published studies on medical therapy for pericarditis,
https://www-uptodate-com.bibliotecavirtual.udla.edu.ec/contents/acute-pericarditis-treatment-and-prognosis/print?search=pericarditis&source=… 10/23
data from three observational studies of steroid treatment showed that steroid use was
associated with a trend toward increased risk of recurrent pericarditis (OR 7.50, 95% CI 0.62-
90.65) [37]. However, low-dose steroids were superior to high-dose steroids for treatment
failure or recurrent pericarditis (OR 0.29, 95% CI 0.13-0.66), rehospitalization for pericarditis
(OR 0.19, 95% CI 0.06-0.63), and adverse effects (OR 0.07, 95% CI 0.01-0.54).
In our experience, rapid tapering of systemic glucocorticoids increases the risk of treatment
failure and recurrence. Although high doses of glucocorticoids (eg, prednisone 1 mg/kg/day)
have been recommended in the ESC guidelines, use of lower doses (eg, prednisone 0.2 to 0.5
mg/kg/day) may be equally efficacious [11]. These lower doses may be useful in reducing the
risk of steroid side effects, which have been reported in up to 25 percent of patients treated
with high doses. (See "Major adverse effects of systemic glucocorticoids".)
We usually begin tapering glucocorticoids at two to four weeks after resolution of symptoms
and CRP normalization. Each decrement in prednisone dose should proceed only if the
patient is asymptomatic and CRP remains normalized, particularly for doses lower than 25
mg/day. A proposed tapering scheme follows:
● Daily dose >50 mg – Taper 10 mg/day every one to two weeks

● Daily dose 25 to 50 mg – Taper 5 to 10 mg/day every one to two weeks
● Daily dose 15 to 25 mg – Taper 2.5 mg/day every two to four weeks
● Daily dose <15 mg – Taper 1.25 to 2.5 mg/day every two to six weeks
Other approaches — The 2015 ESC guidelines recommended that systemic steroid
therapy be restricted to patients with the following conditions [11]:
● Patients with symptoms refractory to standard therapy

● Acute pericarditis due to connective tissue disease
● Uremic pericarditis
The 2015 ESC guidelines recommend use of low to moderate doses of glucocorticoids (eg,
prednisone 0.2 to 0.5 mg/kg/day) when indicated. In contrast to our suggestions, the ESC
guidelines recommend rapid tapering to reduce the risk of systemic side effects [11,37]. In
patients with a coexisting pericardial effusion, intrapericardial steroid administration is an
option that limits systemic toxicity [11].
Adjunctive therapies — Most patients with uncomplicated low risk acute pericarditis are
managed effectively with medical therapy alone. On occasion, however, patients with
pericarditis may require adjunctive therapies for:
● For patients with elevated heart rate (eg, heart rate >70 to 75 beats per minute), no
evidence of cardiac tamponade, and persistent symptoms despite full anti-
inflammatory therapies, adjunctive use of betablockers, if not contraindicated, can be
helpful to improve symptom control by reducing heart rate and exacerbation of chest
pain at higher heart rates [39].
● Management of pericardial effusion is discussed separately. (See "Pericardial effusion:

Approach to management".)
Patients with cardiac tamponade require urgent pericardial fluid removal. (See "Cardiac
tamponade".)
● Management of recurrent (or incessant) pericarditis is discussed separately. (See

"Recurrent pericarditis", section on 'Treatment'.)
● Management of constrictive pericarditis is discussed separately. (See "Constrictive

pericarditis: Management and prognosis".)
Pericardiectomy — Surgical removal of all or part of the pericardium is virtually never

required for the treatment of acute pericarditis. The role of pericardiectomy in patients with
recurrent pericarditis is discussed separately. (See "Recurrent pericarditis", section on 'Role
of pericardiectomy'.)
Treatment in patients with chronic kidney disease — Treatment for pericarditis in

patients with advanced chronic kidney disease involves initiation or intensification of dialysis
when uremia is the underlying cause, along with selective use of NSAIDs, colchicine, and
corticosteroids. Patients with uremic pericarditis who are not already receiving dialysis
should initiate dialysis. In patients already receiving dialysis for over two months (dialysis-
associated pericarditis), the dialysis prescription is usually intensified. However, the
frequency of improvement in pericarditis in these patients is lower than in patients in whom
dialysis was recently initiated, and medical therapies are often required. The approach to
medical therapy is similar to patients without chronic kidney disease.
PROGNOSIS
Patients with acute idiopathic or viral pericarditis have a good long-term prognosis. Cardiac
tamponade rarely occurs in patients with acute idiopathic pericarditis and is more common
in patients with a specific underlying etiology such as malignancy, tuberculosis, or purulent
pericarditis. Constrictive pericarditis may occur in approximately 1 percent of patients with
acute idiopathic pericarditis and is also more common in patients with a specific etiology.
(See "Constrictive pericarditis: Diagnostic evaluation".)
Approximately 15 to 30 percent of patients with idiopathic acute pericarditis who are not
treated with colchicine develop either recurrent or incessant disease. Immune mechanisms
appear to be of primary importance in the majority of cases, and the term "chronic
autoreactive" pericarditis has been used. Risk factors for recurrent pericarditis include lack of
response to NSAIDs, the need for corticosteroid therapy, and creation of a pericardial
window. The pathogenesis, course, and treatment of recurrent pericarditis are discussed
separately. (See "Recurrent pericarditis".)
Sex may also predict the likelihood of complications. In a series of 453 consecutive cases of
acute pericarditis, women were at increased risk of complications (hazard ratio 1.65, 95% CI
1.08-2.52) [9]. A possible explanation of this finding is the higher frequency of autoimmune
etiologies (eg, connective tissue diseases) in women.
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Pericardial disease".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Pericarditis in adults (The Basics)")
● Beyond the Basics topic (see "Patient education: Pericarditis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
● Indications for hospitalization – Patients with acute pericarditis with one or more
high-risk markers (eg, fever, evidence of cardiac tamponade, immunosuppression, etc)
should be admitted to the hospital in order to initiate appropriate therapy and expedite
a thorough initial evaluation ( algorithm 1). Conversely, patients with uncomplicated
(ie, low-risk) acute pericarditis can usually be evaluated and sent home, with outpatient
follow-up. (See 'Which patients require hospitalization?' above.)
● Initial antiinflammatory therapy ( algorithm 1) (see 'General approach to

treatment' above)
• General regimen – For nearly all patients with acute idiopathic or viral pericarditis,
we recommend combination therapy with a nonsteroidal antiinflammatory drug
(NSAID) plus colchicine rather than an NSAIDs alone (Grade 1A). This is based upon
a reduced rate of recurrent pericarditis and a low incidence of side effects with
colchicine ( table 2). We generally administer ibuprofen or aspirin plus colchicine.
An acceptable alternative is indomethacin plus colchicine in cases that are poorly
responsive to ibuprofen or aspirin. (See 'Nonsteroidal antiinflammatory drugs'
above and 'Colchicine' above.)
• Following acute myocardial infarction – In patients with acute pericarditis

occurring within days following a myocardial infarction (MI), we suggest aspirin plus
colchicine ( table 2) rather than another NSAID plus colchicine (Grade 2C). These
patients already have an indication to use aspirin at lower doses. Moreover, other
NSAIDs may interfere with healing and scar formation. Glucocorticoids and NSAIDs
other than aspirin should generally be AVOIDED in patients with acute pericarditis
following an acute MI, but may be considered in those with persistent pericardial
effusion not responding to aspirin and colchicine and with evidence of constrictive
physiology and organization. (See 'Nonsteroidal antiinflammatory drugs' above and
"Pericardial complications of myocardial infarction", section on 'Management of
PIP'.)
• For patients with NSAID contraindications or a specific indication for

glucocorticoid therapy – Glucocorticoids are used for initial treatment of acute
pericarditis only in patients with contraindications to NSAIDs (eg, renal failure or
pregnancy at ≥20 weeks gestation), or for specific indications (eg, systemic
inflammatory diseases), and should be used at the lowest effective dose. The latter
recommendation results from the greater likelihood of recurrent pericarditis when
glucocorticoid therapy is used early in the course of the disease, along with a
number of potentially significant side effects of systemic glucocorticoid therapy. (See
'Glucocorticoids' above.)
For patients who require glucocorticoid therapy for acute pericarditis, we suggest
the use of moderate initial dosing (eg, 0.2 to 0.5 mg/kg/day of prednisone) followed
by a slow taper rather than high doses with a rapid taper ( table 2) (Grade 2C).
(See 'Our approach to glucocorticoid dosing' above.)
● Specific therapy – In cases of pericarditis due to identifiable causes other than viral
infection (eg, bacterial infection or malignancy), management is focused upon the
underlying disorder and, if necessary, drainage of an associated pericardial effusion.
(See 'Adjunctive therapies' above and 'General approach to treatment' above.)
● Activity restriction – Strenuous physical activity may trigger recurrence of symptoms;

therefore, such activity should be avoided until symptom resolution and normalization
of biomarkers. (See 'Activity restriction' above.)
● Adjunctive therapies – Most patients with uncomplicated low risk acute pericarditis
are managed effectively with medical therapy alone. Patients with one or more of the
following clinical features may require adjunctive therapies such as pericardial drainage
or pericardiectomy: a moderate or large pericardial effusion (particularly if
hemodynamically significant and causing cardiac tamponade or suspicion of a
neoplastic or bacterial etiology), frequent highly symptomatic recurrences of acute
pericarditis with pericardial effusion, or the late development of constrictive
pericarditis. Beta blockers may be considered for those with symptoms despite full
antiinflammatory therapies and high heart rates (eg, heart rate >70 to 75 beats per
minute at rest) to achieve better and faster control of symptoms.
● Prognosis – Patients with acute idiopathic or viral pericarditis generally have a good
long-term prognosis. Cardiac tamponade and late constrictive pericarditis rarely occur
in patients with acute idiopathic pericarditis. (See 'Prognosis' above.)
Use of UpToDate is subject to the Terms of Use.
REFERENCES
1. Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of

pericardial diseases. Circulation 2010; 121:916.
2. Imazio M, Brucato A, Derosa FG, et al. Aetiological diagnosis in acute and recurrent
pericarditis: when and how. J Cardiovasc Med (Hagerstown) 2009; 10:217.
3. Imazio M, Brucato A, Mayosi BM, et al. Medical therapy of pericardial diseases: part I:
idiopathic and infectious pericarditis. J Cardiovasc Med (Hagerstown) 2010; 11:712.
4. Imazio M, Brucato A, Mayosi BM, et al. Medical therapy of pericardial diseases: part II:
Noninfectious pericarditis, pericardial effusion and constrictive pericarditis. J Cardiovasc
Med (Hagerstown) 2010; 11:785.
5. Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic
Review. JAMA 2015; 314:1498.
6. Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J. Primary acute pericardial disease:

a prospective series of 231 consecutive patients. Am J Cardiol 1985; 56:623.
7. Zayas R, Anguita M, Torres F, et al. Incidence of specific etiology and role of methods for
specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol 1995; 75:378.
8. Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment of acute pericarditis: a
management program for outpatient therapy. J Am Coll Cardiol 2004; 43:1042.
9. Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute
pericarditis. Circulation 2007; 115:2739.
10. Pelliccia A, Solberg EE, Papadakis M, et al. Recommendations for participation in
competitive and leisure time sport in athletes with cardiomyopathies, myocarditis, and
pericarditis: position statement of the Sport Cardiology Section of the European
Association of Preventive Cardiology (EAPC). Eur Heart J 2019; 40:19.
11. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and
management of pericardial diseases: The Task Force for the Diagnosis and Management
of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The
European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2015; 36:2921.
12. Imazio M, Brucato A, Maestroni S, et al. Prevalence of C-reactive protein elevation and
time course of normalization in acute pericarditis: implications for the diagnosis,
therapy, and prognosis of pericarditis. Circulation 2011; 123:1092.
13. Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for
acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation
2005; 112:2012.
14. Arunasalam S, Siegel RJ. Rapid resolution of symptomatic acute pericarditis with
ketorolac tromethamine: a parenteral nonsteroidal antiinflammatory agent. Am Heart J
1993; 125:1455.
15. Spodick DH. Acute pericarditis: current concepts and practice. JAMA 2003; 289:1150.
16. McGinn JT, Rosati M, McGinn TG. Indomethacin in treatment of pericarditis. N Y State J
Med 1970; 70:1783.
17. Berman J, Haffajee CI, Alpert JS. Therapy of symptomatic pericarditis after myocardial
infarction: retrospective and prospective studies of aspirin, indomethacin, prednisone,
and spontaneous resolution. Am Heart J 1981; 101:750.
18. Imazio M, Trinchero R. Clinical management of acute pericardial disease: a review of
results and outcomes. Ital Heart J 2004; 5:803.
19. Hammerman H, Alker KJ, Schoen FJ, Kloner RA. Morphologic and functional effects of
piroxicam on myocardial scar formation after coronary occlusion in dogs. Am J Cardiol
1984; 53:604.
20. Imazio M, Trinchero R. Triage and management of acute pericarditis. Int J Cardiol 2007;
118:286.
21. Imazio M, Cecchi E, Demichelis B, et al. Myopericarditis versus viral or idiopathic acute
pericarditis. Heart 2008; 94:498.
22. Imazio M, Brucato A, Trinchero R, et al. Colchicine for pericarditis: hype or hope? Eur
Heart J 2009; 30:532.
23. Imazio M. Contemporary management of pericardial diseases. Curr Opin Cardiol 2012;
27:308.
24. Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute
pericarditis. N Engl J Med 2013; 369:1522.
25. Sambola A, Roca Luque I, Mercé J, et al. Colchicine Administered in the First Episode of
Acute Idiopathic Pericarditis: A Randomized Multicenter Open-label Study. Rev Esp
Cardiol (Engl Ed) 2019; 72:709.
26. Imazio M. Why Colchicine Should Continue To Be The First Line Therapy For Acute And
Recurrent Pericarditis. Rev Esp Cardiol (Engl Ed) 2019; 72:705.
27. Imazio M, Brucato A, Forno D, et al. Efficacy and safety of colchicine for pericarditis
prevention. Systematic review and meta-analysis. Heart 2012; 98:1078.
28. Alabed S, Cabello JB, Irving GJ, et al. Colchicine for pericarditis. Cochrane Database Syst
Rev 2014; :CD010652.
29. Imazio M, Brucato A, Belli R, et al. Colchicine for the prevention of pericarditis: what we
know and what we do not know in 2014 - systematic review and meta-analysis. J
Cardiovasc Med (Hagerstown) 2014; 15:840.
30. Melendo-Viu M, Marchán-Lopez Á, Guarch CJ, et al. A systematic review and meta-
analysis of randomized controlled trials evaluating pharmacologic therapies for acute
and recurrent pericarditis. Trends Cardiovasc Med 2023; 33:319.
31. Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med 2004; 351:2195.
32. Shabetai R. Often neglected yet important: the pericardium and its diseases. Herz 2000;
25:717.
33. Imazio M, Demichelis B, Parrini I, et al. Recurrent pain without objective evidence of
disease in patients with previous idiopathic or viral acute pericarditis. Am J Cardiol 2004;
94:973.
34. Imazio M, Bobbio M, Cecchi E, et al. Colchicine as first-choice therapy for recurrent
pericarditis: results of the CORE (COlchicine for REcurrent pericarditis) trial. Arch Intern
Med 2005; 165:1987.
35. Artom G, Koren-Morag N, Spodick DH, et al. Pretreatment with corticosteroids
attenuates the efficacy of colchicine in preventing recurrent pericarditis: a multi-centre
all-case analysis. Eur Heart J 2005; 26:723.

36. Imazio M, Demichelis B, Parrini I, et al. Management, risk factors, and outcomes in
recurrent pericarditis. Am J Cardiol 2005; 96:736.
37. Lotrionte M, Biondi-Zoccai G, Imazio M, et al. International collaborative systematic
review of controlled clinical trials on pharmacologic treatments for acute pericarditis
and its recurrences. Am Heart J 2010; 160:662.
38. Imazio M, Brucato A, Cumetti D, et al. Corticosteroids for recurrent pericarditis: high
versus low doses: a nonrandomized observation. Circulation 2008; 118:667.
39. Imazio M, Andreis A, Agosti A, et al. Usefulness of Beta-Blockers to Control Symptoms in
Patients With Pericarditis. Am J Cardiol 2021; 146:115.
Topic 15800 Version 41.0
GRAPHICS
Acute pericarditis etiologies: Data from published clinical studies with

unselected populations
Western Europe Africa

(2007-2012) [1] (1995-2001) [2]
Idiopathic * 516 (55.3%) 32 (13.7%)
Specific etiology 417 (44.7%) 201 (86.3%)
Neoplastic ¶ 85 (8.9%) 22 (9.4%)
Tuberculosis ¶ 4 (<1.0%) 161 (69.5%)
Autoimmune etiologies ¶ 25 (2.6%) Δ 12 (5.2%)
Purulent ¶ 29 (3.0%) 5 (2.1%)
* Most idiopathic cases are likely viral.
¶ As a fraction of the entire sample.
Δ Autoimmune pericarditis can be caused by autoimmune disease or as a complication of myocardial

infarction (MI) or cardiac surgery. In this table, we only report pericarditis caused by autoimmune
disease, while the original paper (Gouriet et al) reports an additional 188 cases related to MI or
cardiac surgery.
Data from:
1. Gouriet F, Levy PY, Casalta JP, et al. Etiology of pericarditis in a prospective cohort of 1162 cases. Am J Med 2015;
128:784.
2. Reuter H, Burgess LJ, Louw VJ, et al. The management of tuberculous pericardial effusion: experience in 233 consecutive
patients. Cardiovasc J S Afr 2007; 18:20.
Graphic 60949 Version 9.0
Initial treatment of acute pericarditis in adults
NSAIDs: nonsteroidal antiinflammatory drugs.
* NSAIDs are the preferred antiinflammatory for nearly all patients with acute idiopathic or viral
pericarditis. Glucocorticoids should be used for initial treatment of acute pericarditis only in patients
with contraindications to NSAIDs or for specific indications (ie, systemic inflammatory diseases,
pregnancy, renal failure), and should be used at the lowest effective dose. Refer to the UpToDate topic
on treatment of acute pericarditis for glucocorticoid dosing information.
¶ Response to treatment includes improvement/resolution of symptoms within 1 to 2 weeks of

initiation of therapy and normalization of C-reactive protein level (if measured).
Δ Refer to UpToDate content on recurrent/refractory pericarditis for therapeutic approach to patients

who are not showing clinical improvement.
Drug therapy in acute and recurrent pericarditis for adult patients
Duration of initial
Antiinflammatory
Drug or maintenance Tapering regimen ¶
dose
dose*
First-line therapy for most patients: Δ
Aspirin ◊ 650 to 1000 mg orally 3 1 to 2 weeks Decrease dose by

times daily about 250 mg per week
or
Ibuprofen ◊ 600 to 800 mg orally 3 1 to 2 weeks Decrease dose by 200

times daily § mg per week
or
Indomethacin ◊ 25 to 50 mg orally 3 1 to 2 weeks Decrease dose by 25

times daily mg per week
plus
Colchicine ¥ ‡ 0.5 to 0.6 mg orally 2 3 months (acute) Usually not tapered

times daily
6 months or more
(recurrent)
Second-line therapy (for refractory cases or patients with a contraindication to NSAID therapy):
Prednisone 0.2 to 0.5 mg/kg daily 2 to 4 weeks (acute or Gradual tapering over 2
recurrent † ) to 3 months; refer to
UpToDate topic review
of treatment of acute
pericarditis, section on
glucocorticoids
plus
Colchicine ¥ ‡ 0.5 to 0.6 mg orally 2 3 months or more Usually not tapered

times daily (acute)
6 months or more
(recurrent)
Colchicine is generally
continued for 4 weeks
or more after
discontinuation of
glucocorticoid
Third-line therapy: Second-line therapy plus NSAID dosed as for first-line therapy
Fourth-line therapy: One of the following agents (or pericardiectomy)
Rilonacept Loading dose of 320 160 mg SC weekly for Slow taper over 3
mg delivered as 2 SC several months months or more
doses of 160 mg on the
same day at 2 different

sites
Anakinra 1 to 2 mg/kg SC daily Several months Slow taper over 3

(maximum dose 100 months or more
mg daily)
Azathioprine 1 mg/kg orally daily Several months Not tapered

increasing to 2 to 3
mg/kg daily (maximum
dose 150 mg daily)
IVIG 400 to 500 mg/kg IV 5 days (may repeat Not tapered

daily after 1 month)
NSAID: nonsteroidal antiinflammatory drug (includes ibuprofen, indomethacin, and aspirin); SC:
subcutaneous injection; IVIG: intravenous immunoglobulin; IV: intravenous; CRP: C-reactive protein.
* This column describes the typical duration of full-dose therapy for symptom control. Except for
colchicine, the duration of full-dose therapy and subsequent tapering should be tailored according to
resolution of symptoms and normalization of markers of inflammation; refer to topic reviews for
approach.
¶ Tapering is begun once symptoms have resolved for at least 24 hours and CRP level has normalized.
Tapering is continued only if the patient remains asymptomatic with normal CRP levels. Some
clinicians taper more slowly than shown in the table by reducing the total daily dose (rather than each
individual dose) by the taper dose amount indicated.
Δ For patients treated with aspirin as an antiplatlet agent (including patients with peri-infarction
pericarditis), NSAIDs (such as ibuprofen and indomethacin) are avoided. Glucocorticoid therapy is also
avoided in patients with peri-infarction pericarditis. Refer to UpToDate content on pericardial
complications of myocardial infarction.
◊ Proton pump inhibitor (eg, omeprazole) gastrointestinal protection may be indicated.
§ Some patients may require ibuprofen every 6 hours (4 times daily), in which case the dose should
not exceed 600 mg every 6 hours.
¥ 0.5 mg colchicine is not available in the United States. It is widely available elsewhere.
‡ Colchicine dose should be reduced to 0.5 to 0.6 mg once daily in patients <70 kg. Refer to UpToDate
content on colchicine dosing for other indications for dosage reduction.
† Patients with acute pericarditis are generally treated with prednisone for a duration at the lower end
of this range, while patients with recurrent pericarditis are generally treated for a duration at the
upper end of this range.
Data from:
1. Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med 2004; 351:2195.
2. Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on the diagnosis and management of pericardial disease: The task
force on the diagnosis and management of pericardial disease of the European Society of Cardiology. European Heart
Journal 2004; 25:587.
3. Imazio M, Brucato A, Trinchero R, et al. Individualized therapy for pericarditis. Expert Rev Cardiovasc Ther 2009; 7:965.

Acute Pericarditis - Treatment and Prognosis - UpToDate

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Acute Pericarditis - Treatment and Prognosis - UpToDate

Uploaded by

Copyright:

Available Formats

23/2/24, 14:11 Acute pericarditis: Treatment and prognosis - UpToDate

Official reprint from UpToDate®

Acute pericarditis: Treatment and prognosis

Literature review current through: Jan 2024.

Diseases of the pericardium present clinically in one of several ways:

● Acute and recurrent pericarditis

"Myopericarditis" and "Cardiac tamponade" and "Constrictive pericarditis: Diagnostic

General approach to treatment — In the treatment of acute pericarditis, the goals of

● Ambulatory versus inpatient treatment – Most low-risk patients with acute

● Activity restriction – Patients should be instructed to restrict strenuous physical

• Glucocorticoids should be used for initial treatment of acute pericarditis only in

● Refractory or recurrent symptoms – Most patients whose symptoms worsen or recur

Which patients require hospitalization? — High-risk patients with acute pericarditis

Features of acute pericarditis associated with a higher risk include [8,9]:

● Fever (>38°C [100.4°F])

Activity restriction — Strenuous physical activity may trigger recurrence of symptoms;

● In cases of myopericarditis or perimyocarditis, we recommend withdrawal from

● Duration of treatment is based upon the resolution of symptoms and normalization of

attempt to reduce the subsequent recurrence rate [8,18]. Indomethacin is associated

In symptomatic pericarditis occurring within days after an acute myocardial infarction, we

Gastrointestinal protection — NSAIDs can lead to gastrointestinal toxicity (ie,

● History of peptic ulcer disease

Patients considered at risk of gastrointestinal toxicity related to NSAID treatment should be

Bleeding risk of NSAIDs combined with other antithrombotics — In patients who

There are no significant reported interactions between NSAIDs or other antiplatelet

● In the ICAP trial, a randomized, double-blind study of colchicine versus placebo in

The daily maintenance dose of colchicine is weight-based:

● Patients weighing ≥70 kg should receive 0.5 to 0.6 mg twice daily

Glucocorticoids — Glucocorticoids should be used for initial treatment of acute pericarditis

In addition to concerns about the efficacy of glucocorticoid therapy as initial treatment of

Our approach to glucocorticoid dosing — For patients who require glucocorticoid

● Daily dose >50 mg – Taper 10 mg/day every one to two weeks

● Patients with symptoms refractory to standard therapy

● Management of pericardial effusion is discussed separately. (See "Pericardial effusion:

● Management of recurrent (or incessant) pericarditis is discussed separately. (See

● Management of constrictive pericarditis is discussed separately. (See "Constrictive

Pericardiectomy — Surgical removal of all or part of the pericardium is virtually never

Treatment in patients with chronic kidney disease — Treatment for pericarditis in

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

● Basics topics (see "Patient education: Pericarditis in adults (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Initial antiinflammatory therapy ( algorithm 1) (see 'General approach to

• Following acute myocardial infarction – In patients with acute pericarditis

• For patients with NSAID contraindications or a specific indication for

● Activity restriction – Strenuous physical activity may trigger recurrence of symptoms;

Use of UpToDate is subject to the Terms of Use.

1. Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of

6. Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J. Primary acute pericardial disease:

all-case analysis. Eur Heart J 2005; 26:723.

Acute pericarditis etiologies: Data from published clinical studies with

Western Europe Africa

Idiopathic * 516 (55.3%) 32 (13.7%)

Specific etiology 417 (44.7%) 201 (86.3%)

Neoplastic ¶ 85 (8.9%) 22 (9.4%)

Tuberculosis ¶ 4 (<1.0%) 161 (69.5%)

Autoimmune etiologies ¶ 25 (2.6%) Δ 12 (5.2%)

Purulent ¶ 29 (3.0%) 5 (2.1%)

* Most idiopathic cases are likely viral.

¶ As a fraction of the entire sample.

Δ Autoimmune pericarditis can be caused by autoimmune disease or as a complication of myocardial

Graphic 60949 Version 9.0