This document discusses the treatment of acute pericarditis. It notes that the goals of treatment are relieving pain, resolving inflammation and preventing recurrence. The general approach involves ambulatory care for low-risk patients and hospitalization for high-risk patients. Treatment typically involves a combination of NSAIDs and colchicines, with glucocorticoids as an alternative. Activity restriction is also recommended until symptoms resolve. Factors that increase risk and may require hospitalization include fever, large pericardial effusions, and failure to improve with NSAIDs/colchicines.

2. • IntroductionThe 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 "Myopericarditis" and "Cardiac
tamponade" and "Constrictive pericarditis: Diagnostic evaluation and management" and "Diagnosis
and treatment of pericardial effusion".)

3. • IntroductionThe 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 "Myopericarditis" and "Cardiac tamponade" and "Constrictive pericarditis: Diagnostic evaluation and management" and "Diagnosis and treatment of pericardial effusion".)
• TreatmentThe 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 malignancy" 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 management" 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

4. • 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.)

5. • 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, systemicinflammatory 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 effectivelywith
medical therapy alone, and outpatient management remains feasible in almost all
cases.

6. • 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'.)

7. • 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 systematicdata to guide recommendations on
activity restriction, our experts' approach to activity restriction is consistentwith 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'.)

8. • Medical Therapies
• Nonsteroidal antiinflammatorydrugs — For nearly all patients with acute idiopathicor viral pericarditis, we recommend NSAIDs (in combination
with colchicine)as the initial treatment (algorithm 1).There are two approaches to determine the durationofNSAID therapyand the proper time to
begin taperingtreatment;long-term data demonstratingsuperiorityofone method over the other are not available.
• ●Duration oftreatment is based upon the resolutionofsymptoms,which usuallyoccurs in two weeks or less, with taperingonce the patient is
symptom-free forat least 24 hours.
• ●Duration oftreatment is based upon the resolutionofsymptoms and normalization ofC-reactiveprotein (CRP).In this approach,CRPis assessed at
presentationand then weekly,using the antiinflammatorydose ofNSAIDs until complete resolution ofsymptoms (for at least 24 hours)and
normalization ofCRP,at which point taperingbegins [12].
• Failure to respond to aspirin orNSAID therapywithin one week (defined as persistence of fever, pleuriticchest pain,a new pericardial effusion,or
worseningof general illness)suggests that a cause other than idiopathicorviral pericarditis is present.In such instances,a thorough search for
the etiologyshould be performed.To expedite the diagnosticevaluation and for symptomcontrol,some patients may require admission to the
hospital.The main causes to be ruled out include tuberculous orother bacterial forms of pericarditis,cancer (especiallylungcancer, breast cancer,
and lymphomas and leukemias),post-cardiacinjurysyndromes,and systemicinflammatorydiseases.(See "Acute pericarditis:Clinical presentation
and diagnosis",section on 'Establishinga definite etiology'.)
• Based on the results of multiple cohort studies and one randomizedstudy,treatment with an antiinflammatory dose ofNSAIDs alone appears to be
effective in approximately70 to 80 percent of pericarditis cases presumed to be of viral or idiopathicorigin [7,8,13]. Primary therapyhas been the
administrationoforal NSAIDs, particularly ibuprofen or aspirin;ketorolac,a parenteral NSAID,is also effective (table 2) [14]. NSAIDs (includingaspirin)
function to both reduce inflammationand relieve pain in most patients [7,8,13,15-17]. Despite these benefits,however, there is no evidence that
NSAIDs alter the natural historyofacute pericarditis.
• In a series of 254 patients deemed to be at low risk who were treated with aspirin as outpatients,98percent of patients who responded to aspirin
were presumed to haveidiopathicorviral disease, while 2 percent of the patients who responded to aspirinwere subsequentlydiagnosedwith an
autoimmune disorder [8].By contrast,amongthe patients who did not respond to aspirin after seven days,only39 percent were deemed idiopathic,
while 43 percent were diagnosed with an autoimmune disorder and 18percent with tuberculous pericarditis.At follow-up,aspirin resistance was
associated with significant increases in the rates of recurrent pericarditis (61versus 10 percent)and constrictivepericarditis (9versus 1 percent).
• A theoretical concern is that the antiplatelet activityof aspirin (or another NSAID)might promote the development ofahemorrhagicpericardial
effusion.However, such a relationshiphas neverbeen convincinglyestablished,and the risk-benefit ratio seems to favor the use of these drugs.
(See 'Bleedingrisk of NSAIDs combined with other antithrombotics' below.)

9. • NSAID dosing — We agree with the 2015 ESC guidelines,which recommended the use of an NSAID for the treatment ofacute pericarditis [11]. One
of the followingNSAIDregimens is commonlyused (table 2):
• ●Ibuprofen – The ibuprofen dose is 600 to 800 mg three times per day(table 2). Followingthe resolutionofsymptoms, 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). Followingthe resolutionofsymptoms,we taper the aspirin dose weekly
in an attempt to reduce the subsequentrecurrence rate [8].
• ●Indomethacin – The indomethacin dose is 25 to 50 mg three times per day(table 2). Followingthe resolution ofsymptoms, we taper the
indomethacindose weekly in an attempt to reduce the subsequent recurrence rate [8,18]. Indomethacinis associated with more side effects, and it is
usuallyconsidered forrecurrences.(See "Recurrent pericarditis",section on 'NSAID or aspirin'.)
• Anyof the listed NSAIDs can be continued fordays orweeks, if necessary,for recurrent or incessant attacks.(See "Recurrent pericarditis",section on
'NSAID or aspirin'.)
• In symptomaticpericarditis occurringwithin 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 antiinflammatorytherapymayimpair scar formation[19]. Aspirin may
also be the first choice in patients who require concomitantantiplatelettherapyfor anyreason.With either regimen, gastrointestinal protection
should be provided.(See "Pericardial complications ofmyocardialinfarction"and "NSAIDs (includingaspirin):Primaryprevention ofgastroduodenal
toxicity" and 'Gastrointestinalprotection' below.)
• Gastrointestinal protection — NSAIDs can lead to gastrointestinal toxicity(ie,gastritis,ulcers,etc), particularlywhen used in high doses or for
prolonged periods oftime.In addition to high doses orprolonged periods oftreatment,patient-relatedfactors associatedwith a higher risk of
gastrointestinal toxicityinclude:
• ●Historyof pepticulcer disease
• ●Age greater than 65 years
• ●Concurrent use of aspirin,corticosteroids,oranticoagulants
• Patients consideredat risk of gastrointestinal toxicityrelatedto NSAIDtreatment should be treated with NSAIDs for the shortest interval possible and
receive concomitant gastroprotectivetherapywhile takingNSAIDs. Proton pump inhibitors (eg, omeprazole,pantoprazole)are generallypreferred for
prevention ofgastrointestinaltoxicitydue to theirefficacy and favorablesafetyprofile. (See "NSAIDs (includingaspirin):Primaryprevention of
gastroduodenal toxicity".)

10. • Bleeding riskof NSAIDs combined with other antithrombotics — In patients who require more than one antiplateletor
anticoagulantas therapy for an underlyingcondition,there is a greater risk of bleeding complications.On occasion,
patients with acute pericarditistreated with NSAIDsmay also havean indication foran additional antiplateletor
anticoagulant,in which case the overallrisk of bleeding should be assessed. Because NSAIDs (especially aspirin) can impact
the metabolism of vitamin K antagonists,patientswill typicallyrequire close monitoring and dose adjustmentsfor the
durationof treatment for acute pericarditis.(See "Managementof warfarin-associatedbleeding or supratherapeuticINR",
section on 'Mitigatingbleedingrisk' and "Biologyof warfarin and modulatorsof INR control",section on 'Aspirin/NSAIDs'.)
• In patientswho require antiplatelettherapy for another indication(eg, following coronary stenting), there are no specific
contraindicationsor additional risksof bleeding when NSAIDs are used during acute pericarditis. In this
setting, however, aspirin is generallythe first choice to treat pericarditis, but doses should be increased to
reach antiinflammatoryeffects (from 100 to 300 mg to up to 650 to 1000 mg three times per day). (See 'NSAID
dosing' above.)
• Concomitantuse of heparinand anticoagulanttherapiesis often perceived as a possible risk factorfor the developmentof a
worsening or hemorrhagic pericardialeffusion that may result in cardiac tamponade,but the availableevidence does
not support this [20].
• ●An analysisof 453 consecutive cases of acute pericarditisdid not show a higher risk of hemorrhagic effusion in patients
on antithrombotics[9].
• ●In another study of 274 patientswith acute pericarditisor myopericarditis,the use of heparin or other anticoagulantswas
not associated with an increased risk of cardiac tamponade(odds ratio [OR] 1.1, 95% CI 0.3-3.5) [21].
• NSAIDs (includingaspirin) alterthe 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 alternativeantiinflammatoryoptions, such as glucocorticoids. Althoughglucocorticoids have the potentialfor
fewer bleeding-relateddrug interactionsin patientsrequiring both antiinflammatorydrugs and chronic anticoagulation
therapy, the potentialbenefits of reduced risk of bleeding should be weighed against potentialside effects and a higher rate
of recurrent pericarditisassociated with glucocorticoids.Because of these glucocorticoidconcerns, we generally prefer
therapy with NSAIDs, with additionalmonitoringfor drug interactionsand bleeding complications.(See "Majorside effects
of systemic glucocorticoids".)
• There are no significantreported interactionsbetween NSAIDs or other antiplatelettherapiesand colchicine

11. • Colchicine — For all patients with acute idiopathicorviral pericarditis (algorithm1),we recommend that colchicine be added to antiinflammatory
therapy(either NSAIDs or glucocorticoids)(table 2) [11,23]. Additionally,colchicine is generallyefficacious for pericarditis caused bysystemic
inflammatorydiseasesand post-cardiacinjurysyndromes.However,for patients with diagnosedbacterial pericarditis,colchicine has not been proven
efficacious and,on the contrary,maytheoreticallyimpair 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 generallywell 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 ofacute pericarditis [11]. Of note, colchicine is not approved forthe prevention ofrecurrent pericarditis in North America and most
European countries (as of 2019, it is approved for this indicationin Italyand Austria),as such its use is off-label.(See "Recurrent pericarditis",section
on 'Colchicine'.)
• The efficacy of colchicine in the primarymanagement of acute pericarditis has been evaluated in randomizedtrials:
• ●In the ICAP trial,a randomized,double-blind studyof colchicine versus placebo in addition to standard antiinflammatory therapyfor treatment ofa
first episode of acute pericarditis (77 percent idiopathic)in 240 patients,colchicine addedto standard antiinflammatory therapysignificantlyreduced
the risk of recurrence (17 versus 38 percent with antiinflammatory therapyalone;relativeriskreduction 0.56, 95% CI 0.30-0.72) [24]. In addition,
colchicine added to antiinflammatory treatment resultedin significantlybetter rates ofremission and fewer hospitalizations comparedwith
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 (84percent idiopathic),the recurrence rate of pericarditis within
18 months was significantlylower 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 idiopathicpericarditis,the additionof colchicine to conventional
antiinflammatory treatment did not reduce the recurrence rate [25]. However, the studyhas important limitations to be acknowledged (eg, probably
underpowered to test colchicine efficacy,diagnosticcriteria forpericarditis not consistent with 2015 ESC guidelines,and possible significant delayin
the administrationofcolchicine from symptoms onset)that maylimit its clinical applicability[26].
• In the COPE and ICAP studies,adult patients were excluded iftheyhad elevated levels of aminotransferases,creatinine, or troponin and liverdiseases,
myopathy,blooddyscrasias,orinflammatorybowel disease.Pregnant orlactatingwomen were also excluded as well as patients with bacterial or
neoplasticpericarditis.
• The efficacy of colchicine in the treatment ofpericarditis has also been assessed in several systematicreviews and meta-analyses (which include
patients with both acute and recurrent pericarditis)[27-30]. In a 2014 systematicreviewand meta-analysis,which included four randomized,double-
blind trials (564 patients)ofcolchicine for both initial and recurrent episodes ofpericarditis,colchicine use was associated with a reduced risk of
recurrent pericarditis at 18 months in patients beingtreatedforacute (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'.)

12. • Colchicinedosing — 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.
• Colchicineside 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 effectsinclude bone marrow suppression, hepatotoxicity,and
myotoxicity. Chronic renal insufficiencyleading 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.

13. • Glucocorticoids— Glucocorticoidsshouldbe usedforinitial treatmentof acute pericarditisonlyinpatientswithcontraindicationstoNSAIDs (eg,renal failure orpregnancyat≥20 weeksgestation), orfor
specificindications(eg,systemicinflammatorydiseases),andshouldbe usedatthe lowesteffectivedose.The numberof suchpatientsrequiringglucocorticoidsshouldbe quitelow(10percentor less),as
illustratedintwostudiesbyanalmost90 percentresponse rate to aspirinalone withinsevendays,withmostof the nonresponders havinganautoimmune diseaseortuberculosis[8,13].Glucocorticoids
may alsobe usedinthe eventof failedinitialtherapywithaspirin/NSAIDplus colchicine,suggestingrecurrentorrefractorypericarditis.(See"Recurrentpericarditis".)
• Limiteddataare available onthe efficacyof glucocorticoidtherapyforacute pericarditis,assuchtherapyisgenerallylimitedtopatientswithnonresponse orcontraindicationstoNSAIDuse [25].
Observationalstudiessuggestthatglucocorticoidtherapyearlyinthe course of the disease ismore likelytobe associated withrecurrentepisodes[13,31-33].The bestdatacome fromthe COPE trial
of colchicine therapyinwhichglucocorticoidswere givenonlywhen aspirinwascontraindicatedornottolerated[13].Glucocorticoiduse wasasignificantpredictorof recurrence (OR4.30, 95% CI1.21-
15.25). The same effecthasbeenreportedforpatientswiththe firstrecurrence ormultiple recurrencesandmaybe due to promotionof viral replication[31,34-36]. Ina subsequentsystematicreview
whichincludedtworandomizedtrialscomparingsteroidtherapywithstandardNSAIDtherapyandone trial of low-dose versushigh-dosesteroidtherapy(withorwithoutothertherapywithNSAIDsor
colchicine),the administrationof steroidswasassociatedwithatrendtowardahigherrate of recurrentpericarditis(OR7.50,95% CI 0.62-90.65) [37].
• In additiontoconcernsaboutthe efficacyof glucocorticoidtherapyasinitialtreatmentof acute pericarditis,chronicuse of systemicglucocorticoidsisassociatedwithanumberof potentiallysignificantside
effects.Assuch,whenglucocorticoidsare required,theyshouldbe givenatthe lowestappropriateandeffectivedose.(See "Majorside effectsof systemicglucocorticoids".)
• Glucocorticoiddosing— While NSAIDsand colchicine remainthe preferredtreatmentoptionsforacute pericarditis,aminorityof patientswill have refractorysymptomsrequiring treatmentwithsystemic
steroidtherapy.There are conflictingdata,mostlyderivedfromobservational studies,regardingthe optimaldosingandtaperingof steroidtherapywhenusedtotreatpericarditis.
• Our approach to glucocorticoiddosing — For patientswhorequire glucocorticoidtherapyforacute pericarditis,we suggestthe use of moderate initialdosing(eg,0.2to 0.5 mg/kg/dayof prednisone)
followedbyaslowtaper(table 2) rather thanhighdoseswitha rapidtaper.We add colchicine duringglucocorticoidtherapyandcontinue colchicine forthree monthsforinitial casesof acute pericarditis
and six monthsinrecurrentcases.We introduce aspirinoranotherNSAIDtowardthe endof taperingorincase of recurrencesinsteadof increasingthe dose of the glucocorticoids. (See "Recurrent
pericarditis".)
• Resultsfromastudyof patientswithrecurrentpericarditissuggestthatlowerglucocorticoiddosesmayalsobe feasible in acute pericarditis,althoughthesepopulationsdiffer.Inanobservational study,
100 patientswithrecurrentpericarditiswere treatedwithglucocorticoids(51with prednisone1mg/kg/dayand49 withprednisone0.2to 0.5 mg/kg/day) [38].Afteradjustmentforpotentialconfounders,
onlyhighdosesof prednisone wereassociatedwithmore sideeffects,recurrences,andhospitalizations(HR3.61, 95% CI 1.96-6.63). In a systematicreviewof publishedstudiesonmedical therapyfor
pericarditis,datafromthree observational studiesof steroidtreatmentshowedthatsteroiduse wasassociatedwithatrend towardincreasedriskof recurrentpericarditis(OR7.50, 95% CI 0.62-90.65)
[37]. However, low-dosesteroidswere superiortohigh-dosesteroidsfortreatmentfailure orrecurrentpericarditis(OR0.29, 95% CI 0.13-0.66), rehospitalizationforpericarditis(OR0.19, 95% CI 0.06-
0.63), andadverse effects(OR0.07, 95% CI0.01-0.54).
• In ourexperience,rapidtaperingof systemicglucocorticoidsincreasesthe riskof treatmentfailureandrecurrence.Althoughhighdosesof glucocorticoids(eg,prednisone1mg/kg/day) have been
recommendedinthe ESCguidelines,use of lowerdoses(eg,prednisone 0.2to0.5 mg/kg/day) maybe equallyefficacious[11].These lowerdosesmaybe useful inreducingthe riskof steroidsideeffects,
whichhave beenreportedinupto25 percentof patientstreatedwithhighdoses.(See "Majorside effectsof systemicglucocorticoids".)
• We usuallybegintaperingglucocorticoidsattwoto fourweeksafterresolutionof symptomsandCRPnormalization.Eachdecrementinprednisone dose shouldproceedonlyif the patientisasymptomatic
and CRPremainsnormalized,particularlyfordoseslowerthan25 mg/day.A proposedtaperingschemefollows:
• ●Dailydose >50 mg – Taper 10 mg/dayeveryone totwo weeks
• ●Dailydose 25 to 50 mg– Taper 5 to10 mg/dayeveryone totwoweeks
• ●Dailydose 15 to 25 mg– Taper 2.5 mg/dayeverytwotofour weeks
• ●Dailydose <15 mg – Taper 1.25 to 2.5 mg/dayeverytwoto six weeks

14. • Other approaches — The 2015 ESC guidelines recommended that systemicsteroid therapy be restricted to
patients with the following conditions [11]:
• ●Patients with symptoms refractory to standardtherapy
• ●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 systemicside effects [11,37]. In patients with a coexisting pericardial effusion, intrapericardial
steroid administration is an option that limits systemictoxicity [11].
• Adjunctive therapies — Most patients with uncomplicated low risk acute pericarditis are managed effectively
with medical therapy alone. On occasion, however, patients may require adjunctive therapies for:
• ●In patients with persistent symptoms and elevated heart rate (eg, heart rate >70 to 75 beats per minute)
despite full antiinflammatorytherapies, 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].
• ●A moderate to large pericardial effusion, particularly if hemodynamically significant and causing cardiac
tamponade or symptomaticand refractory to medical therapy.
• ●Suspicion of a neoplastic or bacterial etiology and moderate to large pericardial effusion.
• ●Frequent, highly symptomaticrecurrences of acute pericarditis with pericardial effusion.
• ●Evidence of constrictive pericarditis (a late occurrence when present).
• Percutaneous and surgical techniques maybe considered for such patients.

15. • Pericardial drainage — Prolonged catheter drainage ofa pericardial effusion is an effective means of preventingfluidreaccumulation.The mechanism
by which this occurs is probablymore related to the obliterationofthe pericardial space followinginflammation provoked by the catheter,rather than
fluid drainage itself.Catheter drainage maybe required forseveral days,and the catheter should not be removed until drainage stops or is minimal.If
significant drainage continuesfor more than three to four days,a pericardial windowshouldbe considered.The management of pericardial effusions
with and without cardiac tamponade is discussed in detail separately.(See "Cardiactamponade" and "Diagnosis and treatment ofpericardial
effusion",section on 'Treatment'.)
• Pericardiectomy — Surgical removal of all or part of the pericardiumis virtuallynever required for the treatment ofacute pericarditis.The role of
pericardiectomyin patients with recurrent pericarditis is discussed separately.(See "Recurrent pericarditis",section on 'Role of pericardiectomy'.)
• Treatment in patients with chronic kidneydisease — Treatment forpericarditis in patientswith advanced chronickidneydisease involves initiation or
intensificationofdialysis when uremia is the underlyingcause, alongwith selective use of NSAIDs, colchicine, and corticosteroids.Patients with
uremic pericarditis who are not alreadyreceivingdialysis should initiate dialysis.In patients alreadyreceivingdialysis for over two months (dialysis-
associated pericarditis),the dialysis prescription is usuallyintensified.However,the frequencyof improvement in pericarditis in these patientsis
lower than in patients in whomdialysis was recently initiated,and medical therapies are often required.The approach to medical therapyis similar to
patients withoutchronickidneydisease.
• PrognosisPatients with acute idiopathicorviral pericarditis havea good long-term prognosis. Cardiactamponade rarelyoccurs in patients with acute
idiopathicpericarditis and is more common in patients with a specific underlying etiology such as malignancy,tuberculosis,or purulent pericarditis.
Constrictive pericarditis mayoccur in approximately1percent of patients with acute idiopathicpericarditis and is also more common in patientswith
a specific etiology.(See "Constrictive pericarditis:Diagnosticevaluation and management".)
• Approximately15to 30 percent of patients with idiopathicacute pericarditis who are not treated with colchicine develop either recurrent or incessant
disease.Immune mechanisms appearto be of primary importance in the majorityof cases, and the term "chronic autoreactive"pericarditis has been
used.Risk factors for recurrent pericarditis include lackof response to NSAIDs, the need for corticosteroid therapy,and creation ofa pericardial
window.The pathogenesis,course, and treatmentofrecurrent pericarditis are discussed separately.(See "Recurrent pericarditis".)
• Sex may also predict the likelihood ofcomplications.In a series of 453 consecutivecases of acute pericarditis,women were at increased risk of
complications(hazardratio1.65, 95% CI 1.08-2.52) [9]. A possible explanationofthis findingis the higher frequencyof autoimmune etiologies(eg,
connectivetissue diseases)in women.
•