Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
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
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. The treatment options available for acute pericarditis will be reviewed here. The etiology of pericarditis, 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 diagnostic evaluation" and "Recurrent pericarditis" and "Cardiac tamponade" and "Constrictive pericarditis" and "Diagnosis and treatment of pericardial effusion".)
TREATMENT — The therapy of acute pericarditis should be targeted as much as possible to the underlying etiology [1-5]. In patients with an identified cause other than viral infection, specific therapy appropriate to the underlying disorder is indicated. However, in developed countries, most cases of acute pericarditis in immunocompetent patients are due to viral infection or are idiopathic. Because of the relatively benign course associated with the common causes of pericarditis (>80 percent of cases), it not necessary to search for the etiology in all patients. As such, most patients are treated for a presumptive viral cause with nonsteroidal anti-inflammatory drugs (NSAIDS) and colchicine. (See "Pericardial disease associated with malignancy" and "Tuberculous pericarditis" and "Purulent pericarditis".)
Most patients with acute pericarditis can be managed effectively with medical therapy alone. However, patients with a large pericardial effusion, a hemodynamically significant pericardial effusion, a suspicion of a bacterial or neoplastic etiology, or evidence of constrictive pericarditis should be evaluated for invasive therapies, such as pericardial drainage and/or pericardiotomy (pericardial window). (See 'Interventional therapeutic techniques' below.)
Some clinical features of acute pericarditis impart a higher risk to the patient; as such, patients felt to be at high risk should be hospitalized for additional evaluation and initiation of treatment [6,7]. Features associated with a higher risk include:
●Fever (>38ºC [100.4ºF]) and leukocytosis
●Evidence suggesting cardiac tamponade
●A large pericardial effusion (ie, an echo-free space of more than 20 mm)
●A history of therapy with vitamin K antagonists (eg, warfarin)
●Failure to respond within seven days to NSAID therapy
●Elevated cardiac troponin, which suggests myopericarditis
Patients with none of the listed high-risk features can be safely treated on an outpatient basis. A protocol has been proposed for outpatient treatment of those at low risk (algorithm 1) . (See "Acute pericarditis: Clinical presentation and diagnostic evaluation".)
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 [8,9]. (See "Constrictive pericarditis" and "Cardiac tamponade".)
Activity restriction — Strenuous physical activity may trigger recurrence of symptoms; therefore, such activity should be avoided until symptom resolution. While there are little if any data to guide recommendations on activity restriction, our experts' approach to activity restriction is consistent with the position of the European Society of Cardiology in a 2006 position paper :
●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 reevaluated by a clinician prior to resuming training and competition.
●Non-competitive athletes should restrict activity until the resolution of symptoms and normalization of biomarkers (this approach has been endorsed by the 2015 European Society of Cardiology guidelines) .
In cases of myopericarditis, we recommend withdrawal from competitive sports for six months and return to play only after normalization of laboratory data (eg, markers of inflammation, ECG, and echocardiogram). (See "Myopericarditis", section on 'Treatment'.)
Nonsteroidal anti-inflammatory drugs — In the treatment of acute pericarditis, the goals of therapy are the relief of pain and resolution of inflammation (and, if present, pericardial effusion). We recommend NSAIDs for all patients without a contraindication, with the duration of treatment based upon the persistence of symptoms, which is usually for two weeks or less. An individualized approach based on symptom control and normalization of C-reactive protein (CRP) has also been proposed, in which CRP is assessed at presentation and then weekly, with anti-inflammatory drugs prescribed until complete resolution of symptoms and normalization of CRP . Long-term data demonstrating that routine measurement of CRP improves outcomes or reduces the risk of recurrent pericarditis are not available.
Based on the results of multiple cohort studies and one randomized study, treatment with NSAIDs alone appears to be effective in approximately 70 to 80 percent of pericarditis cases presumed to be of viral or idiopathic origin [6,9,13]. Primary therapy has been the administration of oral NSAIDs, particularly ibuprofen or aspirin; ketorolac, a parenteral NSAID, is also effective (table 1) . NSAIDs and aspirin function to both reduce inflammation and relieve pain in most patients [6,9,13,15-17]. Despite these benefits, however, there is no evidence that NSAIDs or aspirin alter the natural history of acute pericarditis.
A theoretical concern is that the antiplatelet activity of aspirin or other 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.
Failure to respond to aspirin or NSAID therapy within one week (defined as persistence of fever, pericarditic chest pain, a new pericardial effusion, or worsening of general illness) suggests that a cause other than idiopathic or viral pericarditis is present. (See "Acute pericarditis: Clinical presentation and diagnostic evaluation".)
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 . In 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 (nine versus one percent).
●Ibuprofen (eg, 600 to 800 mg three times per day as attack dose) – Depending on the severity of the pericarditis and individual medication response, ibuprofen three times daily is usually adequate for symptom relief (table 1). Ibuprofen can be continued for days or weeks for recurrent or incessant attacks as needed. NSAID dose tapering may be prescribed in an attempt to reduce the subsequent recurrence rate [6,18].
●Aspirin (eg, 650 to 1000 mg three times per day as attack dose) – Aspirin can be given every six to eight hours (table 1) followed by gradual tapering every two to three days for a treatment period of three to four weeks .
●Indomethacin – Indomethacin can be administered at a dose of 50 mg three times daily for one to two weeks followed by gradual tapering every two to three days for a treatment period of three to four weeks.
In symptomatic pericarditis occurring within days after an acute myocardial infarction, aspirin is preferred, and the use of an NSAID other than aspirin should be AVOIDED, since anti-inflammatory therapy may impair scar formation . 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.)
One practical approach is the initial administration of an NSAID at a full dose (ie, "attack dose") every six to eight hours to achieve better symptom control than with a lower dose. The attack dose is maintained empirically for one to two weeks or until complete symptom resolution. Tapering should be considered following the attack dose in an attempt to reduce the subsequent risk of recurrence. Normalization of C-reactive protein may be used to tailor the duration of treatment .
Gastrointestinal protection — Nonsteroidal anti-inflammatory drugs (NSAIDs) can lead to gastrointestinal toxicity, 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".)
Concomitant use of antiplatelet and anticoagulation therapies — 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. However, there are no apparent increased risks of hemorrhagic pericardial effusion, cardiac tamponade, or recurrent pericarditis in such patients. (See "Anticoagulation in older adults", section on 'Risk of bleeding'.)
There are no specific contraindications or additional risks of bleeding when antiplatelet therapies are used during acute pericarditis. In this setting aspirin is generally the first choice to treat pericarditis, but doses should be increased to reach anti-inflammatory effects (from 100 to 300 mg to up to 750 to 1000 mg three times per day). (See 'NSAID regimens' above.)
In contrast to antiplatelet therapies, 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. Use of anticoagulant therapy has also been considered a possible poor prognostic predictor in the setting of acute pericarditis, but the available evidence does not support this .
●A multivariable analysis of nearly 500 consecutive cases of acute pericarditis did not show this to be the case .
●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 (OR 1.1, 95% CI 0.3 to 3.5) .
NSAIDs and aspirin may, however, interfere with the metabolism of vitamin K antagonists (eg, warfarin), thus enhancing the anticoagulant effect of vitamin K antagonists. Consequently, careful monitoring is needed. Additionally, consideration should be given to using alternative anti-inflammatory options such as glucocorticoids that have the potential for fewer bleeding-related drug interactions in patients requiring both anti-inflammatory drugs and chronic anticoagulation therapy. However, the potential benefits of using glucocorticoids to lower the risk of bleeding must be balanced with the potential side effects associated with glucocorticoids. (See "Major side effects of systemic glucocorticoids".)
Colchicine — The majority of patients have prompt resolution of symptoms without recurrent pericarditis when treated with NSAIDS alone. However, when used as an adjunct to NSAID therapy, colchicine reduces symptoms, decreases the rate of recurrent pericarditis, and is generally well tolerated. As such, we recommend that colchicine be added to NSAIDs in the management of a first episode of acute pericarditis [11,23] (table 1).
The effect of colchicine in the primary management of acute pericarditis has subsequently been evaluated in two randomized trials:
●In the ICAP trial, a randomized, double-blind study of colchicine versus placebo in addition to standard anti-inflammatory therapy for treatment of a first episode of acute pericarditis (77 percent idiopathic), colchicine added to standard anti-inflammatory therapy significantly reduced the risk of recurrence (17 percent versus 38 percent with anti-inflammatory therapy alone; relative risk reduction 0.56; 95% CI 0.30-0.72) . In addition, colchicine added to anti-inflammatory treatment resulted in significantly better remission rates and fewer hospitalizations compared to anti-inflammatory treatment alone. Colchicine was given without a loading dose colchicine 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. Overall adverse effects and rates of study-drug discontinuation were similar in the two study groups. 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 percent versus 32 percent with aspirin alone; number needed to treat to prevent one recurrence equals five). .
Two systematic reviews have evaluated the efficacy of colchicine in the treatment of pericarditis:
●A 2012 systematic review and meta-analysis (published prior to the ICAP results) included the results of five published trials (795 patients, mean follow-up 13 months) that evaluated the efficacy and safety of colchicine for pericarditis prevention, including three double-blind, randomized trials and two open-label, randomized trials . Colchicine use was associated with a reduced risk of recurrent pericarditis during follow-up (RR = 0.40, 95% CI 0.30-0.54) without a significantly higher risk of adverse events.
●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, reported similar results . Colchicine use was associated with a reduced risk of recurrent pericarditis at 18 months in patients being treated for acute (HR 0.40; 95% CI 0.27-0.61) or recurrent (HR 0.37; 95% CI 0.24-0.58) pericarditis. There was no significant increase in adverse effects related to colchicine therapy .
The 2015 ESC guidelines concluded that the weight of evidence supported the efficacy of colchicine (0.5 to 1 mg/day, no loading dose and weight adjusted doses: 0.5 mg once of <70 kg, otherwise 0.5 mg twice daily for three months), alone or in combination with NSAIDs, in the treatment of acute pericarditis . Findings of the COPE and ICAP studies are applicable only to adults without elevated levels of aminotransferases, creatinine, or troponin and those without liver disease, myopathy, blood dyscrasias, or inflammatory bowel disease. Pregnant or lactating women were also excluded as well as patients with bacterial or neoplastic pericarditis.
Moreover, colchicine appears to be effective in the prevention of postpericardiotomy syndrome following cardiac surgery. This is discussed in greater detail separately. (See "Post-cardiac injury syndromes".)
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. (See "Treatment of acute gout", section on 'Safety of colchicine'.)
Glucocorticoids — Glucocorticoids should be considered only if acute pericarditis results in symptoms that are clearly refractory to NSAIDs and colchicine, and a specific cause for the pericarditis has been excluded . Corticosteroids may also be used in case of contraindications or failure of aspirin/NSAID, or rarely for specific indications (ie, systemic inflammatory diseases, pregnancy, renal failure). The number of such patients is quite low as illustrated in the COPE trial and in an observational series of 254 low risk patients in which almost 90 percent of patients responded to aspirin alone within seven days and most of the nonresponders had an autoimmune disease or tuberculosis [6,13].
A number of studies, mostly observational, suggest that glucocorticoid therapy early in the course of the disease is more likely to be associated with recurrent episodes [13,28-30]. However, a concern with observational evidence related to glucocorticoid therapy is that such therapy may be more likely to be used in patients with disease resistant to initial therapy, which would be a predictor of recurrence independent of prior administration of glucocorticoid.
The best data come from the COPE trial of colchicine therapy in which glucocorticoids were given only when aspirin was contraindicated or not tolerated . On multivariate analysis, glucocorticoid use was a significant predictor of recurrence (OR 4.30, 95% CI 1.21 to 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 [28,31-33].
A subsequent systematic review evaluated the results of two randomized trials comparing steroid therapy to 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 to 90.65).
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. (See "Major side effects of systemic glucocorticoids".)
Approaches to glucocorticoid use — 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.
European Society of Cardiology guidelines — The 2015 European Society of Cardiology (ESC) guidelines recommended that systemic steroid therapy be restricted to patients with the following conditions :
●Patients with symptoms refractory to standard therapy
●Acute pericarditis due to connective tissue disease
●Uremic pericarditis (see "Pericarditis in renal failure")
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 with rapid tapering to reduce the risk of systemic side effects . . In patients with a coexisting pericardial effusion, intrapericardial steroid administration is an option that limits systemic toxicity .
Our approach to glucocorticoid use — Our approach to glucocorticoid dosing has been endorsed by the 2015 ESC guidelines (table 1) . 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 0.25 to 0.50 mg/kg/day) may be equally efficacious. 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 side effects of systemic glucocorticoids".)
We generally add colchicine during glucocorticoid therapy and continue colchicine for several months after glucocorticoid discontinuation (ie, with an overall length of treatment of three months for acute pericarditis, 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.
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 treated with high-dose prednisone 1.0 mg/kg/day and 49 treated with prednisone 0.2 to 0.5 mg/kg/day) . After adjustment for potential confounders only high doses of prednisone were associated with more side effects, recurrences, and hospitalizations (hazard ratio, 3.61; 95% CI 1.96 to 6.63).
We usually begin tapering glucocorticoids at two to four weeks, after resolution of symptoms and/or C-reactive protein normalization. Each decrement in prednisone dose should proceed only if the patient is asymptomatic, 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 5-10 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
In a systematic review of published studies on medical therapy for pericarditis, 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 to 90.65) . However, low-dose steroids were superior to high-dose steroids for treatment failure or recurrent pericarditis (OR 0.29, 95% CI 0.13 to 0.66), rehospitalization for pericarditis (OR 0.19, 95% CI 0.06 to 0.63), and adverse effects (OR 0.07, 95% CI 0.01 to 0.54).
Interventional therapeutic techniques — Most patients with acute pericarditis can be managed effectively with medical therapy alone. On occasion, however, patients may require invasive therapies for:
●A moderate to large pericardial effusion, particularly if hemodynamically significant and causing cardiac tamponade or symptomatic and refractory to medical therapy
●Suspicion of a neoplastic or bacterial etiology and moderate to large pericardial effusion
●Frequent, highly symptomatic recurrences of acute pericarditis with pericardial effusion
●Evidence of constrictive pericarditis (a late occurrence when present)
Percutaneous and surgical techniques may be considered for such patients.
Pericardial drainage — Prolonged catheter drainage of a pericardial effusion is an effective means of preventing fluid reaccumulation. The mechanism by which this occurs is probably more related to the obliteration of the pericardial space following inflammation provoked by the catheter, rather than fluid drainage itself. Catheter drainage may be required for several days and the catheter should not be removed until drainage is less than 20 to 30 ml/24 hours. (See "Cardiac tamponade" and "Diagnosis and treatment of pericardial effusion", section on 'Treatment'.)
Pericardiotomy, pericardial window and pericardiectomy — Surgical removal of all or part of the pericardium is virtually never required for the treatment of acute pericarditis. However, pericardiectomy may be considered for frequent and highly symptomatic recurrences of pericarditis resistant to medical treatment or recurrent cardiac tamponade . The efficacy of pericardiectomy in the management of recurrent idiopathic pericarditis is unproven and should be considered only in exceptional cases. Other situations in which to consider pericardiectomy include repeated recurrences of pericardial effusions resulting in cardiac tamponade, evidence of serious steroid toxicity limiting further medical treatment, or the late occurrence of constrictive pericarditis. (See "Recurrent pericarditis" and "Cardiac tamponade" and "Constrictive pericarditis".)
Surgical decompression of the pericardium (also known as pericardiotomy, pericardiostomy, and "window" pericardiectomy) can be achieved either by conventional heart surgery or video-assisted thoracoscopy. These techniques may result in a lower incidence of effusion recurrence compared with pericardiocentesis and prolonged catheter drainage. However, surgical experiences are not always concordant, and the efficacy of pericardiectomy remains largely unproven.
Less-invasive options (eg, balloon pericardiotomy) for the management of recurrent symptomatic pericardial effusions are mainly derived from the experience of management of neoplastic pericardial effusions and include prolonged catheter drainage and the creation of the so-called "pericardial window". These techniques, which involve inserting balloon catheters into the pericardial space using a subxiphoid approach under fluoroscopic or echocardiographic guidance, are highly successful in preventing recurrent effusions, especially for patients with a reduced life expectancy since reaccumulation of fluid may occur with longer follow-up. However, stretching of the pericardium is often painful so appropriate analgesia is necessary. (See "Pericardial disease associated with malignancy".)
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
●In cases of pericarditis due to an identifiable cause (eg, bacterial infection or malignancy), management is focused upon the underlying disorder and, if necessary, drainage of an associated pericardial effusion. (See 'Treatment' above.)
●For most patients with acute idiopathic or viral pericarditis, we recommend combination therapy with colchicine plus NSAIDs rather than NSAIDs alone (Grade 1A). This is based upon a reduced rate of recurrent pericarditis and a low incidence of side effects with colchicine (table 1). We generally administer ibuprofen plus colchicine. An acceptable alternative is indomethacin plus colchicine. Because NSAIDs do not alter the natural history of pericarditis, NSAID treatment duration is based upon the persistence of symptoms, which is usually for two weeks or less, while colchicine is generally continued for three months. Individualized treatment length may be based on a weekly assessment of markers of inflammation (ie, C-reactive protein). Intravenous administration of NSAIDs may be useful to control acute and severe symptoms at the beginning of therapy. (See 'Nonsteroidal anti-inflammatory drugs' above and 'Colchicine' above.)
●In patients with acute pericarditis occurring within days following a myocardial infarction (MI), we suggest aspirin plus colchicine (table 1) rather than another NSAID plus colchicine (Grade 2C). This is principally due to the possibility that other NSAIDs may interfere with healing and scar formation. Although the evidence of potential harm from glucocorticoids and NSAIDs other than aspirin is modest, there is no evidence that these medications improve outcomes. For these reasons glucocorticoids and NSAIDs other than aspirin should generally be AVOIDED in patients with acute pericarditis following an acute MI. (See 'Nonsteroidal anti-inflammatory drugs' above and "Pericardial complications of myocardial infarction", section on 'Management of PIP'.)
●Patients treated with aspirin or another NSAID should also receive gastrointestinal protection (eg, a proton pump inhibitor). (See 'Gastrointestinal protection' above and "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity".)
●Among patients with acute pericarditis, initial management with systemic glucocorticoid therapy should be restricted to patients with pericarditis due to connective tissue disease, autoreactive (immune-mediated) pericarditis, uremic pericarditis not responding to dialysis, and to patients who have contraindications to NSAID therapy. Glucocorticoid therapy is also used for patients with idiopathic or viral pericarditis that is refractory to combination therapy with NSAIDs and colchicine. (See 'Glucocorticoids' above.)
●For patients who require glucocorticoid therapy for acute pericarditis, we suggest the use of moderate initial dosing (eg, 0.25 to 0.50 mg/kg/day of prednisone) followed by a slow taper rather than high doses with a rapid taper (table 1) (Grade 2C). (See 'Our approach to glucocorticoid use' above.)
- Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of pericardial diseases. Circulation 2010; 121:916.
- 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.
- 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.
- 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.
- Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic Review. JAMA 2015; 314:1498.
- 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.
- Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute pericarditis. Circulation 2007; 115:2739.
- 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.
- 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.
- Pelliccia A, Corrado D, Bjørnstad HH, et al. Recommendations for participation in competitive sport and leisure-time physical activity in individuals with cardiomyopathies, myocarditis and pericarditis. Eur J Cardiovasc Prev Rehabil 2006; 13:876.
- 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.
- 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.
- 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.
- Arunasalam S, Siegel RJ. Rapid resolution of symptomatic acute pericarditis with ketorolac tromethamine: a parenteral nonsteroidal antiinflammatory agent. Am Heart J 1993; 125:1455.
- Spodick DH. Acute pericarditis: current concepts and practice. JAMA 2003; 289:1150.
- McGinn JT, Rosati M, McGinn TG. Indomethacin in treatment of pericarditis. N Y State J Med 1970; 70:1783.
- 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.
- Imazio M, Trinchero R. Clinical management of acute pericardial disease: a review of results and outcomes. Ital Heart J 2004; 5:803.
- 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.
- Imazio M, Trinchero R. Triage and management of acute pericarditis. Int J Cardiol 2007; 118:286.
- Imazio M, Cecchi E, Demichelis B, et al. Myopericarditis versus viral or idiopathic acute pericarditis. Heart 2008; 94:498.
- Imazio M, Brucato A, Trinchero R, et al. Colchicine for pericarditis: hype or hope? Eur Heart J 2009; 30:532.
- Imazio M. Contemporary management of pericardial diseases. Curr Opin Cardiol 2012; 27:308.
- Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis. N Engl J Med 2013; 369:1522.
- 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.
- Alabed S, Cabello JB, Irving GJ, et al. Colchicine for pericarditis. Cochrane Database Syst Rev 2014; :CD010652.
- 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.
- Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med 2004; 351:2195.
- Shabetai R. Often neglected yet important: the pericardium and its diseases. Herz 2000; 25:717.
- 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.
- 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.
- 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.
- Imazio M, Demichelis B, Parrini I, et al. Management, risk factors, and outcomes in recurrent pericarditis. Am J Cardiol 2005; 96:736.
- 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.
- Imazio M, Brucato A, Cumetti D, et al. Corticosteroids for recurrent pericarditis: high versus low doses: a nonrandomized observation. Circulation 2008; 118:667.