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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 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 "Clinical presentation and diagnostic evaluation of acute pericarditis" 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 [1-4]. 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 [5,6]. Features associated with a higher risk include:
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 "Clinical presentation and diagnostic evaluation of acute pericarditis", section on 'Determination of risk and need for hospitalization'.)
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 [7,8]. (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. Athletes should not participate in competitive sports until there is no longer evidence of active disease (eg, resolution of symptoms). 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 [5,8,10]. 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 [5,8,10,12-14]. 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 "Clinical presentation and diagnostic evaluation of acute pericarditis", section on 'Identifying the etiology'.)
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).
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:
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 .
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  (table 1).
The effect of colchicine in the primary management of acute pericarditis has subsequently been evaluated in two randomized trials:
A 2012 systematic review and meta-analysis (published prior to the ICAP results) included the results of five published clinical 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.
The 2004 ESC guidelines, published before the COPE and ICAP trials and the 2012 meta-analysis, concluded that the weight of evidence supported the efficacy of colchicine (0.5 to 1 mg/day), alone or in combination with NSAIDs, in the treatment of acute pericarditis . The findings in the COPE and ICAP trials and subsequent meta-analysis, including the relative lack of toxicity, provide additional support for the efficacy and minimal toxicity of colchicine when added to NSAIDs in acute pericarditis and suggest to use weight-adjusted doses without a loading dose as suggested by 2004 ESC guidelines (table 1). 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. In the multicenter, randomized COlchicine for the Prevention of the Post-Pericardiotomy Syndrome (COPPS) trial, colchicine significantly reduced the incidence of the postpericardiotomy syndrome at 12 months compared to placebo (respectively, 9 percent versus 21 percent; NNT equals eight) . (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). 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 [5,10].
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 [10,25-27]. 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 [25,28-30].
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 2004 European Society of Cardiology (ESC) guidelines recommended that systemic steroid therapy be restricted to patients with the following conditions :
The 2004 ESC guidelines recommend use of high doses of glucocorticoids (eg, prednisone 1 mg/kg/day) when indicated with rapid tapering to reduce the risk of systemic side effects. However, others have used the lowest steroid dose that provides symptomatic relief . 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 differs from the 2004 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:
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:
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".)
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