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Acute Pericarditis

Sally A. Arif, PharmD, BCPS
Assistant Professor of Pharmacy Practice
Chicago College of Pharmacy, Midwestern University
Downers Grove, Illinois


US Pharm. 2011;36(2):HS-18-HS-20.

Acute pericarditis is an inflammatory process involving the pericardium, a fibroelastic sac containing the heart and the roots of the great blood vessels.1 In the United States, acute pericarditis accounts for approximately 1 of every 1,000 hospital admissions and 1% of emergency room visits in patients presenting with ST-segment elevation on ECG.2 A variety of infectious and noninfectious causes may be responsible, including systemic disease. Acute pericarditis is classified as idiopathic if a viral etiology is presumed and no secondary cause (i.e., autoimmune problem, malignancy, drug) can be identified (TABLE 1). Acute pericarditis occurs more often in men than in women, and in more adults than children.3


The pericardium is composed of layers, including the visceral pericardium and the parietal pericardium. Between the visceral and parietal layers of the pericardium is a potential space, or cavity. The pericardial cavity contains approximately 20 mL of plasmalike fluid, and it can accommodate another 120 mL of fluid without causing significant hemodynamic changes.4

Inflammation of the pericardium and increased fluid in the pericardial cavity can lead to pericardial effusion (accumulation of excess fluid around the heart). The rate of accumulation and the type of fluid (serous, sanguineous, lymph, or pus) that accumulates vary by the type of pericardial effusion. A major sequela of pericardial effusion occurs when compression of the heart from the fluid buildup interferes with its normal functioning (i.e., compromises the heart’s ability to pump blood, leading to decreased cardiac output and stroke volume). This potentially fatal condition, called cardiac tamponade, occurs in up to 15% of patients with idiopathic pericarditis.1,5

Clinical Features and Diagnosis

The classic findings in acute pericarditis are chest pain, pericardial friction rub, and ECG changes. In general, the course of disease is short (lasting days to weeks), although it is critical to watch for progression to cardiac tamponade.6

The chest pain associated with acute pericarditis has a sudden onset and is pleuritic, meaning that the pain is sharp and occurs with inspiration or coughing. The pain may be over the anterior chest or the back and trapezius ridge; it also may resolve with upright posture. Unlike chest pain associated with myocardial ischemia, it is uncommon for the pain to radiate to the arms. Patients may also be tachycardic, and chest pain may be preceded by a low-grade fever.

Upon physical examination, 85% of patients with acute pericarditis present with pericardial friction rub, which is a highly specific finding. This rub, which is audible upon auscultation of the chest cavity throughout the respiratory cycle, is caused by the friction of the two inflamed layers of pericardium. This may sound like a pleural rub; however, a pleural rub does not persist when the patient holds his or her breath, while a pericardial rub would still be heard.7 Best detected with the patient in the supine or left lateral decubitus position, pericardial rub is most often described as a superficial scratchy sound.

The diagnosis of acute pericarditis may require some objective testing to obtain useful clinical data. The ECG changes that occur with acute pericarditis may be delayed for days and may resemble features similar to acute myocardial infarction (MI), making diagnosis more difficult.3 Such ECG changes typically occur in four stages.8 The first stage involves an ST elevation (convex upward); in stage 2, there is a normalization of the ST and PR segments. In stage 3, the T wave may become inverted, followed by stage 4, when the ECG becomes normal. Such changes may occur within days to weeks of the onset of inflamed pericardial tissue.

It is recommended that all patients undergo an echocardiogram, more emergently in patients with suspected pericardial effusion or cardiac tamponade.9 A chest radiograph is usually found to be normal in patients with acute pericarditis, unless there is a large effusion with an accumulation of more than 200 mL of fluid. In such cases, an enlarged distinct “water bottle–like” cardiac silhouette may be seen. C-reactive protein levels and erythrocyte sedimentation rates are often elevated, indicative of the inflammatory state. Cardiac biomarkers should also be evaluated; a study found that 32% of patients with acute pericarditis have elevated troponin I levels.10


Most viral and idiopathic cases of pericarditis are self-limiting. Management should focus on both symptom relief and treatment of the underlying disease.11 Most cases of acute pericarditis can be managed on an outpatient basis. If a pericardial effusion is suspected, or if the patient presents with hemodynamic instability, hospital admission may be warranted to better diagnose and manage any complications that may arise. Nonpharmacologic and pharmacologic considerations when treating pericarditis are presented in TABLE 2.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): NSAIDs are the drugs of choice for treating pericarditis, based on European Society of Cardiology (ESC) guidelines published in 2004.9 Historically, indomethacin (25-50 mg 3 times/day) has been commonly prescribed; however, it carries an unfavorable adverse-reaction (AR) profile and a propensity for reducing coronary blood flow compared with ibuprofen (300-800 mg 3-4 times/day).12 Aspirin (325-650 mg 3 times/day) may be used if the patient has suffered a recent (7-10 days) MI, in which case other NSAIDs are contraindicated. Overall, the NSAIDs have similar efficacy, with chest-pain relief seen within days in approximately 85% to 90% of patients.13 Treatment should be continued until the patient is asymptomatic and/or afebrile for several days; the dose may be gradually tapered. Parenteral ketorolac tromethamine may also be used for more immediate relief of symptoms in hospitalized patients, but there is a higher risk of gastrointestinal (GI) bleeds in patients who are elderly, have renal insufficiency, or have low body weight.14

Colchicine: For patients with symptoms that persist beyond 2 weeks of NSAID treatment, colchicine maybe a viable option alone or in combination. The primary treatment of acute pericarditis with colchicine may be based on results from the randomized, open-label COPE trial, in which colchicine (1-2 mg for day 1, then 0.5-1 mg/day for 3 months) was added to aspirin therapy and administered for 3 months.15 At 18 months, there was a reduced recurrence of first episode of viral or idiopathic pericarditis for colchicine plus aspirin versus aspirin alone (32.3% vs. 10.7%, P = .004). Colchicine reduced symptoms in as little as 72 hours (11.7% vs. 36.7%, P £.03). Diarrhea led to discontinuation in five patients in the colchicine arm. Although the ESC guidelines support its efficacy, colchicine should be avoided or used only if benefit outweighs risk in patients with hepatobiliary disease, renal insufficiency, or macrolide therapy (CYP 450 interaction), all of which can elevate drug levels and increase the risk of ARs.16,17

Corticosteroids: Although pericarditis is typically self-limiting, one-quarter of patients may have recurrence and require prolonged therapy with NSAIDs or colchicine. In patients who may become intolerant to such therapies or lack adequate response, high-dose oral corticosteroids (prednisone 20-60 mg/day) may be used for several weeks. Corticosteroid use has been identified as an independent risk factor for recurrence based on observational studies in which its use in early disease was associated with recurrent episodes of percarditis.18 Based on current evidence and the ESC guidelines, corticosteroids should be reserved only for refractory cases or for patients with connective-tissue disease or autoreactive or uremic pericarditis.19 Corticosteroids should be avoided in patients with recent MI, as these agents have been shown to increase the likelihood of myocardial-wall rupture.

If patients lack symptomatic relief after starting corticosteroid therapy, the dose should be increased to 1 to 1.5 mg/kg body weight daily, with tapering begun at 2-4 weeks.20 One retrospective observational study of 100 patients found that a lower dose (0.2-0.5 mg/kg/day) maintained for 4 weeks and followed with a slow taper yielded significantly fewer severe ARs (2.0% vs. 23.5%, P = .002), lower recurrence (32.6% vs. 64.7%, P = .002), and fewer hospitalizations (8.2% vs. 31.4%, P = .005) than high-dose steroids (1 mg/kg/day).21

Other Considerations: Unless it is necessary, anticoagulation (e.g., heparin, warfarin) should be avoided in acute pericarditis to reduce the risk of hemopericardium. Aspiration of fluid from the pericardial cavity (pericardiocentesis) may be beneficial in the presence of severe tamponade or in patients with symptomatic pericardial effusion. Patients should be advised to avoid strenuous physical activity during the early phase of acute pericarditis, as it may worsen symptoms.

Role of the Pharmacist

Acute pericarditis is diagnosed clinically and has a viral or idiopathic etiology. Fortunately, most patients with acute pericarditis have a short and uncomplicated course, with treatment occurring mostly in the ambulatory setting. Anti-inflammatory agents are the cornerstone of treatment. The use of NSAIDs, with or without colchicine, is considered first-line therapy, and corticosteroids are reserved for refractory cases. The use of these agents requires the pharmacist to assist with dose adjustment based on renal function and comorbidities, to screen for drug–drug interactions, and to counsel patients about ARs associated with these drugs in the setting of acute pericarditis.

If high-dose NSAIDs and steroids are started while the patient is hospitalized, the pharmacist should recommend GI prophylaxis with either proton pump inhibitors or histamine2 antagonists, especially if the patient has a history of gastroesophageal reflux disease or peptic ulcer disease. If steroid treatment is initiated, the patient should be counseled about the proper tapering doses and schedule. Since most steroid therapy is continued for several weeks, the pharmacist should recommend supplementation with calcium (1,500 mg/day) and vitamin D (800 IU/day) to prevent steroid-induced osteoporosis. For patients with recurrent acute pericarditis who have been placed on several steroid tapers, it may also be appropriate to recommend bisphosphonate therapy.22,23


1. Little WC, Freeman GL. Pericardial disease. Circulation. 2006;113:1622-1632.
2. Lorell BH. Pericardial diseases. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 5th ed. Philadelphia, PA: Saunders; 1997:1478-1534.
3. Troughton RW, Asher CR, Klein AL. Percarditis. Lancet. 2004;363:717-727.
4. Shabetai R. Diseases of the pericardium. In: Hurst JW, Schlant RC, Rackley CE, et al, eds. The Heart: Arteries and Veins. 7th ed. New York, NY: McGraw-Hill; 1990:1348-1353.
5. Permanyer-Miralda G. Acute pericardial disease: approach to the aetiologic diagnosis. Heart. 2004;90:252-254.
6. Lange RA, Hillis LD. Acute pericarditis. N Engl J Med. 2004;351:2195-2202.
7. Zayas R, Anguita M, Torres F, et al. Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol. 1995;75:378-382.
8. Dehmer GJ, O’Meara JJ. Update on acute pericarditis. Hosp Med. 1995;31:39-44.
9. Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary: the Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology. Eur Heart J. 2004;25:587-610.
10. Imazio M, Demichelis B, Cecchi E. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol. 2003;42:2144-2148.
11. Press OW, Livingston R. Management of malignant pericardial effusion and tamponade. JAMA. 1987;257:1088-1092.
12. Schifferdecker B, Spodick DH. Nonsteroidal anti-inflammatory drugs in the treatment of pericarditis. Cardiol Rev. 2003;11:211-217.
13. 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;43:1042-1046.
14. Arunasalam S, Siegel RJ. Rapid resolution of symptomatic acute pericarditis with ketorolac tromethamine: a parenteral nonsteroidal antiinflammatory agent. Am Heart J. 1993;125(pt 1):1455-1458.
15. 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;112:2012-2016.
16. Hung IF, Wu AK, Cheng VC, et al. Fatal interaction between clarithromycin and colchicine in patients with renal insufficiency: a retrospective study. Clin Infect Dis. 2005:41:291-300.
17. Adler Y, Finkelstein Y, Guindo J, et al. Colchicine treatment for recurrent pericarditis. A decade of experience. Circulation. 1998;97:2183-2185.
18. Spodick DH. Intrapericardial treatment of persistent autoreactive pericarditis/myopericarditis and pericardial effusion. Eur Heart J. 2002;23:1481-1482.
19. Shabetai R. Recurrent pericarditis: recent advances and remaining questions. Circulation. 2005;112:1921-1923.
20. Marcolongo R, Russo R, Laveder F, et al. Immunosuppressive therapy prevents recurrent pericarditis. J Am Coll Cardiol. 1995;26:1276-1279.
21. Imazio M, Brucato A, Cumetti D, et al. Corticosteroids for recurrent pericarditis: high versus low doses: a nonrandomized observation. Circulation. 2008;118:667-671.
22. American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis. Recommendations for the prevention and treatment of glucocorticoid induced osteoporosis: 2001 update. Arthritis Rheum. 2001;44:1496-1503.
23. Sambrook PN. How to prevent steroid induced osteoporosis. Ann Rheum Dis. 2005;64:176-178.

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