Acute : Diagnosis and Management MATTHEW J. SNYDER, DO, Nellis Family Medicine Residency Program, Nellis Air Force Base, Nevada JENNIFER BEPKO, MD, David Grant Medical Center Family Medicine Residency Program, Travis Air Force Base, California MERIMA WHITE, DO, Nellis Family Medicine Residency Program, Nellis Air Force Base, Nevada

Acute pericarditis, of the , is found in approximately 5% of patients admitted to the emer- gency department for chest unrelated to acute myocardial . It occurs most often in men 20 to 50 years of age. has a number of potential etiologies including , acute , use, trauma to the thoracic cavity, and systemic , such as . However, most etiologic evalu- ations are inconclusive. Patients with acute pericarditis commonly present with acute, sharp, retrosternal that is relieved by sitting or leaning forward. A is found in up to 85% of patients. Classic electro- cardiographic changes include widespread concave upward ST-segment elevation without reciprocal T-wave inversions or Q waves. First-line treatment includes nonsteroidal anti-inflammatory drugs and . Glucocorticoids are traditionally reserved for severe or refractory cases, or in cases when the cause of pericarditis is likely connective tissue , autoreactivity, or . consultation is recommended for patients with severe disease, those with pericarditis refractory to empiric treatment, and those with unclear etiologies. (Am Fam Physician. 2014;89(7):553- 560. Copyright © 2014 American Academy of Family Physicians.)

CME This clinical content cute pericarditis is the most common causes must be considered.9 Localized to the conforms to AAFP criteria affliction of the pericardium. It is , acute pericarditis can occur second- for continuing medical (CME). See diagnosed in approximately 0.1% ary to an MI or a dissecting aortic . CME Quiz Questions on of patients hospitalized for chest Systemic conditions, such as malignancy, page 515. A pain and in 5% of patients admitted to the inflammatory responses, autoimmune dis- Author disclosure: No rel- for chest pain unre- orders (e.g., rheumatoid arthritis), and evant financial affiliations. lated to acute myocardial infarction (MI).1 uremia, can precipitate acute pericarditis. ▲ Patient information: Although acute pericarditis occurs in all External causes other than viral A handout on this topic, age groups and in men and women, it pres- include pharmacologic agents (e.g., hydrala- written by the authors ents most often in men 20 to 50 years of age.2 zine, ), radiation treatment, blunt of this article, is avail- Acute pericarditis by itself confers low mor- or sharp trauma to the thoracic cavity, and able at http://www.aafp. 9 org/afp/2014/0401/ tality; however, the high rate of recurrence bacterial infection. Most etiologic evalua- p553-s1.html. Access to and the difficulty of controlling symptoms tions are inconclusive. the handout is free and contribute to high morbidity. After an initial unrestricted. episode of acute pericarditis, 30% of patients Clinical Presentation and Diagnosis have a recurrence.3 Factors associated with HISTORY AND increased morbidity are shown in Table 1.4-6 In more than 95% of cases, patients with acute pericarditis present with acute Etiology retrosternal, sharp, pleuritic chest pain that Healthy pericardium consists of the inner varies in severity.10 The pain may radiate serous visceral layer and the outer fibrous into the neck, jaw, or arms, similar to an parietal layer that envelop the heart. About 15 MI. In contrast to the pain from myocardial to 50 mL of fluid, an ultrafiltrate of plasma, , chest pain from acute pericardi- separates these layers. Acute pericarditis can tis is exacerbated in the supine position, by result from a systemic disease or a process coughing, and with inspiration. The pain isolated to the pericardium (Table 2).2,7,8 In usually improves in the seated position or most immunocompetent patients, viral or by leaning forward, which reduces pres- idiopathic etiologies are common, but other sure on the parietal pericardium, but it is

AprilDownloaded 1, 2014 from ◆ Volume the American 89, Number Family Physician 7 website at www.aafp.org/afp.www.aafp.org/afp Copyright © 2014 American Academy of FamilyAmerican Physicians. Family For the Physician private, noncom 553- mercial use of one individual user of the website. All other rights reserved. Contact [email protected] for copyright questions and/or permission requests. Acute Pericarditis SORT: KEY RECOMMENDATIONS FOR PRACTICE

Evidence Clinical recommendation rating References

Evaluation of patients with acute pericarditis should include a history, C 2, 7, 15 physical examination, , chest radiography, and baseline laboratory studies (i.e., , basic metabolic panel, -I and levels, erythrocyte sedimentation rate, and serum C-reactive protein levels). Additional laboratory testing and imaging are dictated by clinical presentation and factors. Transthoracic should be performed in all patients with C 19 suspected acute pericarditis to exclude and . Patients with acute pericarditis should be treated empirically with nonsteroidal C 7 anti-inflammatory drugs. Colchicine may be used as monotherapy or in combination with a nonsteroidal C 23 anti-inflammatory drug for the first episode of acute pericarditis.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evi- dence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort.

not relieved with nitrates.2 Acute chest pain Additional clinical findings reflective of may or may not occur in patients with ure- the underlying etiology, such as those con- mic pericarditis or pericarditis associated sistent with specific autoimmune disorders with rheumatologic disorders, although or malignancies, may occur in patients with pleuritic chest pain may be the initial pre- acute pericarditis. Patients with a bacterial sentation of systemic erythematosus. etiology may present with , chills, and Dull, oppressive chest pain radiating to the , whereas those with a viral eti- trapezius ridges or shoulders may occur ology may present with -like or with acute pericarditis, making it difficult gastrointestinal symptoms. to differentiate from other common or life- A pericardial friction rub, which is highly threatening causes of chest pain, such as MI specific and for acute pericar- or (Tables 311 and 49). ditis, occurs in up to 85% of patients, but its absence does not exclude the diagnosis.12 Fric- tion rubs are characterized by a superficial scratchy or squeaking quality with varying Table 1. Predictors of Severe Illness in Patients with Acute Pericarditis intensity that may come and go over a period of hours, and may be heard best with the

Major absence of a pericardial effusion. The intensity Fever > 100.4°F (38°C) of the friction rub may be increased during Subacute onset by having the patient for- Evidence suggestive of cardiac tamponade ward or rest the elbows on the knees, applying Large pericardial effusion (an echo-free space firm pressure on the stethoscope diaphragm greater than 20 mm) during suspended respiration.9 Respiration Nonsteroidal anti-inflammatory drug therapy does not affect a pericardial friction rub and ineffective after seven days thus allows differentiation from a pleural rub. Minor Immunosuppressed state ELECTROCARDIOGRAPHIC FINDINGS History of oral therapy Electrocardiographic changes caused by sig- Acute trauma nificant pericardial inflammation occur in Elevated cardiac troponin level (suggestive of approximately 90% of patients with acute ) pericarditis,2 with the possible exception of

NOTE: Major predictors have been validated in multi- those with uremic pericarditis, and typi- variate analysis. cally evolve in four stages (Figure 12,9). Classic Information from references 4 through 6. changes include widespread concave upward ST-segment elevation and PR-segment

554 American Family Physician www.aafp.org/afp Volume 89, Number 7 ◆ April 1, 2014 Acute Pericarditis Table 2. Etiologies of Acute Pericarditis

Infectious Noninfectious Hypersensitivity- or autoimmunity- Viral* Acute idiopathic* related Adenovirus Acute myocardial infarction* Medication induced (select drugs)* Coxsackie A and B Neoplastic* Echovirus Primary tumors Epstein-Barr virus Fibroma Isoniazid Hepatitis Lipoma Minoxidil Human virus Mesothelioma Phenytoin (Dilantin) Influenza Sarcoma Procainamide Metastatic tumors Metabolic disorders* Bacterial* Breast Gout Haemophilus Leukemia Myxedema Legionella Renal insufficiency (i.e., pericarditis) Meningococcus Lymphoma Uremia Neisseria Melanoma Postcardiac Pneumococcus Sarcoma Postmyocardial infarction (Dressler Salmonella Trauma syndrome) Staphylococcus Direct pericardial injury Postpericardiotomy syndrome Streptococcus Cardiac injury (e.g., , Posttraumatic (in children) catheterization) vascular disease Syphilis Pericardial perforation (e.g., gastric/ esophageal perforation, chest trauma) Ankylosing spondylitis Indirect pericardial injury Dermatomyositis Whipple disease Blunt chest trauma Familial Mediterranean fever Fungal Radiation Aspergillosis Aortic dissection (with leakage into Rheumatoid arthritis Blastomycosis pericardial sac) Sarcoidosis Chylopericardium Scleroderma Coccidioidomycosis Familial pericarditis Sjögren syndrome Pregnancy Systemic lupus erythematosus Other Wegener granulomatosis Parasitic Protozoal

*—Most common or clinically important in each category. Adapted with permission from Ariyarajah V, Spodick DH. Acute pericarditis: diagnostic cues and common electrocardiographic manifestations. Cardiol Rev. 2007;15(1):25, with additional information from references 7 and 8. depression without T-wave inversions. In con- trast, pathologic Q waves, regional convex ST- Table 3. segment elevations, and reciprocal changes of Acute Pericarditis commonly occur with myocardial ischemia or infarction. When the ratio of ST-segment Common Less common elevation to T-wave amplitude (in mm) in pectoris Esophageal spasm Esophagitis Pulmonary lead V6 exceeds 0.25, acute pericarditis is usu- ally present.13 Electrocardiographic manifes- (acute) Tension tations of acute pericarditis, acute MI, and Gastroesophageal Rare reflux disease early repolarization are shown in Table 5.2,9,14 Aortic dissection Myocardial infarction DIAGNOSIS AND FURTHER EVALUATION Myocardial ischemia Diagnosis requires at least two of the follow- Pleuritis ing criteria: characteristic sharp, pleuritic chest pain; pericardial friction rub; suggestive changes on electrocardiography; and a new or Information from reference 11. worsening pericardial effusion.15 In addition

April 1, 2014 ◆ Volume 89, Number 7 www.aafp.org/afp American Family Physician 555 Acute Pericarditis Table 4. Features That Differentiate Acute Pericarditis from Myocardial Ischemia or Infarction and

Symptom and clinical finding Acute pericarditis Myocardial ischemia or infarction Pulmonary embolism

Chest pain Location Retrosternal Retrosternal Anterior, posterior or lateral

Duration Hours to days Minutes (ischemia); hours Hours to days (infarction)

Character Sharp, stabbing, occasionally dull Pressure-like, heavy, squeezing Sharp, stabbing

Change with position Worse when patient is supine, No No improved when sitting up or leaning forward

Change with respiration Worsened with inspiration No In phase with respiration (absent when the patient is apneic)

Radiation Jaw, neck, shoulder, one or both Jaw, neck, shoulder, one or both Shoulder arms, trapezius ridge arms

Response to No change Improved No change

Physical examination Friction rub Present (in 85% of patients) Absent (unless pericarditis is Rare; a pleural friction rub is present) present in 3% of patients

S3 sound, pulmonary Absent May be present Absent congestion

Reprinted with permission from Massachusetts Medical Society. Lange RA, Hillis LD. Clinical practice. Acute pericarditis [published correction appears in N Engl J Med. 2005;352(11):1163]. N Engl J Med. 2004;351(21):2197.

to a history, physical examination, and elec- of patients who have acute pericarditis (pri- trocardiography, evaluation includes chest marily associated with epicardial inflamma- radiography and laboratory studies to support tion rather than myocyte ), with or the diagnosis, such as complete blood count, without an elevation in the MB fraction of basic metabolic panel, troponin-I and creatine serum creatine kinase.9,17 The rise in cardiac kinase levels, erythrocyte sedimentation rate, troponin-I levels is transient, typically resolves and serum C-reactive protein [CRP] level2,7,15 within seven to 14 days after presentation, and (Figure 2). Chest radiography can rule out does not have an adverse prognosis.17,18 abnormalities of the and mediastinum, Transthoracic echocardiography should specifically pericardial effusion. Cardio- be performed to exclude a pericardial effu- megaly in the absence of known cardiac dis- sion and cardiac tamponade.19 Small (less ease indicates a pericardial effusion of at least than 10 mm of echo-free space in ) 250 mL.9 The white count, erythro- and moderate (10 to 20 mm) pericardial cyte sedimentation rate, and serum CRP level effusions (79% and 10%, respectively) were usually are elevated.9 found in 180 of 300 consecutive patients In a prospective cohort study of 200 (60%) with acute pericarditis.10 If suspected patients 18 to 90 years of age with acute peri- purulent, tuberculous, or neoplastic peri- , high-sensitivity CRP levels were ele- carditis or an effusion that is refractory to vated in 76% of patients, and normalization treatment causes hemodynamic compro- occurred within two weeks after treatment in mise or cardiac tamponade, then pericar- 85% of patients.16 Persistent high-sensitivity diocentesis and possible pericardial biopsy CRP elevation at one week may indicate con- are indicated.9 may also tinued inflammation and need for prolonged be indicated for large (greater than 20 mm) therapy. Plasma cardiac troponin-I levels or symptomatic pericardial effusions refrac- are elevated in approximately 30% to 50% tory to medical treatment.15 The absence of

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Acute Pericarditis Electrocardiographic Changes

Stage I: Diffuse, concave ST-segment elevation Stage II: ST segments normalize, J point returns to baseline, T-wave amplitude begins to decrease, PR-segment depression begins to appear Stage III: Symmetric, diffuse T-wave inversions Stage IV: Changes normalize or T-wave inversions may become permanent

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Figure 1. Acute pericarditis electrocardiographic changes, stage 1. Diffuse concave ST-segment elevation and PR-segment depression are best demonstrated in leads I, II, aVL, and V3-5. Also note ST/T ratio > 0.25 in V6 (vertical height of ST segment from end of PR segment to J point/ amplitude of ) and lack of reciprocal ST-segment changes (ST depression in II and aVF). Information from references 2 and 9.

Table 5. Electrocardiographic Manifestations of Acute Pericarditis, Acute Myocardial Infarction, and Early Repolarization

Electrocardiographic finding Acute pericarditis Myocardial infarction Early repolarization

ST-segment shape Concave upward Convex upward Concave upward

Q waves Absent Present Absent

Reciprocal ST-segment changes Absent Present Absent

Location of ST-segment elevation Limb and precordial leads Area of involved Precordial leads

ST/T ratio in lead V6 > 0.25 Not applicable < 0.25 Loss of R-wave voltage Absent Present Absent

PR-segment depression Present Absent Absent

Arrhythmia Atrial (uncommon Atrioventricular blocks, ventricular Occasional in absence of heart disease) ,

Information from references 2, 9, and 14.

April 1, 2014 ◆ Volume 89, Number 7 www.aafp.org/afp American Family Physician 557 Acute Pericarditis Diagnosis and Treatment of Acute Pericarditis Perform history and physical examination, electrocardiography, chest radiography, echocardiography, and laboratory tests (e.g., complete blood count, basic metabolic panel, cardiac enzyme levels, erythrocyte sedimentation rate, C-reactive protein level)

Do results meet diagnostic criteria?

No Yes

Consider other etiologies Do results meet criteria for high risk of severe illness (Table 1)?

No Yes

Admit patient for further studies to Treat as outpatient with determine underlying cause; treat NSAIDs or colchicine with NSAIDs or colchicine

Do symptoms improve Do symptoms improve with no with treatment? evidence of pericardial effusion?

No Yes No Yes

Continue search Continue outpatient Cardiologist consultation Exclude infection for etiology treatment Pericardiocentesis or systemic disease as possible etiology Consider hospital No etiologic search Computed tomography of admission needed the chest and Exclude infection or systemic disease as possible etiology

Figure 2. Algorithm for the diagnosis and treatment of acute pericarditis. (NSAIDs = nonste- roidal anti-inflammatory drugs.)

a pericardial effusion does not exclude acute Treatment pericarditis. Cardiac tamponade is present Many patients with pericarditis can be suc- in 5% to 15% of patients with acute idio- cessfully treated in the outpatient setting pathic pericarditis and in 60% of those with (Figure 2). Clinical presentation, presumed neoplastic, tuberculous, or purulent peri- etiology, medical history, and response to carditis.20 Pericardial calcifications noted previous treatments help determine man- on transthoracic echocardiography suggest agement options. Patients at higher risk constrictive pericarditis.2 should be treated in the hospital (Table 14-6). Clinical presentation should dictate other testing and imaging to determine the etiol- NSAIDS ogy of the pericarditis. Human immunode- Although there are no randomized con- ficiency virus assay, antinuclear antibody, trolled trials to date, pericarditis usually is rheumatoid factor, tuberculin skin testing, or treated empirically with nonsteroidal anti- quantiferon tuberculosis assay should be con- inflammatory drugs (NSAIDs).7 Patients sidered in immunocompromised or high-risk with presumed viral or idiopathic pericar- patients.2 Viral cultures and antibody titers ditis should start on NSAIDs and continue are not indicated because of their low yield until symptom resolution, which usually and lack of influence on management.9 Fur- takes two weeks.22 Although many differ- ther imaging via computed tomography and ent NSAIDs are available, there is no evi- magnetic resonance imaging may be indi- dence that any particular one is superior to cated for symptoms not responding to empiric another for treating acute pericarditis. How- treatment or in the setting of suspected com- ever, the preferred agent to treat acute peri- plex etiologies, such as malignancy.21 carditis caused by MI is in a dosage

558 American Family Physician www.aafp.org/afp Volume 89, Number 7 ◆ April 1, 2014 Acute Pericarditis

of 650 to 1,000 mg four times per day with a (relative risk = 0.56; 95% confidence inter- taper over four weeks.6,10 val, 0.30 to 0.72; = 4; An observational study with aspirin P < .001). Colchicine also reduced the rate of (800 mg orally every six to eight hours for symptom persistence at 72 hours (19.2% vs. seven to 10 days followed by a two- to three- 40%; P = .001), reduced the number of recur- week taper) and gastroprotection showed a rences per patient (0.21 vs. 0.52; P = .001), and resolution rate of 87% with follow-up for 38 improved the remission rate at one week (85% months.10 , which may be preferred vs. 58.3%; P < .001).23 because of the adverse effect profile, can be Colchicine should not be taken with macro- prescribed at 300 to 800 mg every six to eight lides and should be used cautiously in patients hours tapered to 800 mg weekly over three with renal insufficiency because colchicine to four weeks.6,7 Indomethacin (Indocin) levels will increase. Maintenance or prophy- should be prescribed at 75 to 150 mg daily.6 lactic doses of colchicine should be reduced Tapering will decrease the risk of recurrences by 50% in patients older than 70 years who and should be guided by symptoms and have impaired renal function and glomerular inflammatory markers (e.g., erythrocyte sed- filtration rates less than 50 mL per minute.6 imentation rate, CRP level).22 Patients should Additional potential adverse effects include limit strenuous activities until they are pain diarrhea (up to 10% of cases), , vom- free and their have normalized.22 iting, myotoxicity, hepatotoxicity, and bone Gastroprotection should be used in appropri- marrow suppression.6 Baseline blood analysis ate patients while they are taking NSAIDs. (including complete blood count, and trans- aminase, creatine kinase, and serum creati- COLCHICINE nine levels) should be performed at the time Colchicine is used to treat recurrent pericar- of colchicine initiation and approximately ditis or pericarditis that does not respond to one month later to assess for adverse effects.6 conventional treatment.23 European guide- lines also suggest colchicine as a possible GLUCOCORTICOIDS initial treatment choice for acute pericardi- In general, glucocorticoids should not be tis.7 In one prospective, randomized, open- used as first-line therapy for patients with label study, patients with acute pericarditis acute pericarditis. Glucocorticoid use during received conventional treatment plus col- acute pericarditis confers a significant risk chicine or conventional treatment alone. of adverse effects and possible recurrence of Patients who received colchicine had a sig- pericarditis (odds ratio = 4.30; 95% confi- nificantly lower recurrence rate at 18 months dence interval, 1.21 to 15.25; P = .024) caused (10.7% vs. 32.3%; P = .004) and symptom by reactivation of a viral infection or an persistence at 72 hours (11.7% vs. 36.7%; increase in viral replication.6 However, gluco- P = .003).24 When combined with an NSAID, corticoids may be considered when the cause colchicine decreased symptoms, decreased of the acute pericarditis is connective tissue rate of recurrence, and was better tolerated disease, autoreactivity, or uremia.7 Predni- than an NSAID alone. sone may be prescribed at 1 mg per kg per day These findings were confirmed in a sub- with a rapid taper or titrated to a dosage that sequent multicenter, randomized, double- achieves clinical benefit (0.25 mg per kg per blind, controlled trial in which colchicine or day). Toward the end of the taper (generally placebo was added to conventional therapy six to eight weeks), NSAIDs or colchicine can in patients with acute pericarditis. Colchicine be introduced to decrease the risk of recur- was given at a dosage of 0.5 mg twice daily for rence.6 The taper is based on clinical symp- three months in patients weighing more than toms and serum biomarkers. If symptoms 154 lb (70 kg) or 0.5 mg once daily in patients return, NSAIDs can be added. If symptoms weighing 154 lb or less. Incessant or recurrent do not improve, the last dosage of glucocor- pericarditis occurred in 16.7% of the colchi- ticoids that suppressed symptoms should be cine group vs. 37.5% of the placebo group restarted. Glucocorticoid treatment should

April 1, 2014 ◆ Volume 89, Number 7 www.aafp.org/afp American Family Physician 559 Acute Pericarditis

be continued for two to three weeks.6 Consul- 8. Spodick DH. Pericardial disease. In: Braunwald E, Zipes tation with a cardiologist is recommended for DP, Libby P, eds. Heart Disease: A Textbook of Cardio- vascular Medicine. 6th ed. Philadelphia, Pa.: Saunders; patients with severe disease, those with peri- 2001. carditis refractory to treatment, and those 9. Lange RA, Hillis LD. Clinical practice. Acute pericar- with unclear etiologies. ditis [published correction appears in N Engl J Med. 2005;352(11):1163] . N Engl J Med. 2004;351(21):2195- Data Sources: PubMed, Ovid, and the Cochrane data- 2202. base were searched using the key words acute pericar- 10. Imazio M, et al. Day-hospital treatment of acute pericar- ditis, acute pericarditis treatment, and acute pericarditis ditis: a management program for outpatient therapy. diagnosis. Essential Evidence Plus was also searched. J Am Coll Cardiol. 2004;43(6):1042-1046. Search dates: September and October 2011, January 11. Gibbons RJ, Chatterjee K, Daley J, et al. ACC/AHA/ACP- 2012, and December 2013. ASIM guidelines for the management of patients with chronic stable angina: a report of the American College Figure 1 courtesy of Alan Hinderliter, MD, Department of Cardiology/American Heart Association Task Force of Medicine, Division of Cardiology, University of North on Practice Guidelines (Committee on Management of Carolina at Chapel Hill. Patients with Chronic Stable Angina [published correc- The opinions and assertions contained herein are the tions appear in J Am Coll Cardiol. 1999;34(1):314, and private views of the authors and are not to be construed J Am Coll Cardiol. 2001;38(1):296]. J Am Coll Cardiol. as official or as reflecting the views of the U.S. Air Force 1999;33(7):2092-2197. Medical Department or the U.S. Air Force at large. 12. Zayas R, et al. Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol. 1995;75(5):378-382. The Authors 13. Ginzton LE, Laks MM. The differential diagnosis of acute MATTHEW J. SNYDER, DO, is the assistant program direc- pericarditis from the normal variant: new electrocardio- graphic criteria. Circulation. 1982;65(5):1004-1009. tor and director of obstetrics at the Nellis Family Medicine Residency Program at Nellis Air Force Base, Nev. 14. Marinella MA. Electrocardiographic manifestations and differential diagnosis of acute pericarditis. Am Fam Phy- JENNIFER BEPKO, MD, is director of for the David sician. 1998;57(4):699-704. Grant Medical Center Family Medicine Residency Program 15. Imazio M, Spodick DH, Brucato A, Trinchero R, Markel at Travis Air Force Base, Calif. At the time the manuscript G, Adler Y. Diagnostic issues in the clinical management was written, Dr. Bepko was director of geriatrics at the of pericarditis. Int J Clin Pract. 2010;64(10):1384-1392. Nellis Family Medicine Residency Program. 16. Imazio M, et al. of C-reactive protein elevation and time course of normalization in acute pericarditis: MERIMA WHITE, DO, is a third-year resident at the Nellis implications for the diagnosis, therapy, and prognosis of Family Medicine Residency Program. pericarditis. Circulation. 2011;123(10):1092-1097. Address correspondence to Matthew J. Snyder, DO, 17. Bonnefoy E, et al. Serum cardiac troponin I and ST- Nellis Family Medicine Residency, 4700 N. Las Vegas segment elevation in patients with acute pericarditis. Blvd., Nellis AFB, NV 89191 (e-mail: mdrnsnyder@gmail. Eur Heart J. 2000;21(10):832-836. com). Reprints are not available from the authors. 18. Imazio M, et al. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol. 2003;42(12):2144-2148. REFERENCES 19. Cheitlin MD, et al. ACC/AHA guidelines for the clini- cal application of echocardiography. A report of the 1. Imazio M, Trinchero R. Current and future treatment for American College of Cardiology/American Heart Asso- pericarditis. Future Cardiol. 2007;3(6):623-634. ciation Task Force on Practice Guidelines (Committee on 2. Ariyarajah V, Spodick DH. Acute pericarditis: diagnostic Clinical Application of Echocardiography). Developed in cues and common electrocardiographic manifestations. collaboration with the American Society of Echocar- Cardiol Rev. 2007;15(1):24-30. diography. Circulation. 1997;95(6):1686-1744. 3. Lotrionte M, et al. International collaborative system- 20. Permanyer-Miralda G. Acute pericardial disease: atic review of controlled clinical trials on pharmacologic approach to the aetiologic diagnosis. Heart. 2004; treatments for acute pericarditis and its recurrences. 90(3):252-254. Am Heart J. 2010;160(4):662-670. 21. Hoey ET, et al. Cardiovascular MRI for assessment of 4. Imazio M, et al. Indicators of poor prognosis of acute infectious and inflammatory conditions of the heart. pericarditis. Circulation. 2007;115(21):2739-2744. AJR Am J Roentgenol. 2011;197(1):103-112. 5. Imazio M, Spodick DH, Brucato A, Trinchero R, Adler Y. 22. Imazio M, et al. Medical therapy of pericardial diseases: Controversial issues in the management of pericardial part I: idiopathic and infectious pericarditis. J Cardio- diseases. Circulation. 2010;121(7):916-928. vasc Med (Hagerstown). 2010;11(10):712-722. 6. Imazio M, Trinchero R. Triage and management of acute 23. Imazio M, Brucato A, Cemin R, et al.; ICAP Investiga- pericarditis. Int J Cardiol. 2007;118(3):286-294. tors. A randomized trial of colchicine for acute pericar- 7. Maisch B, Seferovic´ PM, Ristic´ AD, et al. Guidelines on ditis. N Engl J Med. 2013;369(16):1522-1528. the diagnosis and management of pericardial diseases 24. Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addi- executive summary: Task Force on the Diagnosis and tion to conventional therapy for acute pericarditis: Management of Pericardial Diseases of the European results of the COlchicine for acute PEricarditis (COPE) Society of Cardiology. Eur Heart J. 2004;25(7):587-610. trial. Circulation. 2005;112(13):2012-2016.

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