AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

The pericardium is composed of the parietal pericardium (an outer fibrous layer) and the visceral pericardium (an inner serous membrane made of a single layer of mesothelial cells). The visceral pericardium is attached to the epicardial fat and reflects back on itself to form the parietal pericardium. The pericardium normally contains as much as 50 mL of an ultrafiltrate of plasma. Drainage occurs via the thoracic duct and the right lymphatic duct into the right pleural space.

Pericardial physiology includes 3 main functions. First, through its mechanical function, the pericardium promotes cardiac efficiency by limiting acute dilation, maintaining ventricular compliance with preservation of the Starling curve, and distributing hydrostatic forces. The pericardium also creates a closed chamber with subatmospheric pressure that aids atrial filling and lowers transmural cardiac pressures. Second, through its membranous function, the pericardium shields the heart by reducing external friction and acting as a barrier against extension of infection and malignancy. Third, through its ligamentous function, the pericardium anatomically fixes the heart.

Acute pericarditis is an inflammation of the pericardium characterized by chest pain, pericardial friction rub, and serial electrocardiographic changes.

Pathophysiology

In most cases of acute pericarditis, the pericardium is acutely inflamed and has an infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. Often, the pericardium manifests a fibrinous reaction with exudates and adhesions. The pericardium may develop a serous or hemorrhagic effusion. A granulomatous pericarditis occurs with tuberculosis, fungal infections, rheumatoid arthritis (RA), and sarcoidosis.

Frequency

United States

Epidemiological data on incidence are lacking, likely because acute pericarditis is frequently inapparent clinically, despite its presence in numerous disorders. Lorell notes a diagnosis of acute pericarditis in approximately 1 per 1000 hospital admissions.¹ Acute pericarditis comprises 1% of emergency room visits in patients with ST-segment elevation.²

Mortality/Morbidity

• Mortality varies greatly depending on etiology. The mortality rate approaches 100% in untreated purulent pericarditis, whereas mortality is virtually nonexistent in acute viral or idiopathic pericarditis.³
• Morbidity also depends on the etiology and development of complications.

Sex

• Acute pericarditis is more common in men than in women.

Age

• Acute pericarditis is more common in adults than in children.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• Chest pain is the cardinal symptom.
• • The quality of the pain may be sharp, dull, aching, burning, or pressing.
  • Intensity varies from barely perceptible to severe.
  • Pain is usually precordial with referral to the trapezius ridge.
  • It is worse during inspiration, when lying flat, or during swallowing and with body motion.
• Dyspnea may be present, especially with tamponade.
• Fever may be present.
• Abdominal pain occurs infrequently in children.

Physical

• A pericardial friction rub is pathognomonic for acute pericarditis.  
• • The rub has a scratching, grating sound similar to leather rubbing against leather.
  • Auscultation with the diaphragm of the stethoscope over the left lower sternal edge allows the best detection of the rub.
  • Auscultation during end expiration with the patient sitting up and leaning forward increases the likelihood of observing this physical finding.
  • Serial examinations may be necessary for detection.
  • More than 50% of rubs are triphasic. They are composed of (1) an atrial systolic rub that precedes S1, (2) a ventricular systolic rub between S1 and S2 and coincident with the peak carotid pulse, and (3) an early diastolic rub after S2 (usually the faintest).
  • The biphasic to-and-fro rub is less common (24%). It can occur with tachycardia and is due to summation of the atrial and early diastolic rub.
  • Monophasic rubs (the ventricular systolic) are the least common but may occur in patients with atrial fibrillation.
  • Especially when it is monophasic, the pericardial friction rub can be mistaken for a systolic murmur. Pericardial rubs may be differentiated if the rub does not change with usual respiratory or positional maneuvers, if 3 components are present, and if the findings on the ECG are typical.
• Tachypnea may be present.
• Tachycardia may be present.
• Patients may have fever.
• The Beck triad (ie, hypotension; elevated systemic venous pressure, often with jugular venous distention; muffled heart sounds) may occur in patients with cardiac tamponade, especially from sudden intrapericardial hemorrhage.
• Pulsus paradoxus is defined as a > 10 mm Hg decrease in arterial systolic pressure with inspiration. This decrease is important in patients with more slowly developing tamponade because they may lack findings of the Beck triad.

Causes

• Idiopathic
• • Between 26% and 86% of cases are idiopathic in nature.⁴
  • No clinical features distinguish idiopathic cases from viral pericarditis.
  • Most likely, most idiopathic cases are undiagnosed viral infections.
  • Seasonal peaks occur in spring and fall.
• Infection
• • Viral
  • • This is the most common cause of acute pericarditis and accounts for 1-10% of cases.
    • Causative viruses include coxsackievirus B, echovirus, adenoviruses, influenza A and B viruses, Enterovirus, mumps virus, Epstein-Barr virus, human immunodeficiency virus (HIV), herpes simplex virus type 1, varicella-zoster virus, measles virus, parainfluenza virus type 2, and respiratory syncytial virus, cytomegalovirus, hepatitis A, hepatitis B, and hepatitis C.
    • Viruses, especially coxsackievirus B and influenza, can occur as seasonal epidemics.
    • It is usually a short self-limited disease that lasts 1-3 weeks.
    • Patients may have associated myocarditis.
    • The treatment is based on the symptoms present, with observation for the development of tamponade.
    • Pericardial involvement is frequent in persons with HIV, but is usually an asymptomatic pericardial effusion of small volume. Persons with advanced HIV infection develop pericardial involvement more frequently, with one study noting right atrial diastolic compression in 5% of cases involving advanced HIV infection.⁵ Symptomatic pericarditis occurs in less than 1% of cases involving HIV, and its etiology can include the usual causes, opportunistic infection, Kaposi sarcoma, and HIV.
  • Bacterial
  • • This accounts for 1-8% of cases and causes purulent pericarditis.
    • Bacterial pericarditis develops from direct pulmonary extension, hematogenous spread, myocardial abscess or endocarditis, penetrating injury to chest wall from either trauma or surgery, or a subdiaphragmatic suppurative lesion.
    • Organisms isolated include gram-positive species such as Streptococcus pneumoniae and other Streptococcus species and Staphylococcus. Isolated gram-negative species include Proteus, Escherichia coli, Pseudomonas, Klebsiella, Salmonella, Shigella, Neisseria meningitidis, and Haemophilus influenzae.
    • Less common organisms include Legionella, Nocardia, Actinobacillus, Rickettsia, Borrelia burgdorferi (Lyme borreliosis), Listeria, Leptospira, Chlamydophila psittaci, and Treponema pallidum (syphilis).
    • Anaerobes also have been isolated in 40% of patients in reviews of the pediatric population.
    • Previously, Pneumococcus was the predominant organism. However, in the antibiotic era, staphylococcal and gram-negative species have become more common. Most cases are now associated with thoracic surgery, renal disease, and immunosuppression.
    • Purulent pericarditis can develop from previous aseptic pericarditis and is associated with a poorer prognosis, with a mortality rate nearing 100% for untreated persons and a mortality rate of 12-40% for treated patients.
    • A high percentage of patients develop constrictive pericarditis.
    • Treatment includes appropriate antibiotics for at least 4 weeks and drainage of pericardial fluid.
    • Intrapericardial fibrinolysis can be a useful treatment to assist with drainage of thick, loculated fluid, but open surgical drainage is preferred.
    • Occasionally, patients require partial to total pericardiectomy.
  • Tubercular
  • • Tuberculosis accounts for 4% of cases.
    • It should be considered in all instances of pericarditis without a rapid course, especially in high-risk groups, such as elderly patients in nursing homes.
    • The diagnostic yield for acid-fast bacilli in pericardial fluid is fairly low (between 30% and 76%).
    • Pericardial biopsy has a much better yield (approximately 100%).
    • Elevated adenosine deaminase in pericardial fluid is useful for diagnosing tuberculosis. Studies note greater than 90% sensitivity and specificity with levels higher than 50-70 U/L.
    • High adenosine deaminase values may indicate a poorer prognosis.
    • Approximately half the patients develop constrictive pericarditis.
    • Treatment is with the usual antituberculous chemotherapy.
    • The mortality rate approaches 50%.
  • Other infectious agents
  • • Fungal organisms include Histoplasma, Blastomyces, Coccidioides, Aspergillus, and Candida.
    • Parasitic organisms include Entamoeba, Echinococcus, and Toxoplasma.
• Inflammatory disorders
• • Rheumatoid arthritis
  • • Autopsy studies show a prevalence of 11-50% in patients with RA.
    • Echocardiography studies note pericardial effusions in 50% of patients with RA with nodules and in only 15% of patients with RA without nodules.
    • Pericardial involvement is usually clinically silent. Diagnosis is made in only 2% of adults and 6% of juveniles.
    • Pericarditis occurs predominantly in males with severely destructive and nodular RA.
    • Rarely, pericarditis precedes the onset of RA.
    • ECG almost never demonstrates typical findings of pericarditis, possibly secondary to masking from RA medications.
    • Diagnosis is suggested by serous or hemorrhagic pericardial fluid with a glucose level of less than 45 mg/dL, a white blood cell count higher than 15,000/µL with cytoplasmic inclusion bodies, a protein level higher than 5 g/dL, a low total serum hemolytic complement (CH₅₀), a high immunoglobulin G (IgG) level, and a high rheumatoid factor. Cholesterol levels may be high in the fluid of patients with RA who have nodules.
    • Only symptomatic RA pericarditis should be treated.
    • Interestingly, symptomatic disease tends to occur in patients with arthritis, pleuritis, and other complications who are already being treated with anti-inflammatory agents such as corticosteroids, gold, and antimalarial drugs.
  • Systemic lupus erythematosus
  • • Clinically evident pericarditis has been reported in 25% of patients with lupus. Autopsy series reveal pericardial involvement in 62%.
    • Pericarditis usually occurs in flare-ups, but it may be the presenting manifestation. In contrast to RA, ECG findings usually demonstrate typical changes of pericarditis.
    • Fluid analysis reveals increased leukocytes of PMN predominance with a high protein level, low-to-normal glucose level, low complement, and, possibly, a pH level of less than 7. In addition, fluid analysis reveals positive autoantibodies, such as the antinuclear antibody or anti–double-stranded DNA.
    • Treat with anti-inflammatory agents and optimization of systemic lupus erythematosus (SLE) treatment.
    • Development of tamponade and constrictive pericarditis is rare.
  • Scleroderma
  • • Pericarditis is recognized in 5-10% of patients with scleroderma. Autopsy prevalence rate is 70%.
    • Pericardial effusions occur in 40% of patients with scleroderma and can be due to scleroderma, myocardial failure (restrictive cardiomyopathy), and renal failure.
    • Restrictive cardiomyopathy and pericardial constriction can coexist. Usually, pulmonary hypertension, right heart failure, and systolic dysfunction occur.
    • Pericardial fluid has a protein value greater than 5 g/dL, has a low cell count, and does not demonstrate the antibodies found in RA and SLE.
    • These patients have a poor prognosis.
  • Rheumatic fever
  • • This occurs more commonly in lower socioeconomic groups and in children.
    • It often accompanies endocarditis and myocarditis, with a worse prognosis.
    • Consider this etiology in any child with pericarditis.
    • In adults, pericarditis may not occur with myocardial or valvular involvement, and it is associated with a better prognosis. It usually appears 7-10 days after onset of fever and arthritis. Often, stage 1 ECG findings are absent.
    • Antistreptolysin O titer is usually greater than 400.
    • Rarely is a large effusion present.
    • This is not a demonstrated cause of constrictive pericarditis.
    • Pericarditis resolves with anti-inflammatory treatment.
  • Sarcoidosis
  • • Echocardiography shows that pericardial involvement is present in 20% of cases.
    • Patients may not have significant myocardial infiltration.
    • It rarely causes cardiac tamponade or constrictive pericarditis.
  • Other inflammatory conditions
  • • Sjögren syndrome
    • Mixed connective-tissue disease
    • Reiter syndrome
    • Ankylosing spondylitis
    • Inflammatory bowel disease
    • Wegener granulomatosis
    • Vasculitis (eg, giant cell arteritis, polyarteritis)
    • Polymyositis
    • Behçet syndrome
    • Whipple disease
    • Familial Mediterranean fever
    • Serum sickness
• Metabolic disorders
• • Renal failure
  • • Renal failure accounts for approximately 12% of cases.
    • In the predialysis era, pericarditis developed in 35-50% of patients with uremia who had chronic renal failure and less commonly in those with acute renal failure. Death often followed in several weeks.
    • With dialysis, the incidence rate is less than 10%.
    • Pericarditis occurs after the onset of dialysis in 8-12% of cases.
    • ECG commonly does not show the typical ST-T segment changes due to lack of inflammation.
    • In uremic patients, heart rates may be deceptively slow with tamponade, fever, and hypotension due to autonomic impairment.
    • Some authors suggest that uremic pericarditis is a different entity from dialysis-associated pericarditis.
    • Asymptomatic pericardial effusions can occur in 36-62% of patients with uremia who require dialysis. They are often small to moderate in size, and they can occur secondary to volume overload. They can lead to significant hemodynamic complications during routine dialysis. The presence of a large pericardial effusion that persists for longer than 10 days after intensive dialysis has a high likelihood of causing tamponade.
    • Treatment is intensive dialysis.
    • If no improvement is noted after 7-10 days or if the patient has hemodynamic instability, proceed with pericardiocentesis or pericardiectomy.
    • Intensive dialysis is beneficial to most patients with uremia who develop pericarditis prior to dialysis. Dialysis-induced pericarditis fails to respond to more intensive dialysis in 25-33% of patients.
  • Hypothyroidism
  • • This accounts for as many as 4% of cases.
    • Pericardial involvement usually occurs with severe hypothyroidism.
    • Patients may develop large pericardial effusions, but they rarely develop tamponade.
    • Pericardial fluid is often clear with high protein and cholesterol levels and with few cells.
    • Low ECG voltage is often observed.
    • Myocardial involvement is common.
    • Treatment is hormone replacement.
  • Cholesterol pericarditis
  • • Cholesterol pericarditis is also called gold-paint pericarditis.
    • Granulomatous pericarditis has been implicated in some cases.
    • Cholesterol pericarditis is a complication of a chronic pericardial effusion exacerbated by cholesterol crystals.
    • It usually presents with large effusions that are not hemodynamically important.
    • Development of constriction is rare.
• Cardiovascular diseases
• • Myocardial infarction
  • • After a transmural infarction, a fibrinous pericardial exudate appears within 24 hours. It begins to organize at 4-8 days, and it completes organization at 4 weeks.
    • If pericardial involvement is confined to the infarct zone, stage 1 ECG findings are often not seen.
    • Positive T waves that last longer than 48 hours after an acute myocardial infarction (AMI) or premature reversal of inverted T waves may indicate pericardial involvement.
    • The pericardial pain occurs less frequently than the friction rub. The rub often is detected on the second or third day after an AMI but may be heard within 24 hours and as late as 10 days.
    • Prior to thrombolytic therapy, infarct-associated pericarditis ranges from 7-23% of cases. At autopsy, almost all patients were noted to have localized fibrinous pericarditis overlying the area of infarction.
    • With thrombolytic therapy and direct infarct angioplasty, the incidence of infarct-associated pericarditis has decreased to 5-8%.
    • Overall, pericardial involvement indicates larger infarction, greater incidence of left ventricular dysfunction, and greater mortality.
    • Pericarditis usually heals without consequence.
    • Effusions may occur, but they rarely lead to tamponade.
    • Pericarditis does not contraindicate thrombolytic or anticoagulant therapy.
    • Anticoagulation should be discontinued if pericardial effusion develops or effusion size increases.
    • Treatment is aspirin.
  • Dressler syndrome
  • • Pericarditis associated with Dressler syndrome is usually observed 2-3 weeks after a myocardial infarction.
    • Initially, the syndrome was described in as many as 4% of patients post-AMI. More recent studies suggest a much lower incidence.
    • Dressler syndrome is rarely described with pulmonary embolism.
    • It may be a unique autoimmune-mediated phenomenon to myocardial antigens, or it may merely be an unrecognized postmyocardial infarction pericarditis.
    • ECG findings may demonstrate diagnostic changes of acute pericarditis, especially if the ECG findings normalize after the infarction.
    • Patients may develop pulmonary infiltrates and large pericardial effusions.
    • Because of the risk of hemorrhagic pericarditis, anticoagulant therapy should be stopped.
    • Treatment is with nonsteroidal anti-inflammatory drugs (NSAIDs).
  • Aortic dissection
  • • This accounts for 1% of cases.
    • This accounts especially for cases with hemorrhage into the pericardium.
  • Takotsubo cardiomyopathy 
  • Neoplasm
  • • This accounts for 5-17% of cases.
    • In patients presenting with acute pericarditis or pericardial effusion, 4-7% have an unsuspected malignancy.
    • Neoplastic disease, particularly advanced, is the most frequent cause of tamponade in the hospital.
    • Symptoms develop over days to weeks. Dyspnea is common and is the most significant symptom.
    • Occasionally, the tumor encases the heart and causes constrictive pericarditis rather than tamponade.
    • Primary neoplasm of the heart and pericardium is rare. Pericardial mesothelioma and angiosarcoma are lethal malignancies with aggressive local spread that respond poorly to treatment. Infants and children can present with a teratoma in the pericardial space. These can often be successfully removed.
    • Most cases are a result of metastatic disease. Autopsy studies have noted that approximately 10% of patients with cancer develop cardiac involvement, and, often, it is clinically silent. The neoplastic cells reach the pericardium through the bloodstream, through the lymphatic system, or via local growth.
    • Lung cancer, including adenocarcinoma and squamous and small cell carcinoma, accounts for approximately 33% of cases. Breast cancer accounts for 25%. Leukemia and lymphoma, including Hodgkin and non-Hodgkin, account for 15% of cases. Malignant melanoma represents another 5%. Almost all other malignancies, except primary brain, comprise the rest of the cases. Kaposi sarcoma also has become a more prominent cause of neoplastic disease with the AIDS epidemic.
    • The pericardial carcinoembryonic antigen (CEA) level is often elevated.
    • Cytology findings are positive in 80-90% of breast and lung cancer cases, but the percentage is lower in other malignancies. Obstruction of the lymphatic drainage can cause the pericardial effusion to be more significant than the tumor mass.
    • Initial treatment includes relief of tamponade, confirmation of the diagnosis, and systemic treatment of the neoplasm.
    • Further treatment options include sclerosis of the pericardial space, instillation of chemotherapeutic agents into the pericardial space, local radiation, or pericardiectomy.
• Miscellaneous causes, including iatrogenic
• • Drugs
  • • Some medications, including penicillin and cromolyn sodium, induce pericarditis through a hypersensitivity reaction.
    • The anthracycline antineoplastic agents, such as doxorubicin and cyclophosphamide, have direct cardiac toxicity and can cause acute pericarditis and myocarditis.
    • Pericarditis can develop from a drug-induced SLE syndrome caused by medications including procainamide, hydralazine, methyldopa, isoniazid, mesalazine, and reserpine.
    • Smallpox vaccination infrequently leads to myocarditis. In a review of a large vaccination program in the US military, approximately 12 per 100,000 vaccinated troops developed myopericarditis within 14 days of vaccination.⁶ Whether this is due to a direct viral cytopathic effect or an immune-mediated phenomenon is unclear.
    • Methysergide causes constrictive pericarditis through mediastinal fibrosis.
    • Dantrolene, phenytoin, and minoxidil produce pericarditis through an unknown mechanism.
    • Treatment includes stopping the administration of the offending agent and anti-inflammatory therapy as needed.
  • Irradiation
  • • Pericardial disease is the most common cardiac toxicity. Others are coronary artery disease, conduction disturbance, and myocardial and valvular disease.
    • High incidence occurs with high doses, especially those greater than 4000 rad.
    • It can present as acute pericarditis, with or without effusion; chronic constrictive pericarditis; or effusive-constrictive pericarditis.
  • Postpericardiotomy syndrome
  • • This is similar to Dressler syndrome, except that postpericardiotomy syndrome occurs after cardiac surgery.
    • Several series note an incidence rate of 10-40%. Approximately 1% develop tamponade.
    • Pericardial effusions can occur in the absence of typical features of postpericardiotomy syndrome.
    • In one study, 56% developed pericardial effusions early after cardiac surgery, without correlation to pericarditis or tamponade. The effusions were more common after heavy postoperative bleeding.
    • Pericarditis may develop with other cardiac instrumentation, including percutaneous transluminal coronary angioplasty (PTCA) and pacemaker implantation. Usually, it is associated with epicardial or pericardial hematoma formation.
    • Treatment is with aspirin or NSAIDs.
  • Trauma
  • • This accounts for approximately 1% of cases.
    • Pericarditis can develop from penetrating and nonpenetrating cardiac trauma, esophageal rupture or perforation, and pancreatitis.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Chest pain

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• CBC count with differential may show leukocytosis.
• Erythrocyte sedimentation rate and C-reactive protein levels are usually elevated.
• BUN and creatinine levels can be measured to evaluate for uremia.
• Evaluate cardiac biomarkers for associated myocarditis or myocardial infarction. In a recent study by Imazio and colleagues, an elevated troponin I level was found in 32% of patients with viral or idiopathic pericarditis. In this study, the troponin I level was related to the extent of myocardial inflammation but was not a negative prognostic marker.⁷
• Further laboratory work may be clinically indicated.
• • Evaluate blood and/or viral cultures.
  • Perform tuberculin testing with sputum for acid-fast bacilli if the illness exceeds one week in duration.
  • Obtain an antistreptolysin titer.
  • Obtain rheumatoid factor, antinuclear antibody, and anti-DNA values, particularly if the illness is prolonged or severe.
  • Evaluate thyroid function in patients with severe pericardial effusion.

Imaging Studies

• Chest radiography  
• • A flask-shaped, enlarged cardiac silhouette may be the first indication of a large pericardial effusion.
  • Patients with small effusions (less than a few hundred milliliters) may present with a normal cardiac silhouette.
  • In one study, pleural effusions were seen in 33% of patients. Approximately 75% of the effusions were left-sided only.
• Echocardiography
• • Echocardiography is recommended in all cases. Any form of pericardial inflammation can induce pericardial effusion.
  • Echocardiography is performed urgently if tamponade is suspected.
  • Echocardiography is particularly helpful if pericardial effusion is suspected on clinical or radiographic grounds, the illness lasts longer than 1 week, or myocarditis or purulent pericarditis is suspected.
  • M-mode demonstrates persistence of the echo-free space between the parietal pericardium and the epicardium during the cardiac cycle.
  • Fluid is distributed from the posterobasal left ventricle apically and anteriorly, then laterally and posteriorly to the left atrium. Fluid adjacent to the right atrium is an early indicator of an effusion. Other causes of echo-free space that must be considered include pleural effusion, pericardial masses, and epicardial fat.
  • To a limited extent, an echocardiogram can characterize the effusion. Thin fibrous strands within the pericardial space can be seen in acute effusive pericarditis. Shaggy exudate may indicate a potentially difficult pericardiocentesis, but this finding is not diagnostic.
  • Echocardiography can also be used to evaluate for chamber size, tamponade, and ventricular dysfunction.
• Computed tomography
• • Effusions are easily detected through different x-ray coefficients of fluid and the pericardium.
  • Similarly, the nature of the effusion may be surmised, given the different attenuation coefficients for blood, exudate, chyle, and serous fluid.
  • Hemopericardium may be difficult to assess without intravenous contrast because blood has the same radiodensity as myocardium.
• Magnetic resonance imaging: This is a sensitive technique for detecting pericardial effusion and loculated pericardial effusion and thickening.

Other Tests

• Electrocardiography
• • Classic acute pericarditis evolves through 4 stages (see Image 1, Image 2, Image 3, and Image 4).
  • Stage 1 accompanies the onset of acute pain and is the hallmark of acute pericarditis. ECG changes include diffuse concave upward ST elevation, except aVR and V₁ (usually depressed). T waves are upright in the leads with ST elevation, and the PR segment deviates opposite to P-wave polarity.
  • Stage 2 occurs several days later with the return of the ST segment to baseline, followed by flattening of the T waves.
  • In stage 3, T waves become inverted.
  • Finally, in stage 4, the ECG returns to the prepericarditis baseline weeks to months after the onset. The T-wave inversion may persist indefinitely in the chronic inflammation observed with tuberculosis, uremia, or neoplasm.
  • Electrical alternans, the beat-to-beat variability in QRS voltage caused by excessive cardiac mobility, may be seen with an effusion.

Procedures

• Cardiac catheterization
• • This is used for tamponade.
  • It can evaluate constrictive pericarditis versus restrictive cardiomyopathy.
• Pericardiocentesis
• • Blind percutaneous pericardial puncture increases the risk of complication to 5-50% and should be performed only in an emergency. Complications include fatal cardiac laceration.
  • Conversely, pericardiocentesis is relatively safe when guided by echocardiography, especially with large free anterior effusion. One study noted only 3 minor complications in 117 procedures with ultrasound guidance.
  • In a large study, diagnostic pericardiocentesis led to a diagnosis in only 6% of cases, versus 29% diagnosed with therapeutic pericardiocentesis. As such, pericardiocentesis should not be performed unless tamponade or suspected purulent pericarditis is present.
  • If a pericardiocentesis is performed for drainage, an indwelling catheter should be placed in the pericardial space for continued drainage over several days. If the catheter continues to drain a large amount, a more definitive procedure should be performed.
  • The pericardial fluid should be analyzed for red cells, total protein level, lactic acid dehydrogenase level, adenosine deaminase activity, and culture (ordinary and Loewenstein media). Directly investigate for tuberculous bacilli and perform a cytologic study.
• Pericardial window
• • This procedure, in which only 9 cm² or less of pericardium is resected, is used for effusive pericarditis therapy.
  • In critically ill patients, a balloon catheter may be used to create a pericardial window.
  • Some studies note the need for repeat operation in nearly 25% of patients who undergo the procedure at 2 years.
• Pericardiectomy
• • This is used for constrictive pericarditis, effusive pericarditis, or recurrent pericarditis with multiple attacks, steroid dependence, and/or intolerance to other medical management.
  • Studies demonstrate that failure rates are proportional to the amount of pericardium removed (ie, the more pericardium removed, the less likely the procedure will fail). In effusive pericarditis, the higher failure rate associated with a pericardial window or partial pericardiectomy is likely secondary to the continued fluid production from the remaining pericardium, with sealing of the remaining pericardium to the heart.
  • The operative mortality rate was 14% in one series, with a range of 1% for New York Heart Association class 1-2, 10% for class 3, and 46% for class 4. The 5-year survival rate was 80% for class 3-4 and approximately 95% for 1-2.
  • As with pericardiocentesis, studies involving pericardiectomy note a greatly improved diagnostic yield if pericardial biopsy is performed as part of a therapeutic procedure. Diagnostic biopsies yielded 5%, whereas therapeutic biopsies were at 22-54%.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

• Oxygen and a cardiac monitor should be provided. Rule out other life-threatening causes of chest pain, such as myocardial infarction or aortic dissection. Evaluate for evidence of hemodynamic instability. Consider whether further management is safe to continue on an outpatient basis. In a recent study, fever of more than 38°C, subacute onset, immunosuppression, trauma, oral anticoagulation therapy, aspirin or NSAID failure, myopericarditis, severe pericardial effusion, and cardiac tamponade were designated as poor prognostic predictors. Patients without these factors were treated on an outpatient basis without serious complications after a mean follow-up of 38 months.⁸
• Given an overall lack of specificity of clinical features, several authors describe diagnostic protocols to determine the etiology for pericarditis.
• • Following specific protocols, several authors have determined a specific etiology in 14-22% of patients.
  • In one study, cardiac tamponade and an unfavorable clinical outcome, with persistence of fever, significant pericardial effusion, or general illness lasting longer than a week, was highly associated with finding a specific etiology.
  • Initial evaluation includes clinical history and physical examination, chest radiograph, ECG, echocardiography as indicated, and initial laboratory work.
  • Consider thoracentesis with adenosine deaminase in addition to conventional studies in patients with a pleural effusion.
  • Pericardiocentesis should be performed on all patients with cardiac tamponade or suspected purulent pericarditis.

Surgical Care

• If tamponade recurs after pericardiocentesis, perform a pericardial biopsy with histologic and bacteriologic examinations of the pericardium.
• If significant clinical activity persists for 3 weeks after admission and without an etiologic diagnosis, some authors recommend pericardial biopsy.

Consultations

• Consult a cardiologist or internist for acute and idiopathic cases.
• In complicated cases, such as tuberculous, purulent uremic etiologies require multidisciplinary involvement, including consultations with a cardiologist, cardiac surgeon, and medical subspecialists (eg, infectious diseases specialist, nephrologist).

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Treatment for specific causes of pericarditis is directed according to the underlying cause. For patients with idiopathic or viral pericarditis, therapy is directed at symptom relief. NSAIDs are the mainstay of therapy. These agents have a similar efficacy with relief of chest pain in about 85-90% of patients within days of treatment. Ibuprofen has the advantage of few adverse effects and increased coronary flow. Indomethacin has a poor adverse effect profile and reduces coronary flow.

Aspirin is recommended for treatment of pericarditis after STEMI.

Colchicine, in combination with an NSAID can be considered in the initial treatment to prevent recurrent pericarditis. Colchicine, alone or in combination with an NSAID, can be considered for patients with recurrent or continued symptoms beyond 14 days.

Corticosteroids should not be used for initial treatment of pericarditis unless it is indicated for the underlying disease, the patient has no response to NSAIDs or colchicine, or both are contraindicated.

Drug Category: Nonsteroidal anti-inflammatory drugs

These agents are effective for chest discomfort and underlying inflammation.

Drug Category: Anti-inflammatory agents

These agents reduce the effects of immune reactions.

Drug Category: Salicylates

These agents reduce inflammation.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Complications

• Recurrence (can cause significant morbidity, secondary to pain)
• Cardiac tamponade
• Constrictive pericarditis
• Combination of effusive and constrictive pericarditis

Prognosis

• The prognosis depends on the etiology.
• Idiopathic and viral etiologies usually have a self-limited course.
• Purulent, tuberculous, and neoplastic pericardial involvement have more complicated courses with worse outcomes.

Patient Education

• For excellent patient education resources, visit eMedicine's Cholesterol Center, Statins Center, and Heart Center. Also, see eMedicine's patient education articles High Cholesterol, Cholesterol FAQs, Atorvastatin (Lipitor), Chest Pain, and Atrial Fibrillation.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Avoid NSAIDs and corticosteroids in AMI pericarditis because they may interfere with ventricular healing, remodeling, or both.
• Pericarditis can be difficult to distinguish from myocardial infarction and repolarization in patients who present with chest pain and ST-segment elevation on ECG.
• • Aside from clues elicited from the history and physical examination, repolarization does not progress through stages and is uncommonly associated with PR depression. Serial monitoring of ECGs in young patients with chest pain helps differentiate early repolarization from acute pericarditis.
  • An ST-segment–to–T-wave ratio of greater than or equal to 0.25 in V₆ can distinguish acute pericarditis from early repolarization.
  • The ST segment in AMI is usually convex, bowing upward with reciprocal changes, as opposed to concave ST segments without reciprocal changes observed in acute pericarditis and repolarization.

Special Concerns

• Children may present with abdominal pain.
• The classic feature of chest pain and dyspnea with pericarditis may be subtle and can be confused with other diagnoses, particularly in elderly individuals.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Stage 1 ECG changes in patient with acute pericarditis.
	View Full Size Image
Media type:  ECG

Media file 2:  Stage 2 ECG changes in patient with acute pericarditis obtained 3 days into clinical course.
	View Full Size Image
Media type:  ECG

Media file 3:  Stage 3 ECG changes of acute pericarditis obtained 18 days into the clinical course. The patient had resolution of symptoms.
	View Full Size Image
Media type:  ECG

Media file 4:  Stage 4 ECG changes in the same patient as in Images 1-3, taken approximately 3 months after acute pericardial illness. The patient remained symptom free despite continued T-wave inversion.
	View Full Size Image
Media type:  ECG

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

1. Lorell BH. Pericardial Diseases. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 5^th ed. Philadelphia, Pa: WB Saunders; 1997:1478-534.
2. Brady WJ, Perron AD, Martin ML, Beagle C, Aufderheide TP. Cause of ST segment abnormality in ED chest pain patients. Am J Emerg Med. Jan 2001;19(1):25-8. [Medline].
3. Sagristà-Sauleda J, Barrabes JA, Permanyer-Miralda G. Purulent pericarditis: review of a 20-year experience in a general hospital. J Am Coll Cardiol. Nov 15 1993;22(6):1661-5. [Medline].
4. Soler-Soler J, Permanyer-Miralda G, Sagristà-Sauleda J. A systematic diagnostic approach to primary acute pericardial disease. The Barcelona experience. Cardiol Clin. Nov 1990;8(4):609-20. [Medline].
5. Silva-Cardoso J, Moura B, Martins L, Mota-Miranda A, Rocha-Gonçalves F, Lecour H. Pericardial involvement in human immunodeficiency virus infection. Chest. Feb 1999;115(2):418-22. [Medline].
6. Eckart RE, Love SS, Atwood JE, Arness MK, Cassimatis DC, Campbell CL, et al. Incidence and follow-up of inflammatory cardiac complications after smallpox vaccination. J Am Coll Cardiol. Jul 7 2004;44(1):201-5. [Medline].
7. Imazio M, Demichelis B, Cecchi E. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol. Dec 17 2003;42(12):2144-8. [Medline].
8. Imazio M, Demichelis B, Parrini I, Giuggia M, Cecchi E, Gaschino G, et al. Day-hospital treatment of acute pericarditis: a management program for outpatient therapy. J Am Coll Cardiol. Mar 17 2004;43(6):1042-6. [Medline].
9. Adler Y, Finkelstein Y, Guindo J, Rodriguez de la Serna A, Shoenfeld Y, Bayes-Genis A, et al. Colchicine treatment for recurrent pericarditis. A decade of experience. Circulation. Jun 2 1998;97(21):2183-5. [Medline].
10. Angomachalelis N, Hourzamanis A, Salem N, Vakalis D, Serasli E, Efthimiadis T, et al. Pericardial effusion concomitant with specific heart muscle disease in systemic sarcoidosis. Postgrad Med J. 1994;70 Suppl 1:S8-12. [Medline].
11. Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction; A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of patients with acute myocardial infarction). J Am Coll Cardiol. Aug 4 2004;44(3):E1-E211. [Medline].
12. Arunasalam S, Siegel RJ. Rapid resolution of symptomatic acute pericarditis with ketorolac tromethamine: a parenteral nonsteroidal antiinflammatory agent. Am Heart J. May 1993;125(5 Pt 1):1455-8. [Medline].
13. Baljepally R, Spodick DH. PR-segment deviation as the initial electrocardiographic response in acute pericarditis. Am J Cardiol. Jun 15 1998;81(12):1505-6. [Medline].
14. Brook I, Frazier EH. Microbiology of acute purulent pericarditis. A 12-year experience in a military hospital. Arch Intern Med. Sep 9 1996;156(16):1857-60. [Medline].
15. Brosius FC 3rd, Waller BF, Roberts WC. Radiation heart disease. Analysis of 16 young (aged 15 to 33 years) necropsy patients who received over 3,500 rads to the heart. Am J Med. Mar 1981;70(3):519-30. [Medline].
16. Callahan JA, Seward JB, Nishimura RA, Miller FA Jr, Reeder GS, Shub C, et al. Two-dimensional echocardiographically guided pericardiocentesis: experience in 117 consecutive patients. Am J Cardiol. Feb 1 1985;55(4):476-9. [Medline].
17. Chen Y, Brennessel D, Walters J, Johnson M, Rosner F, Raza M. Human immunodeficiency virus-associated pericardial effusion: report of 40 cases and review of the literature. Am Heart J. Mar 1999;137(3):516-21. [Medline].
18. Correale E, Maggioni AP, Romano S, Ricciardiello V, Battista R, Santoro E. Pericardial involvement in acute myocardial infarction in the post-thrombolytic era: clinical meaning and value. Clin Cardiol. Apr 1997;20(4):327-31. [Medline].
19. Dacso CC. Pericarditis in AIDS. Cardiol Clin. Nov 1990;8(4):697-9. [Medline].
20. Fairley CK, Ryan M, Wall PG, Weinberg J. The organisms reported to cause infective myocarditis and pericarditis in England and Wales. J Infect. May 1996;32(3):223-5. [Medline].
21. Fowler NO. Recurrent pericarditis. Cardiol Clin. Nov 1990;8(4):621-6. [Medline].
22. Friedman PL, Brown EJ Jr, Gunther S, Alexander RW, Barry WH, Mudge GH Jr, et al. Coronary vasoconstrictor effect of indomethacin in patients with coronary-artery disease. N Engl J Med. Nov 12 1981;305(20):1171-5. [Medline].
23. Friman G, Fohlman J. The epidemiology of viral heart disease. Scand J Infect Dis Suppl. 1993;88:7-10. [Medline].
24. Ginzton LE, Laks MM. The differential diagnosis of acute pericarditis from the normal variant: new electrocardiographic criteria. Circulation. May 1982;65(5):1004-9. [Medline].
25. Gregoratos G. Pericardial involvement in acute myocardial infarction. Cardiol Clin. Nov 1990;8(4):601-8. [Medline].
26. Guevara R, Aguinaga-Meza M, Hazin MI, Hazin R, McCord J. Takotsubo cardiomyopathy complicated with acute pericarditis and cardiogenic shock. J Natl Med Assoc. Mar 2007;99(3):281-3. [Medline].
27. Gunukula SR, Spodick DH. Pericardial disease in renal patients. Semin Nephrol. Jan 2001;21(1):52-6. [Medline].
28. Hall IP. Purulent pericarditis. Postgrad Med J. Jul 1989;65(765):444-8. [Medline].
29. Hancock EW. Neoplastic pericardial disease. Cardiol Clin. Nov 1990;8(4):673-82. [Medline].
30. Hoit BD. Imaging the pericardium. Cardiol Clin. Nov 1990;8(4):587-600. [Medline].
31. Imazio M, Bobbio M, Cecchi E, Demarie D, Demichelis B, Pomari F, et al. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. Sep 27 2005;112(13):2012-6. [Medline].
32. Imazio M, Cecchi E, Demichelis B, Ierna S, Demarie D, Ghisio A, et al. Indicators of poor prognosis of acute pericarditis. Circulation. May 29 2007;115(21):2739-44. [Medline].
33. Imazio M, Demichelis B, Parrini I, Favro E, Beqaraj F, Cecchi E, et al. Relation of acute pericardial disease to malignancy. Am J Cardiol. Jun 1 2005;95(11):1393-4. [Medline].
34. Juneja R, Kothari SS, Saxena A, Sharma R, Joshi A. Intrapericardial streptokinase in purulent pericarditis. Arch Dis Child. Mar 1999;80(3):275-7. [Medline].
35. Khan AH. The postcardiac injury syndromes. Clin Cardiol. Feb 1992;15(2):67-72. [Medline].
36. Klacsmann PG, Bulkley BH, Hutchins GM. The changed spectrum of purulent pericarditis: an 86 year autopsy experience in 200 patients. Am J Med. Nov 1977;63(5):666-73. [Medline].
37. Komsuoglu B, Göldelï O, Kulan K, Komsuoglu SS. The diagnostic and prognostic value of adenosine deaminase in tuberculous pericarditis. Eur Heart J. Aug 1995;16(8):1126-30. [Medline].
38. Krainin FM, Flessas AP, Spodick DH. Infarction-associated pericarditis. Rarity of diagnostic electrocardiogram. N Engl J Med. Nov 8 1984;311(19):1211-4. [Medline].
39. Krikorian JG, Hancock EW. Pericardiocentesis. Am J Med. Nov 1978;65(5):808-14. [Medline].
40. Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med. Nov 18 2004;351(21):2195-202. [Medline].
41. Lorbar M, Spodick DH. 'Idiopathic' pericarditis--the clinician's challenge [nothing is idiopathic]. Int J Clin Pract. Jan 2007;61(1):138-42. [Medline].
42. Maisch B. Pericardial diseases, with a focus on etiology, pathogenesis, pathophysiology, new diagnostic imaging methods, and treatment. Curr Opin Cardiol. May 1994;9(3):379-88. [Medline].
43. Maisch B, Pankuweit S, Brilla C, Funck RC, Simon BC, Grimm W, et al. Intrapericardial treatment of inflammatory and neoplastic pericarditis guided by pericardioscopy and epicardial biopsy--results from a pilot study. Clin Cardiol. Jan 1999;22(1 Suppl 1):I17-22. [Medline].
44. Maisch B, Seferovic PM, Ristic AD, Erbel R, Rienmüller R, Adler Y, 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. Apr 2004;25(7):587-610. [Medline].
45. Maruyama T, Hanaoka T, Nakajima H. Acute pericarditis in the recovery phase of transient left ventricular apical ballooning syndrome (takotsubo cardiomyopathy). Intern Med. 2007;46(22):1857-60. [Medline].
46. Mehta M, Jain AC, Mehta A. Early repolarization. Clin Cardiol. Feb 1999;22(2):59-65. [Medline].
47. Mercé J, Sagristà-Sauleda J, Permanyer-Miralda G, Soler-Soler J. Should pericardial drainage be performed routinely in patients who have a large pericardial effusion without tamponade?. Am J Med. Aug 1998;105(2):106-9. [Medline].
48. Moder KG, Miller TD, Tazelaar HD. Cardiac involvement in systemic lupus erythematosus. Mayo Clin Proc. Mar 1999;74(3):275-84. [Medline].
49. Moores DW, Dziuban SW Jr. Pericardial drainage procedures. Chest Surg Clin N Am. May 1995;5(2):359-73. [Medline].
50. Mueller XM, Tevaearai HT, Hurni M, Ruchat P, Fischer AP, Stumpe F, et al. Etiologic diagnosis of pericardial disease: the value of routine tests during surgical procedures. J Am Coll Surg. Jun 1997;184(6):645-9. [Medline].
51. Permanyer-Miralda G, Sagristà-Sauleda J, Soler-Soler J. Primary acute pericardial disease: a prospective series of 231 consecutive patients. Am J Cardiol. Oct 1 1985;56(10):623-30. [Medline].
52. Posner MR, Cohen GI, Skarin AT. Pericardial disease in patients with cancer. The differentiation of malignant from idiopathic and radiation-induced pericarditis. Am J Med. Sep 1981;71(3):407-13. [Medline].
53. Rombola F, Spinoso A, Bertuccio SN. [Cardiac manifestations during viral acute hepatitis]. Infez Med. Mar 2006;14(1):29-32. [Medline].
54. Rostand SG, Rutsky EA. Pericarditis in end-stage renal disease. Cardiol Clin. Nov 1990;8(4):701-7. [Medline].
55. Sagristà-Sauleda J, Permanyer-Miralda G, Soler-Soler J. Tuberculous pericarditis: ten year experience with a prospective protocol for diagnosis and treatment. J Am Coll Cardiol. Apr 1988;11(4):724-8. [Medline].
56. Sagristà-Sauleda J, Permanyer-Miralda G, Candell-Riera J, Angel J, Soler-Soler J. Transient cardiac constriction: an unrecognized pattern of evolution in effusive acute idiopathic pericarditis. Am J Cardiol. Apr 15 1987;59(9):961-6. [Medline].
57. Shabetai R. Acute pericarditis. Cardiol Clin. Nov 1990;8(4):639-44. [Medline].
58. Spodick DH. Arrhythmias during acute pericarditis. A prospective study of 100 consecutive cases. JAMA. Jan 5 1976;235(1):39-41. [Medline].
59. Spodick DH. Diagnostic electrocardiographic sequences in acute pericarditis. Significance of PR segment and PR vector changes. Circulation. Sep 1973;48(3):575-80. [Medline].
60. Spodick DH. Differential diagnosis of acute pericarditis. Prog Cardiovasc Dis. Sep 1971;14(2):192-209. [Medline].
61. Spodick DH. Electrocardiogram in acute pericarditis. Distributions of morphologic and axial changes by stages. Am J Cardiol. Apr 1974;33(4):470-4. [Medline].