Pericarditis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Homa Najafi, M.D.[2]

Pericarditis is a condition in which the sac-like covering surrounding the heart (the pericardium) becomes inflamed. Symptoms of pericarditis include chest pain which increases with deep breathing and lying flat.

The pericardium is a double-walled sac that contains the heart and the roots of the great vessels. Morphologically, it is a conical-shaped, double-walled fibro-serous membrane. It rests posteriorly to the sternum at the level of second to sixth costal cartilages and T5-T8 vertebrae.

Pericarditis may be classified according to duration of the disease and recurrence into acute, Incessant, recurrent and chronic. Moreover, pericarditis can be classified based on the etiology in two groups of infectious and non-infectious causes.

Pericarditis is inflammation of the pericardium, which is the double-walled sac that contains the heart and the roots of the great vessels. There can be an accompanying accumulation of fluid that can be either serous (free flowing fluid) or fibrinous (an exudate, which is a thick fluid composed of proteins, fibrin strands, inflammatory cells, cell breakdown products, and sometimes bacteria). Vascular congestion of the pericardium is also present. The underlying myocardium may or may not be inflamed as well. If the myocardium is involved in the inflammatory process, it is called myopericarditis, and CK and troponin levels may be elevated. Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. Most patients with viral pericarditis recover completely with few developing recurrences. Some patients develop constrictive pericarditis which could be disabling. Bacterial pericarditis results from contiguous spread of infection within the chest, either de novo or after surgery or trauma, spread from infective endocarditis, hematogenous, or direct inoculation as a result of penetrating injury or cardiothoracic surgery.

The causes of pericarditis can be divided into infectious and non-infectious ones. Infectious causes include bacterial, viral, fungal and, parasitic. While, non-infectious causes include autoimmune, neoplastic, metabolic, traumatic and iatrogenic, and drug-related. Acute myocardial infarction, Addisonian crisis, aortic dissection and rupture, blunt or penetrating chest trauma, esophageal perforation, gastric perforation, and myocardial rupture are life threatening causes of pericarditis. Common causes of pericarditis include viral, bacterial organisms, neoplasms, autoimmune and renal failure.

Pericarditis must be differentiated from diseases presenting with chest pain, shortness of breath and tachypnea which include myocardial infarction, pulmonary embolism, congestive heart failure, pneumonia, vasculitis, and chronic obstructive pulmonary disease (COPD). Manifestation of the pericarditis can help in differentiation from myocardial infarction. Moreover, other differential diagnosis include aortic stenosis, coronary artery vasospasm, esophageal rupture, esophageal spasm, esophagitis,acute gastritis, gastroesophageal reflux disease, and peptic ulcer disease should be considered.  

The incidence of acute pericarditis is approximately 27.7 per 100,000 individuals annually. The recurrence of disease is seen in almost 30% of patients after first episode. The mortality rate of acute pericarditis is approximately 1.1% in developed countries. Patients of all age groups may develop acute pericarditis. Although it commonly affects men in 20 to 50 years of age. Pericarditis in developed countries is most commonly due to malignancy or viral infection. It usually follows respiratory infections, most commonly echovirus or coxsackie virus. In children, it is most commonly caused by adenovirus or coxsackie virus. In developing countries pericarditis is usually secondary to tuberculosis or HIV infection. Tuberculous pericarditis, caused by Mycobacterium tuberculosis, is found in approximately 1% of all autopsied cases of TB and in 1% to 2% of instances of pulmonary TB.

There is insufficient evidence to recommend routine screening for pericarditis.  

Pericarditis is often self-limited and most people recover in 2 weeks to 3 months. However, the condition can be complicated by significant fluid buildup around the heart (a pericardial effusion or cardiac tamponade) and may require urgent intervention including pericardiocentesis. If scarring of the sac around the heart (the pericardium) occurs, then this is called constrictive pericarditis which may require surgical stripping of the scar.

Patients with pericarditis commonly present with chest pain that changes with position, cough, fever, breathlessness, and fatigue are the other common symptoms. Less common symptoms include palpitations, hiccup, odynophagia, faint, dizziness, and abdominal pain which is seen mostly in children.

A careful physical examination must be performed to exclude the presence of cardiac tamponade, a dangerous complication of pericarditis. If cardiac tamponade is present, then pulsus paradoxus, hypotension, an elevated jugular venous pressure and peripheral edema may be present.

Non-specific markers of inflammation are generally elevated in pericarditis. These include the leukocyte count, C-reactive protein, and ESR. The cardiac troponin is elevated if there is an injury to the underlying myocardium, a condition termed as myopericarditis. Diagnostic pericardiocentesis and biopsy help in identifying an underlying infectious or malignant process.Non-specific markers of inflammation are generally elevated in pericarditis. These include the leukocyte count, C-reactive protein, and ESR. The cardiac troponin is elevated if there is an injury to the underlying myocardium, a condition termed as myopericarditis. Diagnostic pericardiocentesis and biopsy help in identifying an underlying infectious or malignant process.

In the presence of a large effusion or tamponade, there may be diminished voltage and electrical alternans (alternation of QRS complex amplitude or axis between beats).

A flask-shaped, enlarged cardiac silhouette will be observed on chest x-ray in pericarditis complicated with pericardial effusion or tamponade. A mass may also be seen when malignancy is the cause. Calcification of pericardium may be noted in constrictive pericarditis.

Echocardiography is generally performed to assess for the presence of a pericardial effusion and to assess and monitor its size. Echocardiography is critical in confirming the clinical suspicion cardiac tamponade.

On CT, pericardial fluid adds to the thickness of pericardium as both have the similar signal intensities. In pericarditis, pericardium can generate an intermediate signal intensity and may enhance after gadolinium administration. In pericardial effusion, hemorrhagic effusions can be differentiated from a transudate or an exudate based on signal characteristics (high signal on T1-weighted images) or density (high-density clot on CT). CT is superior to MRI in the visualization of pericardial calcification which is often seen in the patient with pericardial constriction. CT imaging also helps in detecting the presence of tumors and the extent of metastasis of the neoplasm.

On MRI, normal pericardium appears as a thin dark band that is bordered by a bright band on both sides on T1 weighted spin imaging. These surrounding bright bands are associated with the surrounding epicardial and pericardial fat. Following the administration of gadolinium, pericardium may appear thick and inflamed in the setting of pericarditis. Lower intensity signal is observed in constrictive pericarditis than in acute pericarditis. Comprehensive visualization of the LV endocardium and the physiologic consequences of abnormal pericardial thickening can also be obtained without exposure to ionizing radiation.

Echocardiography guided pericardiocentesis may be helpful in the diagnosis of the pericarditis etiology. Pericardial fluid aspiration for cytology and immunohistochemistry analysis should be done in pericarditis with effusion. Pericardiocentesis should be done in patients with high susceptibility of neoplastic pericarditis which cytology analysis for malignancy was negative.

The management of pericarditis depends on whether the patient has an uncomplicated vs. complicated disease course. Uncomplicated pericarditis is generally treated with non-steroidal anti-inflammatory drugs, such as Ibuprofen in cases of either viral or idiopathic pericarditis, and Aspirin in cases of post-MI pericarditis. Pericarditis complicated with either effusion or cardiac tamponade is generally treated with urgent pericardiocentesis in the case of cardiac tamponade, antibiotics in the case of purulent pericardial effusion, and either steroids or colchicine among patients with recurrent or refractory disease.

Percutaneous pericardiocentesis is a procedure where fluid is aspirated from the pericardium (the sac enveloping the heart) using a needle via a percutaneous approach. Pericardiocentesis can provide a diagnostic sampling of pericardial fluid and can be used as a therapeutic maneuver to evacuate pericardial fluid and lower the pericardial pressure.

Creation of a pericardial window is a cardiac surgical procedure in which an opening is made in the pericardium to drain fluid that has accumulated around the heart by creating a fistula or “window” from the pericardial space to the peritoneal cavity. Flow of fluid into the peritoneal cavity prevents the accumulation of fluid around the heart (a pericardial effusion), which might cause compression and impaired filling of the heart (cardiac tamponade), a dangerous complication. The procedure is performed for both diagnostic and therapeutic purposes. The creation of a pericardial window is usually performed by a cardiac surgeon or thoracic surgeon who makes an incision, commonly sub-xiphoid, and cuts a small hole in the pericardium. This surgery is performed with local anesthesia. An incision is made either below the sternum, or alternately between the ribs of the left chest. The resection can be with scissors, cautery, a stapling device, or a harmonic scalpel, with no one technique demonstrably better than another. It is best to have a combination of techniques available to resect the pericardium adequately. The surgeon may place a catheter in the pericardial window so that fluid can continue to drain for a short period of time after the surgery. Chest tubes are removed in 2-3 days once the drainage is less than 200cc/24hrs.

Pericardiectomy is the surgical removal of part or most of the pericardium. This operation is performed to relieve constrictive pericarditis or to remove a pericardium that is calcified and fibrous. Constrictive pericarditis is a progressive disease without spontaneous reversal of pericardial thickening. Some patients can be medically managed for several years. Edema can be controlled with diuretics and slowing the heart rate can maximize the diastolic filling time. Many patients eventually develop significant debility from impaired cardiac output and elevated right and left sided filling pressures. The definitive treatment for constrictive pericarditis is pericardiectomy which is also known as pericardial stripping. This is a surgical procedure where the entire pericardium is peeled away from the heart. Due to the significant risks involved with pericardial stripping, many patients are treated medically, with judicious use of diuretics.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor(s)-in-Chief: Rim Halaby

The pericardium is a double-walled sac that contains the heart and the roots of the great vessels. Morphologically, it is a conical-shaped, double-walled fibro-serous membrane. It rests posteriorly to the sternum at the level of second to sixth costal cartilages and T5-T8 vertebrae.

• The pericardium is made up of two layers:
  • Fibrous pericardium
    • Hard protective external layer
    • Attached to sternum anteriorly by sterno-pericardial ligaments and fused with the central tendon of the diaphragm and great vessels to allow mobility of the pericardial sac against sudden cardiac overfilling
  • Serous pericardium
    • Smooth internal layer made up of 2 components:
      • Parietal: reflects onto fibrous pericardium
      • Visceral: reflects onto heart and great vessels and forms the epicardium, the external layer of the heart wall
• Pericardial cavity: Potential space between parietal and visceral layers. It contains a serous fluid film that occupies the cavity and functions as lubricant against friction by all chest movements.^[1][2][3]

• There are two small chambers or sinuses located where the visceral and parietal pericardia are continuous with one another within the pericardial cavity.
• Transverse sinus:
  • Located posterior to the pulmonary trunk and ascending aorta at the level between the superior vena cava and aortic arch
  • Formed after dorsal mesocardium rupture embryonically
  • Functional role is to allow the unhindered expansion of great arteries posteriorly during cardiac systole
  • Utilized surgically to pass surgical clamps or place ligatures around great arteries.
• Oblique sinus:
  • A blind recess (cul-de-sac) posterior to the left atrium between superior vena cava, right and left pulmonary veins inferior to the transverse sinus
  • Formed embryonically by the incorporation of the pulmonary vein tributaries into the left atrium
  • Functional role believed to be the expansion of the left atrium upon normal collapse of the thorax^[4][5][6]

• Pericarditis is an inflammatory condition of the pericardium.
• Pericardial effusion is fluid accumulation in the pericardial sac.
• Constrictive pericarditis occurs when there is a scar encasing, the heart that chronically constricts the filling of the heart.
• Cardiac tamponade is a medical emergency in which fluid in the pericardial sac acutely restricts the filling of the heart. This requires surgical drainage or pericardiocentesis.

• 
  The phrenic nerve and its relations with the vagus nerve.
• 
  Thoracic portion of the sympathetic trunk.
• 
  Liver with the septum transversum. Human embryo 3 mm long.
• 
  The thymus of a full-time fetus, exposed in situ.

de:Herzbeutel it:Pericardio la:Pericardium ms:Perikardium nl:Pericard nn:Hjartepose fi:Perikardium

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Homa Najafi, M.D.[2]

Pericarditis may be classified according to duration of the disease and recurrence into acute, Incessant, recurrent and chronic. Moreover, pericarditis can be classified based on the etiology in two groups of infectious and non-infectious causes.

• Pericarditis may be classified according to duration of the disease and recurrence into four groups:^[1][2][3][4]
  • Acute
  • Incessant
  • Recurrent
  • Chronic

• Moreover, pericarditis can be classified based on the etiology in two groups:^[1][2][3][5]
  • Infectious:
    • Viral
    • Bacterial
    • Fungal
    • Parasitic
  • Non-infectious:
    • Autoimmune
    • Neoplastic
    • Metabolic
    • Traumatic and iatrogenic
    • Drug-related

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S., Cafer Zorkun, M.D., Ph.D. [2], Rim Halaby Homa Najafi, M.D.[3]

Pericarditis is inflammation of the pericardium, which is the double-walled sac that contains the heart and the roots of the great vessels. There can be an accompanying accumulation of fluid that can be either serous (free flowing fluid) or fibrinous (an exudate, which is a thick fluid composed of proteins, fibrin strands, inflammatory cells, cell breakdown products, and sometimes bacteria). Vascular congestion of the pericardium is also present. The underlying myocardium may or may not be inflamed as well. If the myocardium is involved in the inflammatory process, it is called myopericarditis, and CK and troponin levels may be elevated. Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. Most patients with viral pericarditis recover completely with few developing recurrences. Some patients develop constrictive pericarditis which could be disabling. Bacterial pericarditis results from contiguous spread of infection within the chest, either de novo or after surgery or trauma, spread from infective endocarditis, hematogenous, or direct inoculation as a result of penetrating injury or cardiothoracic surgery.

• The pericardium is made up of two layers:^[1][2][3]
  • Fibrous pericardium:
    • Hard protective external layer
    • Attached to sternum anteriorly by sterno–pericardial ligaments and fused with the central tendon of the diaphragm and great vessels to allow mobility of the pericardial sac against sudden cardiac overfilling
  • Serous pericardium:
    • Smooth internal layer made up of 2 components:
      • Parietal: reflects onto fibrous pericardium
      • Visceral: reflects onto heart and great vessels and forms the epicardium, the external layer of the heart wall
• Pericardial cavity: Potential space between parietal and visceral layers. It contains a serous fluid film that occupies the cavity and functions as lubricant against friction by all chest movements.

• There are two small chambers or sinuses located where the visceral and parietal pericardium are continuous with one another within the pericardial cavity.^[4][5][6]
• Transverse sinus:
  • Located posterior to the pulmonary trunk and ascending aorta at the level between the superior vena cava and aortic arch
  • Formed after dorsal myocardium ruptured embryonically
  • Functional role is to allow the unhindered expansion of great arteries posteriorly during cardiac systole
  • Utilized surgically to pass surgical clamps or place ligatures around great arteries.
• Oblique sinus:
  • A blind recess (cul-de-sac) posterior to the left atrium between superior vena cava, right and left pulmonary veins inferior to the transverse sinus
  • Formed embryonically by the incorporation of the pulmonary vein tributaries into the left atrium
  • Functional role believed to be the expansion of the left atrium upon normal collapse of the thorax

• Pericarditis is an inflammatory condition of the pericardium.
• Pericardial effusion is fluid accumulation in the pericardial sac.
• Constrictive pericarditis occurs when there is a scar encasing, the heart that chronically constricts the filling of the heart.
• Cardiac tamponade is a medical emergency in which fluid in the pericardial sac acutely restricts the filling of the heart. This requires surgical drainage or pericardiocentesis.

• 
  The phrenic nerve and its relations with the vagus nerve.
• 
  Thoracic portion of the sympathetic trunk.
• 
  Liver with the septum transversum. Human embryo 3 mm long.
• 
  The thymus of a full-time fetus, exposed in situ.

• Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. This may cause pericardial effusion and fibrinous change of the pericardium. The pericardium may also develop a serous or hemorrhagic effusion. Most patients with viral pericarditis recover completely with few developing recurrences. Some patients develop constrictive pericarditis which could be disabling.^[7][8][9]

• Bacterial pericarditis results from:^{[10][11][12][13][14]}

1. Contiguous spread of infection within the chest, either de novo or after surgery or trauma.
2. Spread from infective endocarditis
3. Hematogenous spread of infection
4. Direct inoculation as a result of penetrating injury or cardiothoracic surgery

• Tuberculous pericarditis develops from lymphatic spread of peritracheal, peribronchial or mediastinal lymph nodes or by contiguous spread from a focus of infection in the lung or pleura. There are four pathologic stages observed:^[15][16][17]

• Stage 1: Presence of diffuse fibrin deposition, granulomas and abundant mycobacterium.

• Stage 2: Development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells.

• Stage 3: Absorption of effusion with the organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen.

• Stage 4: Development of constrictive pericarditis. The pericardial space is obliterated by dense adhesions with marked thickening of the parietal layer and replacement of granulomas by fibrous tissue.

These types of granulomatous pericarditis also occur with fungal infections, rheumatoid arthritis (RA), and sarcoidosis.

• Pericarditis in renal failure is thought to result from inflammation of the visceral and parietal layers of the pericardium by metabolic toxins such as urea, creatinine, uric acid, methylguanidine, guanidinoacetate, parathyroid hormone, beta2-microglobulin, and others. It may be associated with hemorrhagic or serous effusion.

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2] Ahmed Zaghw, M.D. [3] Homa Najafi, M.D.[4]

The causes of pericarditis can be divided into infectious and non-infectious ones. Infectious causes include bacterial, viral, fungal and, parasitic. While, non-infectious causes include autoimmune, neoplastic, metabolic, traumatic and iatrogenic, and drug-related. Acute myocardial infarction, Addisonian crisis, aortic dissection and rupture, blunt or penetrating chest trauma, esophageal perforation, gastric perforation, and myocardial rupture are life threatening causes of pericarditis. Common causes of pericarditis include viral, bacterial organisms, neoplasms, autoimmune and renal failure.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated and include:^[1][2][3][4]

• Acute myocardial infarction
• Addisonian crisis
• Aortic dissection
• Aortic rupture
• Blunt or penetrating chest trauma
• Esophogeal perforation
• Gastric perforation
• Myocardial rupture

• Acute myocardial infarction
• Cardiac catheterization
• Staphylococcus aureus (MSSA, MRSA)
• Streptococcus pneumoniae
• Neisseria meningitidis
• Enterobacteriaceae
• Tuberculosis
• Histoplasmosis
• Coxsackie B virus
• Echovirus
• HIV
• Adenovirus
• Influenza
• Neoplasm
• Renal Failure
• Sulfa drugs
• Aminosalicylic acid
• Amiodarone
• Systemic lupus erythematosus
• Rheumatoid arthritis
• Idiopathic

• 5-Fluorouracil
• Actinomycosis
• Acute myocardial infarction
• Acute rheumatic fever
• Addisonian crisis
• Adenovirus
• Amebiasis
• Aminosalicylic acid
• Amiodarone
• Amyloidosis
• Angioma
• Ankylosing spondylitis
• Anticoagulants
• Aortic dissection
• Aortic rupture
• Asbestosis
• Behcet’s disease
• Benign obstruction of thoracic duct
• Blunt or penetrating chest trauma
• Borrelia
• Breast cancer
• Bromocriptine
• Carcinoid
• Cardiac catheterization
• Cardiopulmonary resuscitation
• Cathether ablation for arrhythmias
• Certolizumab pegol
• Chlamydia psittaci
• Cholesterol pericarditis
• Chylopericardium
• Coccidioidomycosis
• Collagen vascular disease
• Coronary artery bypass grafting
• Coxsackie B virus
• Cromolyn sodium
• Cyclophosphamide
• Cyclosporine
• Cytarabine
• Cytomegalovirus
• Dantrolene
• Daunorubicin
• Dermatomyositis
• Dialysis
• Dissecting aortic aneurysm
• Doxorubicin
• Dressler’s syndrome
• EBV
• Echinococcosis
• ECHO virus
• Endocarditis
• Esophageal rupture
• Esophogeal perforation
• Familial mediterranean fever
• Fibroma
• Francisella
• Gastric perforation
• Gaucher disease
• Heart surgery
• Herpes viruses
• Histoplasmosis
• HIV
• Hydantoin
• Hydralazine
• Hypothyroidism
• Idiopathic
• Infectious mononucleosis
• Inflammatory bowel disease
• Influenza virus
• Isoniazid
• Jacobs arthropathy-camptodactyly syndrome
• Kaposi’s sarcoma
• Kawasaki disease
• Leiomyoma
• Legionella
• Leukemia
• Lipoma
• Lung cancer
• Lymphoma
• Melanoma
• Meningococci
• Mesalazine
• Mesothelioma
• Methyldopa
• Methysergide
• Minoxidil
• Mixed connective tissue disease
• Mulibrey nanism syndrome
• Mumps virus
• Mycoplasma
• Myocardial rupture
• Myocarditis
• Myxedema
• Neisseria gonorrhoeae
• Neoplasia that has spread to the pericardium,
• Ovarian cancer
• Pacemaker syndrome
• Pancreatic-pericardial fistula
• Penicillin
• Percutaneous coronary intervention
• Pergolide
• Phenylbutazone
• Pneumococci
• Pneumonia
• Polyarteritis nodosa
• Polymyositis
• Polytetrafluoroethylene inhalation
• Postpericardiotomy syndrome
• Practolol
• Procainamide
• Radiation therapy
• Recurrent hereditary polyserositis
• Rhabdomyosarcoma
• Reiter’s syndrome
• Renal failure
• Reserpine
• Rheumatoid arthritis
• Rickettsia
• Sarcoidosis
• Sarcoma
• Scleroderma
• Serum sickness
• Silicosis
• Sipple syndrome
• Staphylococci
• Streptococci
• Streptokinase
• Streptomycin
• Sulfa drugs
• Systemic lupus erythematosus
• TAVI
• Temporal arteritis
• Teratoma
• Thiazides
• Thiouracil
• Thoracic surgery
• Thorax trauma
• Thrombolytics
• Tocainide
• Toxoplasmosis
• Treponema pallidum
• Tuberculosis
• Ureaplasma
• Uremia
• Vaccines (smallpox, yellow fever)
• Valvuloplasty
• Varicella virus
• Wegener’s granulomatosis
• Whipple’s Disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [3] Homa Najafi, M.D.[4]

Pericarditis must be differentiated from diseases presenting with chest pain, shortness of breath and tachypnea which include myocardial infarction, pulmonary embolism, congestive heart failure, pneumonia, vasculitis, and chronic obstructive pulmonary disease (COPD). Manifestation of the pericarditis can help in differentiation from myocardial infarction. Moreover, other differential diagnosis include aortic stenosis, coronary artery vasospasm, esophageal rupture, esophageal spasm, esophagitis,acute gastritis, gastroesophageal reflux disease, and peptic ulcer disease should be considered.

• Pericarditis must be differentiated from diseases presenting with chest pain, shortness of breath and tachypnea.
  • For a full discussion of the differential diagnosis of chest pain click here
  • For an expert algorithm that aids in the diagnosis of the cause of chest pain click here
• Pericarditis must be differentiated from myocardial infarction as an important cause of chest pain.The differentiating features include:^[1]

The differentials include the following:^{[2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21]}

Pericarditis also resembles the following disorders and needs to be differentiated from them:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. Homa Najafi, M.D.[2]

The incidence of acute pericarditis is approximately 27.7 per 100,000 individuals annually. The recurrence of disease is seen in almost 30% of patients after first episode. The mortality rate of acute pericarditis is approximately 1.1% in developed countries. Patients of all age groups may develop acute pericarditis. Although it commonly affects men in 20 to 50 years of age. Pericarditis in developed countries is most commonly due to malignancy or viral infection. It usually follows respiratory infections, most commonly echovirus or coxsackie virus. In children, it is most commonly caused by adenovirus or coxsackie virus. In developing countries pericarditis is usually secondary to tuberculosis or HIV infection. Tuberculous pericarditis, caused by Mycobacterium tuberculosis, is found in approximately 1% of all autopsied cases of TB and in 1% to 2% of instances of pulmonary TB.

• The incidence of acute pericarditis is approximately 27.7 per 100,000 individuals annually.^[1][2][3][4]
• The incidence of hospitalization for acute pericarditis was estimated to be 3.32 cases per 100,000 individuals annually.
• The recurrence of pericarditis is seen in almost 30% of patients after first episode of disease.

• The mortality rate of acute pericarditis is approximately 1.1% in developed countries.^[2]

• Patients of all age groups may develop acute pericarditis. Although it commonly affects people in 20 to 50 years of age.^[5]

• There is no racial predilection to acute pericarditis.

• Men are more commonly affected by acute pericarditis than women.

• Pericarditis in developed countries is most commonly due to malignancy or viral infection.^[6][7][8]
• It usually follows respiratory infections, most commonly echovirus or coxsackie virus.
• In children, it is most commonly caused by adenovirus or coxsackie virus.
• The incidence and prevalence of viral pericarditis vary with season and region.

• In developing countries pericarditis is usually secondary to tuberculosis or HIV infection.^{[9][10][11][12]}
• Tuberculous pericarditis, caused by Mycobacterium tuberculosis, is found in approximately 1% of all autopsied cases of TB and in 1% to 2% of instances of pulmonary TB. It accounted for 69.5% (162 of 233) of cases referred for diagnostic pericardiocentesis in a study in Western Cape Province of South Africa, while the same accounts for 4% of cases in developed countries.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. Homa Najafi, M.D.[2]

Pericarditis can lead to the development of pericardial effusion, cardiac tamponade and constrictive pericarditis. Cardiac tamponade, or compression of the heart by fluid in the pericardial sac, reduces the ability of the heart to pump blood. It is a medical emergency that requires urgent pericardiocentesis or a pericardial window. The prognosis depends on the complications of pericarditis, the underlying etiology, and the associated co-morbidities. Pericarditis secondary to malignancy, MI, autoimmune disease and renal failure carries a poor prognosis.

Pericarditis is inflammation of the pericardium, the double-walled sac that contains the heart and the roots of the great vessels. There can be an accompanying accumulation of fluid that can be either serous (free flowing fluid) or fibrinous (an exudate, which is a thick fluid composed of proteins, fibrin strands, inflammatory cells, cell breakdown products, and sometimes bacteria), which leads to development of pericardial effusion and cardiac tamponade. Vascular congestion of the pericardium is also present. The underlying myocardium may or may not be inflamed as well. If the myocardium is involved in the inflammatory process, it is called myopericarditis, and the CK and troponin levels may be elevated. Subsequent scarring of the pericardium may lead to constrictive pericarditis.

Common complications of pericarditis include:^[1]

• Pericardial Effusion
  • Many forms of pericarditis can be complicated by significant fluid buildup around the heart, which is known as a pericardial effusion.
• Pericardial Tamponade
  • If the fluid accumulates too rapidly or is too large, then cardiac tamponade, a condition in which the heart is compressed by the fluid and cannot pump enough blood forward, may occur. Cardiac tamponade may require urgent intervention including pericardiocentesis or a pericardial window. This complication is more common in patients with specific underlying etiologies such as malignancy, tuberculosis, or purulent pericarditis. It rarely occurs in idiopathic pericarditis.
• Constrictive Pericarditis
  • If scarring of the sac around the heart (pericardium) occurs, then this is called constrictive pericarditis which may require surgical stripping of the scar (pericardiectomy).

The prognosis associated with pericarditis depends on the underlying cause and associated condition(s).^[2][3][4][5]

• Idiopathic Pericarditis:
  • Idiopathic pericarditis is often self-limited and most patients recover in 2 weeks to 3 months. Idiopathic or viral pericarditis is associated with a favorable long-term prognosis with few developing recurrences. Approximately 15-30% of patients with idiopathic acute pericarditis who are not treated with colchicine will develop recurrent pericarditis.
• Post MI Pericarditis or Dressler’s Syndrome:
  • Post MI pericarditis is usually associated with larger infarcts, and therefore these patients have a poorer long term prognosis.
• Tuberculous Pericarditis:
  • The mortality rate associated with tuberculous pericarditis in the preantibiotic era was 80-90%. The mortality is 17-34% if the tuberculous pericarditis is associated with HIV.
• Traumatic Pericardial Injury:
  • In penetrating injuries, pericardial effusion and tamponade may develop rapidly. Early detection and early treatment of cardiac tamponade is associated with a good prognosis. Minor perforations, isolated right ventricular wounds, and a systolic blood pressure more than 50 mm Hg are all associated with better outcomes.
• Malignant Pericarditis:
  • Pericarditis associated with malignancy is associated with poorer outcomes and a more complicated course.
• Autoimmune Disease:
  • Pericarditis associated with scleroderma and rheumatic fever is associated with worse outcomes.
• Renal Failure:
  • Pericarditis associated with renal failure is associated with significant morbidity and may result in hemorrhagic pericarditis.

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