An Overview of Acute Pericarditis

Acute PericarditisAcute Pericarditis


Acute pericarditis is the inflammation of the pericardium. the possible cause of acute pericarditis can be classified into three groups: infectious, non-infectious, and hypersensitivity reactions.  The most common cause of acute pericarditis is a viral infection.

Patients with acute pericarditis may complain of chest pain, dyspnea, and acute infectious state and may be complicated by pericardial effusions or cardiac tamponade.

Diagnosis relies on clinical presentation, physical examination, ECG, imaging, and laboratory studies. Treatment of acute pericarditis is primarily symptomatic and supportive; in selected cases, it may involve surgery.

Introduction to Acute Pericarditis

The pericardium consists of an outer sac known as the fibrous pericardium and an inner sac known as the serous pericardium. The inner sac, serous pericardium, is further divided into an outer parietal layer and an inner visceral layer. These layers are separated by a potential space containing 15 to 60 mL fluid which is serous in nature. The main function of the pericardium is to reduce the friction between the heart and surrounding tissues (1). The inflammation of the pericardium is called pericarditis and is the most common inflammatory heart disease, followed by myocarditis and endocarditis (2). It is usually benign and self-limiting but can lead to complications if not managed properly. It can be caused by both infectious and non-infectious etiologies. In clinical practice, pericarditis and myocarditis may co-exist due to overlapping etiologies (3). Depending on the history, duration, and severity, pericarditis can be classified into acute, subacute, chronic, and recurrent pericarditis. Other pericardial syndromes may also be associated with the disease, including cardiac tamponade, pericardial effusion, constrictive pericarditis, and effusive-constrictive pericarditis.

Epidemiology of Acute Pericarditis

Pericarditis is the most common inflammatory disease of the heart. Approximately 27.7 cases per 100,000 population are reported annually, as shown by a study conducted in an Italian urban area (4); while the hospital admission rate of pericarditis is 3.32 per 100,000 person-years (5). Almost 5% of patients presenting in the emergency department with chest pain are diagnosed with pericarditis, whereas 0.1% of all hospital admissions are due to pericarditis (6, 7). The mortality rate for admitted patients with pericarditis is 1.1%, and it increases with age and associated infections (such as pneumonia and sepsis) (5). The recurrence rate of pericarditis is 30% in all cases within 18 months of the first episode (8, 9).

As shown in many studies, men are more prone to pericarditis than women. The incidence is two times higher among men as compared to women (5). The reason for this sex difference is yet unknown, but sex hormones are considered the main point of difference, as shown in experimental studies of myocardial inflammation. Testosterone contributes to the development of myocarditis, as an experimental study shows enhanced viral replication caused by exogenous testosterone. On the other hand, gonadectomy causes a decrease in inflammation of the heart in experimental viral myocarditis. In females, estrogen and progesterone are the main contributors to the risk of cardiac inflammation. Estrogen has a protective effect of inhibiting cardiac inflammation, while progesterone aggravates it. The risk of cardiac inflammation and incidence of pericarditis is highest in women after menopause due to decreased estrogen concentration and loss of protective effects. Contrary to this, women are found to have more chances of developing systemic diseases associated with pericarditis (for example systemic lupus erythematosus and rheumatoid arthritis). However, more studies need to be done regarding this fact. (5)

Etiology of Acute Pericarditis

The causes of pericarditis can be classified into three main categories:

Infectious causes:

  • Pericarditis can be caused by viruses, bacteria, fungi, and even sometimes parasites. Viral pericarditis accounts for almost 80-85% of all cases, and viruses are considered the most common infective agents (10). These include Coxsackie viruses A and B, Influenza virus, Human Immunodeficiency virus (HIV), Adenoviruses, Parvovirus B19, Echovirus, and Herpesviridae family of viruses, such as Epstein-Barr virus (EBV) and Cytomegalovirus (CMV). A recent study has shown that there is a viral infection history (upper respiratory tract infection or gastroenteritis) in almost 40% of patients with the diagnosis of pericarditis (11). However, the confirmation of viral infection can not always be done on serology, as IgM antibodies are usually not detectable. Molecular techniques, such as polymerase chain reaction (PCR) on pericardial biopsy or fluid, helps identify the causative agent, but these are invasive procedures and are not recommended routinely. According to guidelines by the European Society of Cardiology (ESC), the identification of viral agents, with the exception of hepatitis C virus and HIV, is not recommended as it does not change the outcome or the management strategies (2, 10).
  • Bacteria involved in pericarditis development are Coxiella Burnetti, Pneumococcus, Streptococcus, Staphylococcus, and Meningococcus. Bacterial pericarditis proves to be life-threatening and can be complicated by purulent cardiac tamponade, as reported in the literature (12). Tuberculous infection is also an important cause of pericarditis, and it may be infrequent in developed countries due to vaccination but is still significantly prevalent in developing countries. Especially HIV patients are very susceptible to tuberculous pericarditis. Tuberculous pericarditis accounts for 70%-80% of bacterial causes of pericarditis, and frequency reaches 90% in HIV patients (13).
  • Pericarditis can also be caused by fungal and parasitic species but are rare. Fungal organisms such as Candida, Histoplasma, Blastomyces, and Coccidioides or parasitic organisms such as Entamoeba Histolytica and Toxoplasma Gondii should be considered in immunocompromised and HIV patients as they are opportunistic organisms and should be ruled out. (12)

Non-Infectious Causes:

These include trauma, familial pericarditis, aortic dissection, neoplastic tumors and malignancy (often secondary to metastasis).

  • Trauma is an important cause of non-infectious pericarditis and may present as early onset following the injury or may result in delayed inflammatory reactions. It may be due to blunt chest trauma or pericardial injury during surgical procedures such as cardiac surgery or catheterization. (14)
  • Primary tumors such as lipoma, fibroma, and myxoma may also be associated with pericarditis. While other malignancies such as breast cancer, lung cancer, lymphoma, leukemia, and sarcomas can metastasize and cause pericarditis. (14)

Hypersensitivity and Autoimmune diseases:

  • Pericarditis may also develop as a result of medications. Certain drugs such as anticoagulants, hydralazine, isoniazid, procainamide, and phenytoin are considered responsible for this. These drugs should be prescribed cautiously, keeping in mind the cardiac status, and the patient should be monitored regularly. (14)
  • Metabolic syndromes can also be associated with pericarditis, such as uremia, myxedema, gout, and renal insufficiency. (14, 15)
  • Autoimmune diseases may also produce pericarditis in the course of the disease. These include rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus (SLE), polyarteritis nodosa, scleroderma, and sarcoidosis.

Pathophysiology of Acute Pericarditis

First of all, we should understand the basic anatomy of the pericardium. It consists of an outer sac known as the fibrous pericardium and an inner sac known as the serous pericardium. The inner sac, serous pericardium, is further divided into an outer parietal layer, which is richly innervated, and an inner visceral layer, which overlies the epicardium. These layers are separated by a potential space containing 15 to 60 mL fluid which is serous in nature. The main function of the pericardium is to act as a barrier against infections, and the pericardial fluid lubricates the surfaces to reduce the friction between the heart and surrounding tissues. (1)

It is an interesting point to note that the pericardium is not necessary for normal heart functions. A study on the congenital absence of pericardium has shown that patients are usually asymptomatic, and the condition is discovered incidentally (16). Although the functions of the pericardium are significant, studies have shown that patients with partial or complete absence of pericardium congenitally have similar left ventricular ejaculation fraction (LVEF) and life expectancy as compared to the general population (17).

As the parietal layer of the pericardium is richly innervated, the inflammation caused by any infectious, non-infectious, or autoimmune cause leads to severe retrosternal chest pain. This is the reason that almost 90% of patients present in the emergency department with chest pain as the chief complaint. Pericardial effusion may also develop in pericarditis. In that case, pericardial compliance can increase with time as a response to fluid accumulation by the dilatation of the pericardial sac over time without compressing the heart chambers. This implies that it is not the volume of fluid that decides the outcome but the rate of accumulation of fluid. This means that even if the pericardial effusion is relatively small in volume, it can still cause life-threatening tamponade if it accumulates very quickly. While a chronic process (for example, malignancy) can lead to a large pericardial effusion without causing symptoms due to adaptive response by pericardial compliance and may take weeks before exerting constrictive pathology. (12)

History and Clinical Features

History should be taken thoroughly, and the focus should be the presence of any risk factors such as a previous history of cardiovascular disease, autoimmune disease or connective tissue disorder, diabetes, hypertension, renal impairment, and dyslipidemias. A positive family history of cardiovascular diseases is also significant. Smoking history is also important as it has a major contribution to cardiovascular diseases. Any history of trauma in the area of pain and evaluation of the gastrointestinal or respiratory system is also important in history. (18)

The most significant symptom of pericarditis is retrosternal chest pain. Chest pain may also be due to causes other than acute pericarditis, and that is why clinical assessment and ruling out other diseases is important for triage and management. Acute pericarditis makes up 5% of non-ischemic chest pain presentations in the emergency department and 0.1% of hospital admissions (12, 18). The chest pain is severe, retrosternal, non-radiating, positional (relieves by leaning forward and aggravates on lying down), and pleuritic (aggravates with deep breathing movements). It may be differentiated from ischemic pain, which is non-positional, non-pleuritic, and does not worsen on palpation. Moreover, ischemic pain is worsened by exertion and improves with rest or nitroglycerine (12, 18, 19).

Other physical examinations involve vitals monitoring (pulse, blood pressure in both arms, oxygen saturation, respiratory rate, and temperature), elevated jugular venous pressure (JVP), pulsus paradoxus, changes in heart or lung sounds, and peripheral edema. Respiratory, abdominal, and musculoskeletal examination is also recommended to rule out other diseases that may present with these complaints (18, 19).

Auscultation is also a major step in physical examination. Classically, a left parasternal pericardial friction rub is present that is scratchy and rubbing sound. It is a triphasic sound that corresponds to friction between the pericardial layers during atrial systole, ventricular diastole, and ventricular systole. It may not be present in all cases but is present in 35-85% of cases, as reported in the literature (20). However, it is not easy to appreciate it on examination, and the physician should try multiple precordial locations and multiple positions of the patient. It is also recommended to auscultate more than once as pericardial rub may appear and disappear intermittently. If present, the pericardial rub is highly specific for the diagnosis of pericarditis, but its absence does not rule out the disease, especially when clinical suspicion is present. It should also be differentiated from pleural rub, which may sound similar on auscultation, but the latter corresponds to respiratory movements rather than the cardiac cycle. Auscultation with a hold of breathing can differentiate between pericardial and pleural rub (21).

Differential Diagnosis

These include:

  • Acute MI;
  • Angina;
  • Aortic dissection;
  • Bony pain;
  • Pulmonary embolus;
  • Pneumothorax;
  • Pleurisy;
  • Pneumonia;
  • Costochondritis.



After history taking and physical examination of the patient, ECG is the next best step for evaluation. Widespread ST-segment elevation is considered the hallmark sign of acute pericarditis (2, 6). These changes are reported to be present in 60% of cases (4). Myocardial infarction, however, should be ruled out first as it is the major differential diagnosis that also involves ST-segment elevation and may prove to be a major contributor to misdiagnosis.

Although there is significant temporal variability, typical ECG changes of acute pericarditis evolve through four stages over a period of a few weeks. Stage I consists of diffuse concave-up ST-elevation with reciprocal ST-depression in aVR, often accompanied by PR segment elevation in lead aVR. This PR segment elevation can accurately differentiate pericarditis from myocardial infarction. Stage II involves the normalization of PR and ST segment elevations, usually within the first week of onset. Stages III and IV show diffuse T wave inversions that normalize eventually. (12)

It is important to differentiate acute pericarditis and myocardial infarction on the basis of ECG changes. In acute pericarditis, there is diffuse ST-segment elevation with reciprocal ST-segment depression in lead aVR and PR segment elevation. While in myocardial infarction, ST-segment elevation is not diffuse but is present only in leads overlying the ischemic area, with reciprocal ST-segment depression in leads showing no-ischemic area. (22, 23)

Another significant difference in ECG changes is the QRS complex widening. Experimental studies have shown that myocardial ischemia in animal models shows widening of the QRS complex in leads showing ST-segment elevation. However, the injury in acute pericarditis is restricted to the epicardium only with no transmural conduction delay. Hence, no widening of the QRS complex is seen. (22)

Despite these differences, it may still be difficult to make the diagnosis in some patients as ECG findings are not fully characteristic, and they are sent for emergent coronary angiography to rule out acute myocardial infarction.

Laboratory Studies

Blood tests such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) with elevated white blood count (WBCs) are also important indicators of the inflammatory process and support the diagnosis of acute pericarditis. They may also prove to be helpful for monitoring the disease and efficacy of therapy. Patients with associated myocarditis may also have raised markers of myocardial injury, such as creatine kinase (CK) and troponins (T & I). Chest X-ray is usually normal but may show cardiomegaly in cases of pericardial effusions of volume greater than 300 mL. (24)

Imaging Studies

Computed tomography (CT) and magnetic resonance imaging (MRI) are also recommended by ESC 2015 guidelines as second-line testing. Cardiac CT in acute pericarditis shows a thickening of the pericardial layers. It may also show pericardial fluid accumulation in cases of pericardial effusion and calcifications in constrictive pericarditis. Cardiac MRI is more informative with late gadolinium enhancement (LGE) within pericardial layers and even within the myocardium if pericarditis is associated with myocarditis. Cardiac MRI is a magnificent investigation to assess myocardial function and to rule out any suspicion of pericardial masses but it is costly. (12)

Certain investigations can also be done to find the underlying cause of pericarditis, especially in the case of autoimmune and metabolic syndromes. Uremic pericarditis is suspected in cases of associated renal failure and uremic encephalopathy. Renal parameters (i.e. blood urea and serum creatinine) are done to check the severity of uremia and the effect of therapy along with CRP and ESR (15). Rheumatoid factor is the characteristic investigation in rheumatoid diseases (24). Systemic lupus erythematosus can be detected clinically, along with blood tests for anti-dsDNA and anti-Smith antibodies (26).


Medical Treatment

  • The goal of treatment in acute pericarditis is relief from pain and resolution of the inflammatory process. The first choice of drugs for this aspect is non-steroidal anti-inflammatory drugs (NSAIDs) for 3-4 weeks if no contraindications are present. It helps relieve the pain and diminish inflammation. Physicians are advised to use safer NSAIDs for the shortest duration possible at their lowest effective dose. The use of NSAIDs may cause gastritis and make the gastric mucosa prone to ulcer formation. For this reason, proton pump inhibitors (PPIs) are prescribed along with NSAIDs to avoid gastrointestinal toxicity. (27)
  • Colchicine is also considered among the first line of drugs as Guidelines for the diagnosis and management of pericardial disease by the European Society of Cardiology (ESC). The ESC supports the use of colchicine along with NSAIDs, especially in recurrent cases. Low-dose colchicine is well-tolerated by the patient and does not cause gastrointestinal upset. However, prolonged use can lead to toxicity if higher doses are prescribed (28, 29). Previously, colchicine was advised along with NSAIDs to prevent recurrent episodes of pericarditis. But now, it is recommended to use colchicine for the first episode of pericarditis. Patients should also be counseled regarding the appropriate storage of medications to prevent accidental overdosage, especially in cases where medicines are prescribed for prolonged durations.
  • Glucocorticoids can also be used in a special set of cases. According to the guidelines of the European Society of Cardiology, it is recommended to use glucocorticoids (e.g. prednisolone) in cases of pericarditis that do not respond to NSAIDs, in uraemic pericarditis and in cases of autoimmune diseases and connective tissue disorders. It is usually given in addition to NSAIDs and colchicine. Starting the therapy with high doses (prednisolone 1mg/kg/day) and tapering it down over two to four weeks is recommended. (2) However, prednisolone has no significant advantage in tuberculous pericarditis management and is also associated with increased cancer risk in HIV patients.

Surgical Treatment

  • Pericardiocentesis is the process of aspiration of fluid from the pericardium by inserting a needle into the pericardium and draining the fluid with the help of a catheter. Emergency pericardiocentesis may be needed in patients presenting with cardiac tamponade, or it may be done less urgently in moderate pericardial effusion without immediate hemodynamic instability. A chest tube used for drainage of pericardial fluid may be left in place for several days. Pericardiocentesis can also be done for diagnostic purposes in order to find the infective agent by fluid microbiological investigation. (12, 30)
  • Pericardiectomy is the surgical removal of the whole pericardium, and it was performed for the first time in 1913 by the German surgeon Ludwig Rehn. It is considered a curative rather than a palliative surgical procedure for pericardial diseases but is not recommended as the first choice in early constriction or in severely advanced diseases when the mortality rate is high.
  • Other surgical procedures, such as median sternotomy and lateral thoracostomy, are under consideration as there is debate on the superiority and pros and cons of these procedures. Median sternotomy gives freedom of more radical clearance of the pericardium while lateral thoracotomy is considered a better approach in cases of purulent and effusive-constrictive pericarditis due to associated pyothorax and risk of infections. (30)

Lifestyle modifications

Along with medical and surgical treatment, lifestyle modification is also necessary for patients with pericarditis. A simple factor in this regard is the restriction of bodily activities, especially in the case of athletes. Restricting physical activity and taking rest is advised until symptoms of the disease resolve. The restriction in the case of competitive athletes is extended to three months after the resolution of symptoms. (31)


Pericarditis is usually benign, and early diagnosis and appropriate management can lead to complete resolution without any complications. However, complications may develop in some cases. These involve pericardial effusion, constrictive pericarditis, effusive-constrictive pericarditis, cardiac tamponade, and recurrent pericarditis. (12, 32)

Prognosis of Acute Pericarditis

The outcome of the disease depends upon the underlying causative factors. The overall prognosis of acute pericarditis is good, especially in idiopathic and viral pericarditis. However, in patients with purulent pericarditis or in case of the malignant cause of the pericarditis (which can be a primary tumor or metastasis from other organs), mortality rates are high even when treated (almost 40%). Advanced age is an independent risk factor for a bad prognosis. Female sex is also associated with high rates of complications but more evidence is needed. (33)


The author does not report any conflict of interest.


This information is for educational purposes and is not intended to treat disease or supplant professional medical judgment. Physicians should follow local policy regarding the diagnosis and management of medical conditions.

See Also

What is Atherosclerosis?

Heart Failure with Preserved Ejection Fraction

Hypertensive Crisis

Dyspnea Due to Respiratory Causes

Approach to Chest Pain

Acute Asthma Exacerbation


  1. Jaworska-Wilczynska M, Trzaskoma P, Szczepankiewicz AA, Hryniewiecki T. Pericardium: structure and function in health and disease. Folia Histochem Cytobiol. 2016;54(3):121-125. doi: 10.5603/FHC.a2016.0014. Epub 2016 Sep 21. PMID: 27654013.
  2. Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, Brucato A, Gueret P, Klingel K, Lionis C, Maisch B, Mayosi B, Pavie A, Ristic AD, Sabaté Tenas M, Seferovic P, Swedberg K, Tomkowski W; ESC Scientific Document Group. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015 Nov 7;36(42):2921-2964. doi: 10.1093/eurheartj/ehv318. Epub 2015 Aug 29. PMID: 26320112; PMCID: PMC7539677.
  3. Doctor NS, Shah AB, Coplan N, Kronzon I. Acute Pericarditis. Prog Cardiovasc Dis. 2017 Jan-Feb;59(4):349-359. doi: 10.1016/j.pcad.2016.12.001. Epub 2016 Dec 10. PMID: 27956197.
  4. Imazio M, Cecchi E, Demichelis B, Chinaglia A, Ierna S, Demarie D, Ghisio A, Pomari F, Belli R, Trinchero R. Myopericarditis versus viral or idiopathic acute pericarditis. Heart. 2008 Apr;94(4):498-501. doi: 10.1136/hrt.2006.104067. Epub 2007 Jun 17. PMID: 17575329.
  5. Kytö V, Sipilä J, Rautava P. Clinical profile and influences on outcomes in patients hospitalized for acute pericarditis. Circulation. 2014 Oct 28;130(18):1601-6. doi: 10.1161/CIRCULATIONAHA.114.010376. Epub 2014 Sep 9. PMID: 25205801.
  6. Imazio M, Gaita F. Diagnosis and treatment of pericarditis. Heart. 2015 Jul;101(14):1159-68. doi: 10.1136/heartjnl-2014-306362. Epub 2015 Apr 8. PMID: 25855795.
  7. LeWinter MM. Clinical practice. Acute pericarditis. N Engl J Med. 2014 Dec 18;371(25):2410-6. doi: 10.1056/NEJMcp1404070. PMID: 25517707.
  8. Imazio M, Bobbio M, Cecchi E, Demarie D, Demichelis B, Pomari F, Moratti M, Gaschino G, Giammaria M, Ghisio A, Belli R, Trinchero R. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. 2005 Sep 27;112(13):2012-6. doi: 10.1161/CIRCULATIONAHA.105.542738. PMID: 16186437.
  9. Imazio M, Brucato A, Cemin R, Ferrua S, Maggiolini S, Beqaraj F, Demarie D, Forno D, Ferro S, Maestroni S, Belli R, Trinchero R, Spodick DH, Adler Y; ICAP Investigators. A randomized trial of colchicine for acute pericarditis. N Engl J Med. 2013 Oct 17;369(16):1522-8. doi: 10.1056/NEJMoa1208536. Epub 2013 Aug 31. PMID: 23992557.
  10. Lazarou E, Tsioufis P, Vlachopoulos C, Tsioufis C, Lazaros G. Acute Pericarditis: Update. Curr Cardiol Rep. 2022 Aug;24(8):905-913. doi: 10.1007/s11886-022-01710-8. Epub 2022 May 20. PMID: 35595949; PMCID: PMC9122084.
  11. Rey F, Delhumeau-Cartier C, Meyer P, Genne D. Is acute idiopathic pericarditis associated with recent upper respiratory tract infection or gastroenteritis? A case-control study. BMJ Open. 2015 Nov 24;5(11):e009141. doi: 10.1136/bmjopen-2015-009141. PMID: 26603247; PMCID: PMC4663417.
  12. Dababneh E, Siddique MS. Pericarditis. 2022 Aug 8. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 28613734.
  13. Isiguzo G, Du Bruyn E, Howlett P, Ntsekhe M. Diagnosis and Management of Tuberculous Pericarditis: What Is New? Curr Cardiol Rep. 2020 Jan 15;22(1):2. doi: 10.1007/s11886-020-1254-1. PMID: 31940097; PMCID: PMC7222865.
  14. Snyder MJ, Bepko J, White M. Acute pericarditis: diagnosis and management. Am Fam Physician. 2014 Apr 1;89(7):553-60. PMID: 24695601.
  15. Nesheiwat Z, Lee JJ. Uremic Pericarditis. 2022 Nov 28. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 30725605.
  16. Kim HJ, Cho YS, Cho GY, Choi SI. Congenital absence of the pericardium. J Cardiovasc Ultrasound. 2014 Mar;22(1):36-9. doi: 10.4250/jcu.2014.22.1.36. Epub 2014 Mar 31. PMID: 24753808; PMCID: PMC3992347.
  17. Shah AB, Kronzon I. Congenital defects of the pericardium: a review. Eur Heart J Cardiovasc Imaging. 2015 Aug;16(8):821-7. doi: 10.1093/ehjci/jev119. Epub 2015 May 23. PMID: 26003149.
  18. Rahman A, Saraswat A. Pericarditis. Aust Fam Physician. 2017 Nov;46(11):810-814. PMID: 29101915.
  19. Ralston, S. H., Penman, I. D., Strachan, M. W. J., & Hobson, R. (2018). Davidson’s Principles and Practice of Medicine E-Book. Elsevier Health Sciences.
  20. Zayas R, Anguita M, Torres F, Giménez D, Bergillos F, Ruiz M, Ciudad M, Gallardo A, Vallés F. Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol. 1995 Feb 15;75(5):378-82. doi: 10.1016/s0002-9149(99)80558-x. PMID: 7856532.
  21. Sarkar M, Madabhavi I, Niranjan N, Dogra M. Auscultation of the respiratory system. Ann Thorac Med. 2015 Jul-Sep;10(3):158-68. doi: 10.4103/1817-1737.160831. PMID: 26229557; PMCID: PMC4518345.
  22. Rossello X, Wiegerinck RF, Alguersuari J, Bardají A, Worner F, Sutil M, Ferrero A, Cinca J. New electrocardiographic criteria to differentiate acute pericarditis and myocardial infarction. Am J Med. 2014 Mar;127(3):233-9. doi: 10.1016/j.amjmed.2013.11.006. Epub 2013 Nov 25. PMID: 24287008.
  23. Spodick DH. Differential characteristics of the electrocardiogram in early repolarization and acute pericarditis. N Engl J Med. 1976 Sep 2;295(10):523-6. doi: 10.1056/NEJM197609022951002. PMID: 950958.
  24. Imazio M, Adler Y. Management of pericardial effusion. Eur Heart J. 2013 Apr;34(16):1186-97. doi: 10.1093/eurheartj/ehs372. Epub 2012 Nov 2. PMID: 23125278.
  25. Tiwari V, Jandu JS, Bergman MJ. Rheumatoid Factor. 2022 Jul 25. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 30422493.
  26. Yu H, Nagafuchi Y, Fujio K. Clinical and Immunological Biomarkers for Systemic Lupus Erythematosus. Biomolecules. 2021 Jun 22;11(7):928. doi: 10.3390/biom11070928. PMID: 34206696; PMCID: PMC8301935.
  27. Schwier N, Tran N. Non-Steroidal Anti-Inflammatory Drugs and Aspirin Therapy for the Treatment of Acute and Recurrent Idiopathic Pericarditis. Pharmaceuticals (Basel). 2016 Mar 23;9(2):17. doi: 10.3390/ph9020017. PMID: 27023565; PMCID: PMC4932535.
  28. Lutschinger LL, Rigopoulos AG, Schlattmann P, Matiakis M, Sedding D, Schulze PC, Noutsias M. Meta-analysis for the value of colchicine for the therapy of pericarditis and of postpericardiotomy syndrome. BMC Cardiovasc Disord. 2019 Sep 2;19(1):207. doi: 10.1186/s12872-019-1190-4. Erratum in: BMC Cardiovasc Disord. 2019 Oct 18;19(1):227. PMID: 31477020; PMCID: PMC6720402.
  29. Vukomanovic V, Prijic S, Krasic S, Borovic R, Ninic S, Nesic D, Bjelakovic B, Popovic S, Stajević M, Petrović G. Does Colchicine Substitute Corticosteroids in Treatment of Idiopathic and Viral Pediatric Pericarditis? Medicina (Kaunas). 2019 Sep 20;55(10):609. doi: 10.3390/medicina55100609. PMID: 31547038; PMCID: PMC6843123.
  30. Depboylu BC, Mootoosamy P, Vistarini N, Testuz A, El-Hamamsy I, Cikirikcioglu M. Surgical Treatment of Constrictive Pericarditis. Tex Heart Inst J. 2017 Apr 1;44(2):101-106. doi: 10.14503/THIJ-16-5772. PMID: 28461794; PMCID: PMC5408622.
  31. Pelliccia A, Corrado D, Bjørnstad HH, Panhuyzen-Goedkoop N, Urhausen A, Carre F, Anastasakis A, Vanhees L, Arbustini E, Priori S. Recommendations for participation in competitive sport and leisure-time physical activity in individuals with cardiomyopathies, myocarditis and pericarditis. Eur J Cardiovasc Prev Rehabil. 2006 Dec;13(6):876-85. doi: 10.1097/01.hjr.0000238393.96975.32. PMID: 17143118.
  32. Pericarditis – Symptoms and causes – Mayo Clinic. (2022, April 30). Mayo Clinic.
  33. Kytö V, Sipilä J, Rautava P. Clinical profile and influences on outcomes in patients hospitalized for acute pericarditis. Circulation. 2014 Oct 28;130(18):1601-6. doi: 10.1161/CIRCULATIONAHA.114.010376. Epub 2014 Sep 9. PMID: 25205801.

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