Acute pericarditis is a condition referring to inflammation of the pericardial sac, lasting for less than 4-6 weeks. It is the most common type of pericardial disease and is estimated to be responsible for 5% of presentations in the emergency department and 0.1-0.2% of inpatient admissions for non-ischaemic chest pain.

There are multiple possible aetiologies for acute pericarditis, including viral infection, myocardial infarction and systemic diseases like rheumatoid arthritis. However, evaluation of aetiology is often inconclusive.

Acute pericarditis is typically characterised by sharp retrosternal chest pain over hours to days, with a pericardial friction rub on auscultation and widespread ST-elevations on ECG. Symptom resolution of uncomplicated pericarditis typically takes 1-2 weeks.

It is important to consider any inciting events of acute pericarditis in order to target management. Many times, however, a cause is not identified; neither is it mandatory to investigate for a cause where there is low clinical suspicion for an identifiable cause.

Idiopathic:

• 80-90% of causes
• Thought to be viral, post-viral or immune-mediated in origin

Infectious:

• Viral (e.g. Coxsackie, echovirus, adenovirus, HIV)
  • Most common cause
• Tuberculous
  • Common in endemic countries and in patients with HIV
• Bacterial, fungal and parasitic causes are rare

Inflammatory:

• Systemic lupus erythematosus, rheumatoid arthritis, systemic scleroderma
• Familial Mediterranean fever

Cardiac:

• Post-myocardial infarction
  • Early (1-3 days): fibrinous pericarditis
  • Late (weeks to months): autoimmune pericarditis (Dressler's syndrome)
• Post-cardiac surgery injury syndromes or chest trauma

Other:

• Paraneoplastic syndromes
  • Particularly lung and breast cancer
• Uraemia or on dialysis
• Post-radiotherapy of the chest wall
  • May occur years after exposure
• Drug-induced: isoniazid, cyclosporin, hydralazine

The exact pathogenesis of pericarditis differs based on its aetiology.

It has been suggested that in viral pericarditis, viruses can have a direct cytolytic or cytotoxic effect on the pericardium or may induce an immune-mediated response against viral nucleic acid found within the pericardium.

The inflammatory response in pericarditis can be:

• Exudative
  • Viral pericarditis is usually serous
  • Neoplastic, tuberculous and bacterial pericarditis are usually purulent and haemorrhagic
• Fibrinous
  • Post-myocardial infarction
  • Uraemic pericarditis (unknown mechanism)

Acute pericarditis usually has a nonspecific presentation. The vast majority of patients will present with chest pain of fairly sudden onset. A pericardial friction rub may also be auscultated in some patients. Other clinical features are largely dependent on aetiology.

Major clinical features of acute pericarditis include:

• Retrosternal chest pain (85-90%)
  • Usually sharp and pleuritic in nature
  • Improved by sitting up and leaning forward
  • Radiation to the trapezius ridge is considered to be specific for pericarditis
• Pericardial friction rub (≤33%)
  • Superficial, scratchy or squeaky quality on auscultation, best heard using the diaphragm of the stethoscope
  • Usually best heard at the left lower sternal border
  • Can be differentiated from pleural rub by asking patient to hold their breath
  • Highly specific for pericarditis but has a low sensitivity

Patients may exhibit other clinical features that suggest an infectious aetiology:

• Low-grade fever
• Prodromal myalgia and malaise

Initial investigations may aid the diagnosis of acute pericarditis and provide important prognostic information.

According to the European Society of Cardiology (ESC) guidelines published in 2015, investigations that should be ordered in all suspected cases of acute pericarditis are as follows.

Bedside tests:

• Electrocardiography (ECG)
  • Classical ECG changes are seen in 60% of patients
  • Widespread concave ST-elevations with PR-segment depression
  • PR-segment depression is 85% specific for acute pericarditis, but not sensitive
  • T-wave changes may last for weeks after resolution of symptoms but are of no clinical significance

Bloods:

• C-reactive protein, ESR, FBC
  • Elevated inflammatory markers have a 90% sensitivity and may support the diagnosis of acute pericarditis
  • Can also be used to monitor progress
• Serum troponins
  • Elevation suggests myocardial involvement ('myopericarditis') and indicates a poorer prognosis
• Urea
  • Elevation suggests uraemic aetiology of the pericarditis

Imaging:

• Echocardiography
  • Mild pericardial effusion seen in 60% of patients
  • While visualising a pericardial effusion supports the diagnosis of pericarditis, absence of pericardial effusion does not exclude it
• Chest X-ray
  • Often normal unless there is a large pericardial effusion or lung pathology that can be visualised, such as lung malignancy
  • New or unexplained cardiomegaly may also suggest acute pericarditis

Further imaging techniques - CT and MRI - can be considered in unclear diagnostic cases to better visualise pericardial inflammation. MRI may also be used to confirm myocardial involvement.

Pericardiocentesis is only indicated where there is suspicion of a bacterial or neoplastic aetiology. It may also be done as a therapeutic intervention for a large pericardial effusion.

Other investigations can be considered if a specific cause is suspected, but are not routine. These include:

• Blood cultures if fever >38ºC, signs of sepsis or concomitant bacterial infection elsewhere
• HIV serology
• Interferon-gamma release assay or tuberculin skin test

Viral studies typically do not yield high results and are therefore not routinely obtained.

The presentation of chest pain in acute pericarditis may resemble other conditions, including:

• Acute coronary syndromes
  • Similarities: sharp chest pain, dyspnoea, may have elevation in troponin levels
  • Differences: pleuritic chest pain is typically described differently, with exacerbation on inspiration and lying supine. A pericardial rub may also be heard. ECG is critical in diagnosis
• Pulmonary embolism
  • Similarities: sudden onset chest pain, which may be pleuritic in nature; pleural rub may uncommonly be heard
  • Differences: risk factors for PE (recent travel, immobility, surgery) are typically different from those of pericarditis. An ECG may show tachycardia with right heart strain, rather than widespread ST-elevation
• Pneumonia
  • Similarities: fever, dyspnoea and chest pain that may be pleuritic in nature
  • Differences: respiratory symptoms are often not present, such as cough and sputum production. A chest radiograph will be able to visualise any areas of consolidation
• Gastroesophageal reflux disease
  • Similarities: retrosternal chest pain that may be aggravated by lying supine
  • Differences: constant pain, not aggravated post-prandially and no other gastrointestinal symptoms involved
• Myocarditis
  • Similarities: 'stabbing' chest pain, dyspnoea and signs of heart failure
  • Differences: patients will myocarditis alone will not exhibit ST-elevation on ECG. If patients have elevated cardiac enzyme biomarkers with widespread ST-elevation on ECG, this is a diagnosis of myopericarditis

Acute myocardial infarction (AMI) is an important condition to exclude. There are a few differences to be aware of on ECG, however:

The use of anti-inflammatories is the mainstay of treatment in acute pericarditis. Most patients can be safely managed in the outpatient or primary care setting. If patients have any poor prognostic factors, they should be admitted for further determination of cause. Follow-up is recommended at 1 week to assess responsiveness to therapy. (Class A recommendation, level B evidence from ESC guidelines)

• High-dose NSAID or aspirin
  • Duration until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks)
  • Tapering of dose recommended over weeks to months
• Adjunct use of colchicine
  • Duration for 3 months
  • Used a low, weight-adjusted doses
  • Loading dose no longer recommended to improve compliance
• Restriction of strenuous physical activity
  • Duration until symptom resolution and normalisation of inflammatory markers
• Consider gastroprotection with a proton pump inhibitor
• Consider low-dose corticosteroids if NSAID and colchicine contraindicated, after exclusion of infectious cause

• Recurrent pericarditis (15-30%)
  • Recurrence after a symptom-free interval of 4-6 weeks
  • Recurrence rate increased to 50% in patients not treated with colchicine
• Acute cardiac tamponade
  • More common in patients with underlying malignancy, TB or purulent pericarditis
  • Treated by pericardiocentesis
• Chronic constrictive pericarditis
  • More common in patients with TB or purulent pericarditis or immune-mediated and neoplastic aetiologies
  • Treated by surgical pericardial resection

The prognosis of patients with acute pericarditis is generally good. There are several predictors of poor prognosis, however. Patients with any of these risk factors will require admission and a search of aetiology.

Major predictive factors:

• Fever >38ºC
• Subacute onset (over days)
• Large pericardial effusion
  • Diastolic echo-free space >20 mm
• Lack of response to NSAIDs after at least 1 week of therapy

Minor predictive factors:

• Myopericarditis
• Immunosuppression
• Trauma
• Oral anticoagulation therapy