Last revised by Joachim Feger on 18 Jun 2024

Pericarditis is defined as inflammation of the pericardium. It is normally found in association with cardiac, thoracic or wider systemic pathology and it is unusual to manifest on its own.

Pericarditis is the most common pericardial disease worldwide and accounts for about 0.1-0.2% of all hospital admissions and about 5% of chest pain admissions to the emergency department  1-4.

The diagnosis of pericarditis is based on clinical criteria and supplemental imaging information 1.

According to the 2015 European Society of Cardiology (ESC) Guidelines for the diagnosis and management of pericardial diseases the diagnosis can be made if ≥2 of the following four criteria are met 1:

  • pericarditic chest pain

  • pericardial rubs

  • new widespread ST elevation and/or PR depression (ECG)

  • new or worsening pericardial effusion

Supporting findings include the following:

  • elevated inflammatory markers (CRP, ESR, WBC)

  • imaging findings on cardiac CT or cardiac MRI suggesting pericardial inflammation

Classically, patients present with abrupt, pleuritic, positional left precordial chest pain after a viral prodrome. The pain is relieved in the sitting position when leaning forward and exacerbated when supine. Tuberculous pericarditis may present with constitutional symptoms, including fever, night sweats, anorexia, and weight loss. The physical exam may demonstrate:

  • a pericardial friction rub

    • classically triphasic, two components in diastole and one in systole

    • may be transient

  • signs of tamponade

  • diffuse ST-segment elevation (STE)

    • with upward concavity

    • the STE in lead II > lead III

    • absence of reciprocal changes or Q waves

  • lead aVR demonstrates ST-segment depression

    • this lead also may demonstrate PR segment elevation

  • diffuse PR segment depression

    • excluding the aforementioned (lead aVR)

  • later, T-wave inversions may develop

Etiologies can be divided into infectious (viarl, bacterial, fungal and parasitic) and non-infectious causes (autoimmune, neoplastic and metabolic), with infections accounting for two thirds of cases and non-infectious causes for the remaining third 1,5.

Pericarditis can be divided into subtypes according to morphology:

There may be an increased cardiothoracic ratio (CTR) with a globular or 'flask-shaped' outline if there is co-existing pericardial effusion. Manifestations of cardiogenic pulmonary edema may also be present.

Echocardiography is recommended when the pericardial disease is suspected and may demonstrate 11

Patients who have a preserved ejection fraction but symptomatic heart failure may (with a suggestive clinical history) be examined for occult constrictive pericarditis, features of which include:

  • right and left atrial enlargement

  • mitral/tricuspid inflow pulsus paradoxus

    • in the absence of an effusion

  • annulus paradoxus

    • elevated filling pressures with a preserved mitral septal annular velocity (septal e')

  • annulus reversus

    • tissue Doppler of the mitral annuli reveals a septal e' > lateral e'

    • the lateral e' is normally always higher than the septal e'

At contrast-enhanced CT, enhancement of the thickened pericardium generally indicates inflammation 1.

Usually, GRE cine, T1, T2 black-blood/STIR and IR GRE sequences are performed. In the setting of suspected pericardial constriction, real-time cine sequences should be acquired 6,7. The presence of an arrhythmia may induce artefacts. For specific features please refer to subtype articles.   

The normal pericardial thickness is considered 2 mm while a thickness of over 4 mm suggests a pericarditis 8,9

Edema of the visceral and parietal pericardium, depicted in T2 black-blood/STIR images, and enhancement usually assessed with late gadolinium enhancement (LGE) images are additional specific MRI features 6,7,10.

In addition, cardiac MRI has the ability to assess the myocardium regarding concomitant myocarditis and viability in a post-myocardial infarction setting or to detect myocardial infarction, if previously unknown.

Focal FDG uptake may be demonstrated in some cases. 

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