Acute pericarditis is the most common pericardial syndrome that is encountered in clinical practice. It is an inflammatory pericardial syndrome with or without pericardial effusion [1, 2].

The usual presentation is acute, with retrosternal “chest pain” with pleuritic features (>85 % of cases; it is increased by inspiration), and it has positional features: worsening when the patient is supine and improves when sitting and leaning forward. It may radiate to the shoulders, arms and jaw and may simulate “ischaemic chest pain”. It is a typical “referred pain” since pericardial afferent fibres show convergence with somatic areas on the chest and arms as for angina pain (Fig. 9.1) [1, 2].

The physical examination may be normal; patients may have a low-degree fever in uncomplicated cases and additional signs and symptoms related to a concomitant febrile syndrome (e.g. gastroenteritis, flu-like syndrome that may also precede pericarditis 1–2 weeks before) or an underlying disease with pericardial involvement (e.g. systemic inflammatory disease, cancer). The most specific physical sign can be the presence of a pericardial rub that is identifiable in no more than 1 of 3 cases. It is a superficial scratchy or squeaking sound best heard with the diaphragm of the stethoscope over the left sternal border and better with the patient sitting up and leaning forward. It is typically compared with the sound produced by walking on fresh snow and it can be evanescent [2–4].

On ECG, the classical reported feature of acute pericarditis is widespread ST-segment elevation (Fig. 9.2), although either this sign or the earlier PR depression (as an atrial current of injury that is the earliest ECG sign) is the expression of concomitant subepicardial involvement and not “pure pericarditis”, since the pericardium is electrically silent [3, 5].

A so-called “typical” ECG can be found in no more than 60 % of cases and ST/T changes are more common in younger male patients, especially with associated myocarditis. The ECG evolves according to classical 4 stages reported by Spodick et al. in no more than 60 %. Presentation times as well as therapies may affect the ECG presentation. Early presentation may show ST-segment elevation, on the contrary a normal ECG or with negative T waves (reflecting an ECG in evolution) can be seen in late presentations or chronic forms. In patients with a fast response to medical therapy, the ECG may be absolutely normal as well as in mild forms; thus, a normal ECG does not exclude pericarditis [2, 5]. The risk of cardiac arrhythmias is very low in simple acute pericarditis, that is, in the absence of myocarditis or structural heart diseases [3, 6].

Chest x-ray may be completely normal (Fig. 9.3) in the absence of concomitant pleuropulmonary disease or large pericardial effusion (>300 ml).

An echocardiogram is mandatory in a patient with a suspicion of acute pericarditis to assess the presence, size and haemodynamic importance of pericardial effusion. About 60 % of patients with acute pericarditis will show a pericardial effusion, generally mild [4]. Alternatively, it is common to find non-specific increase of pericardial brightness, probably related to fibrinous exudation in pericardial layers (Fig. 9.4). On this basis, also the absence of a pericardial effusion does not exclude pericarditis.

All the symptoms and signs are due to inflamed pericardial layers with increased attrition (pericardial pain, rubs), possible increased production of pericardial effusion (pericardial effusion) and subepicardial inflammatory involvement (ECG changes, concomitant myocarditis) (See also Fig. 3.​5 in Chap. 3).

Chemistry may show elevation of markers of inflammation in most cases (e.g. elevation of C-reactive protein and white blood cells count) but not all because of a possible early presentation or effect of empiric anti-inflammatory therapies; thus, normal markers of inflammations do not exclude pericarditis [7].

The aetiology of acute pericarditis largely depends on the prevalence of tuberculosis. In developed areas with a low prevalence of tuberculosis (e.g. Western Europe and North America), most cases are presumed to be viral and usually preceded or concomitant with a flu-like syndrome or gastroenteritis [1, 7, 8]. The most common viral agents, which may be also responsible for myocarditis, include Enteroviruses (especially Coxsackieviruses), herpes viruses (especially Epstein-Barr virus (EBV) and reactivation of cytomegalovirus (CMV)), parvovirus and only in a minority of cases influenza viruses, HCV and HBV. In children either Enteroviruses or Adenoviruses or herpes viruses are implicated [1, 2]. Nevertheless, in clinical practice most cases remain “idiopathic” with a conventional diagnostic approach and account for about 85 % of cases. In developing countries, tuberculosis is the most common cause of pericarditis and pericardial diseases, and it is often associated with HIV infection, especially in specific geographic areas, such as sub-Saharan Africa (Table 9.1) [9].

The clinical diagnosis can be made with two of the following criteria (Table 9.2) [2, 10, 11]:

In case of atypical or doubtful presentation, elevation of markers of inflammation or imaging evidence of pericardial inflammation may be helpful [10, 11]. Imaging evidence of pericardial inflammation may be provided by second level imaging techniques, such as computed tomography (CT; as enhanced pericardial imaging after contrast injection) and cardiac magnetic resonance (CMR; as evidence of oedema on T2-weighted dark blood images and late gadolinium enhancement as evidence of organizing pericarditis and/or fibrosis after injection of gadolinium chelates; see chapter on multimodality imaging of the pericardium).

Major differential diagnoses include acute coronary syndromes with ST-segment elevation and early repolarization (see chapter on the diagnosis of pericardial diseases).

Patients with concomitant myocarditis may present with an elevation of markers of myocardial injury (e.g. especially troponin) [11–13].