Recurrent pericarditis is one of the most common and troublesome complications of acute pericarditis affecting 20–30 % of patients with a first episode of pericarditis and 20–50 % of those with one or multiple recurrences, especially if not treated with colchicine [1].

A true recurrence occurs when there is a symptom-free interval from the previous episode of pericarditis. A minimal time is required since anti-inflammatory therapy with its tapering may be as long as several weeks. This interval has been arbitrarily defined as 4–6 weeks. In the absence of this symptom-free interval, the term “incessant pericarditis” is proposed rather than “recurrent pericarditis”, since incessant pericarditis is characterized by continuous symptoms without remission. The term “chronic” is generally referred, especially for pericardial effusions, to disease processes lasting for >3 months, and “chronic pericarditis” is an arbitrary term used by experts for disease lasting >3 months (Table 11.1). All these definitions are consistent with current European guidelines on the management of pericardial diseases [2].

The usual complain is the recurrence of “pericarditic chest”, very often well recognized by patients with the possible association of other symptoms and signs supporting the diagnosis. However, as a general rule, recurrences are essentially manifested by recurrent pain and other manifestations are milder compared with the initial attack of pericarditis and the disease seems to wean slowly with several episodes that are milder and milder with a longer and longer interval between the episodes till complete disappearance of the disease [3–5].

The aetiology of recurrent pericarditis is poorly understood. It is supposed to be immune-mediated in most cases, and this statement is supported by the evidence of non-organ-specific autoantibodies and anti-heart antibodies in patients with recurrences as well as response to corticosteroids and colchicine [5–9].

In addition recurrences may be promoted by an underlying disease (e.g. systemic inflammatory disease, cancer), new or recurrent viral infection (as reported in the Marburg experience in 20–30 % of recurrent pericardial effusions), but especially inappropriate treatment of the previous episode of pericarditis (either for low doses of drugs or too short duration of therapy, or too fast tapering), or missed restriction of physical activities (Table 11.2) [4–9].

The diagnosis of recurrent pericarditis is based on an established evidence of a previous attack of acute pericarditis plus “pericarditic pain” and another objective evidence of activity of pericardial inflammatory disease (e.g. pericardial rubs, ECG changes, new or worsening pericardial effusion, elevation of markers of inflammation or white blood cell count). In atypical or doubtful cases, the evidence of pericardial inflammation by an imaging technique is helpful (e.g. pericardial contrast enhancement on CT or evidence of oedema and delayed enhancement on CMR) (Table 11.3) [2, 3].

In patients with recurrences, the diagnostic evaluation is essentially based on (1) confirmation of the diagnosis (according to previously stated diagnostic criteria), (2) evaluation of possible risk factors for complications or non-viral aetiology (e.g. especially moderate to large pericardial effusions or worsening pericardial effusions, cardiac tamponade, incomplete or lacking response to anti-inflammatory therapy), and (3) exclusion of potential specific aetiologies that were missed in the evaluation of the first attacks or previous recurrences for those with multiple recurrences [1–5].

The same high-risk features or red flags presented for acute pericarditis should be considered in patients with recurrent pericarditis. If there are no risk factors and no clues or suspicion of a missed aetiology, there is no reason to repeat aetiological diagnostic tests for each recurrence [2].

The mainstay of therapy for recurrences is physical restriction as non-pharmacological measure till symptom resolution and C-reactive protein normalization and anti-inflammatory therapy based on aspirin or NSAID plus colchicine as first choice as for acute pericarditis (Table 11.4) [7, 10, 11]. Corticosteroids should be considered only after failure of aspirin/NSAID (and more than one of these drugs) [10, 11]. A stepwise approach may be considered: aspirin and NSAID plus colchicine first, then if the patient is still not responding or has additional recurrences, corticosteroids plus colchicine [12–14]. If additional therapy is necessary, a triple therapy may be considered with aspirin or an NSAID plus corticosteroid plus colchicine. In patient on steroids, it is critical to use low to moderate doses (e.g. prednisone 0.2–0.5 mg/day or equivalent) for 4 weeks then slowly tapering after symptom resolution and normalization of C-reactive protein (Table 11.5) [10]. In case of recurrence of symptoms during steroid tapering, which is very common at doses below 15 mg/day of prednisone or equivalent, do not increase again the corticosteroid but try to control the disease increasing or reinstituting aspirin or an NSAID plus colchicine (Fig. 11.1).