Most episodes of acute pericarditis settle, and treatment is usually straightforward. What determines whether an episode stays simple is whether the inflammation returns and whether a specific cause needs more than anti-inflammatory treatment. Fluid that arrives faster than the pericardium can stretch causes cardiac tamponade, and chronic inflammation can leave behind a fibrotic sac that restricts filling — constrictive pericarditis. Management therefore runs on two tracks: an anti-inflammatory regimen that is much the same for most patients, and treatment directed at the underlying cause.
Anti-inflammatory treatment
Aspirin or a non-steroidal anti-inflammatory drug (NSAID, such as ibuprofen or indomethacin) is the first-line treatment, and it is given together with colchicine, an anti-inflammatory drug, rather than colchicine being kept in reserve. The doses below are the ones recommended in current European guidance, and they are full anti-inflammatory doses, not analgesic doses.
| Drug | Starting dose | Initial course | Tapering |
|---|---|---|---|
| Aspirin | 750–1000 mg three times daily | 1–2 weeks | reduce by 250 mg every 1–2 weeks |
| Ibuprofen | 600–800 mg three times daily | 1–2 weeks | reduce by 200 mg every 1–2 weeks |
| Indomethacin | 25–50 mg three times daily | 1–2 weeks | reduce by 25 mg every 1–2 weeks |
| Colchicine | 0.5 mg twice daily; 0.5 mg once daily if under 70 kg or with severe renal impairment | 3–6 months | not required |
| Prednisone | 0.2–0.5 mg/kg once daily | 2–4 weeks | taper over several months |
Two rules matter more than the choice of drug. First, treatment is continued at full dose until symptoms have resolved and C-reactive protein (a blood marker of inflammation) has normalised, and only then tapered — tapering early is one of the commonest reasons pericarditis comes back. Second, a proton pump inhibitor, an acid-suppressing drug, is added for gastroprotection while the NSAID is running. The taper follows the clinical response and the inflammatory markers, and if symptoms return the dose is increased again rather than tapered further.
Colchicine roughly halves the rate of recurrence when it is added to an NSAID, which is why it is part of first-line treatment rather than a second step. It is cleared by the kidney, so the twice-daily dose becomes a single daily dose in severe renal impairment and in patients under 70 kg. Diarrhoea is the usual reason it has to be stopped.
Corticosteroids relieve symptoms quickly, which is exactly why they are easy to overuse. Exposure to corticosteroids — particularly at high dose, and particularly when they are used first-line instead of an NSAID — is associated with a higher risk of recurrence. They are therefore reserved for patients who fail first-line treatment, or for a specific indication such as a systemic autoimmune disease or uraemic pericarditis. When they are used, the dose is low to moderate and the taper runs over months.
Interleukin-1 blockade is the newest step. Interleukin-1 is an inflammatory signalling molecule, and the two drugs that block it are anakinra, a recombinant interleukin-1 receptor antagonist, and rilonacept, a soluble interleukin-1 trap. They are recommended for patients with recurrent pericarditis that has failed first-line therapy and corticosteroids and who have raised C-reactive protein; they reduce recurrences and allow corticosteroids to be withdrawn. Both drugs were tested in randomised trials, AIRTRIP for anakinra and RHAPSODY for rilonacept.
Treatment directed at the cause
For the common idiopathic and viral episodes, anti-inflammatory treatment alone is enough. Treatment of a specific cause follows a different logic. Purulent bacterial pericarditis needs antibiotics plus drainage. Uraemic pericarditis usually resolves with dialysis. Tuberculous pericarditis needs antituberculous chemotherapy. Neoplastic pericarditis is managed by treating the tumour, with drainage of fluid that is causing symptoms. A haemorrhagic effusion after trauma may need surgical evacuation.
After a myocardial infarction the choice narrows: aspirin is preferred, and non-aspirin NSAIDs and glucocorticoids are avoided because they have been associated with impaired healing and rupture. The three problems that produce chest pain, a changing electrocardiogram and a raised troponin after infarction — early post-infarct pericarditis, Dressler syndrome and reinfarction — are separated in Complications of Myocardial Infarction.
Recurrent pericarditis
Recurrence means a new episode after at least 4 to 6 symptom-free weeks. It is usually an immune-mediated reaction rather than a fresh infection, so it is treated with anti-inflammatory therapy rather than antibiotics. Recurrent or incessant disease (symptoms that continue without a symptom-free interval) develops in about 15–30% of patients with idiopathic acute pericarditis who are not given colchicine, usually within 18 months of the first episode. Several factors raise the risk, and most of them are iatrogenic, meaning caused by treatment: too low an initial dose, tapering before symptoms and C-reactive protein have settled, and corticosteroid exposure. A genetic and autoinflammatory contribution is also recognised in patients who recur repeatedly.
Management repeats the first-line regimen and lengthens it. Colchicine is continued for at least 6 months in recurrent disease rather than for 3 months as in a first episode, the taper is slower, and interleukin-1 blockade is added when episodes keep returning despite adequate treatment and steroids. The rare late evolution of long-standing inflammation is a fibrotic, non-compliant pericardium — constrictive pericarditis.
Who needs hospital care
Alongside the choice of drug, each episode needs a decision about where it will be treated. Most patients with a first, uncomplicated episode can be treated as outpatients with early review. Guidelines group the features that argue for admission into major and minor risk factors.
- Major: fever above 38 °C, a subacute onset where the illness has developed over days to weeks, a large effusion — for example a diastolic echo-free space over 20 mm — tamponade, and no response to anti-inflammatory treatment after about a week.
- Minor: a myocardial component with a troponin rise, immunosuppression, recent trauma or cardiac surgery, and anticoagulant therapy.
The reasoning behind the list is straightforward. Fever and subacute onset suggest a cause other than a simple viral episode, a large effusion and tamponade are the situations in which the heart can be compressed, failure to respond to treatment means the diagnosis or the cause is probably wrong, and immunosuppression, trauma and anticoagulation each raise the odds of a bacterial, haemorrhagic or atypical effusion.