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Cardiology›Condition·Updated Jun 27, 2026·v1

Acute Pericarditis

Acute pericarditis is diagnosed clinically by ≥2 of 4 ESC criteria. First-line therapy consists of high-dose NSAIDs plus colchicine for 3 months, which reduces recurrence from 37.5% to 16.7% (NNT 5). High-risk features (fever >38°C, large effusion, tamponade, immunosuppression) warrant hospitalization. Recurrent pericarditis is an autoinflammatory condition effectively treated with IL-1 inhibitors. Corticosteroids should be avoided in uncomplicated cases.

High Evidence75 references·8,493 words·34 min read·v1
CardiologyPericarditisChest PainInflammatory Heart Disease

Quick Reference

RxDrug of choiceNSAID (ibuprofen 600-800 mg TID or aspirin 750-1000 mg TID) + colchicine (0.5 mg BID if >70 kg, QD if ≤70 kg) for 3 months
AltAlternativesFor refractory/recurrent: IL-1 inhibitors (anakinra 100 mg SC daily, rilonacept 320 mg load then 160 mg weekly); second-line corticosteroids (prednisone 0.2-0.5 mg/kg/day) if infection excluded
⊘AvoidHigh-dose corticosteroids as initial monotherapy; indomethacin (high GI toxicity)
DxTest of choiceTransthoracic echocardiography (assess effusion, tamponade)
ScKey scoreESC diagnostic criteria (≥2 of: pleuritic positional chest pain, pericardial rub, typical ECG changes, new/worsening effusion)
→When to referHospitalization if high-risk features present: fever >38°C, subacute onset, effusion >20 mm, tamponade, immunosuppression, anticoagulation, NSAID failure within 7 days; refer to cardiologist for recurrent disease
First-episode idiopathic pericarditis is a self-limited condition; combine colchicine with NSAIDs for 3 months to cut recurrence by half (NNT=5), and never use high-dose steroids as first-line therapy.
Acute pericarditis, inflammation of the pericardial sac, accounts for 5% of emergency visits for nonischemic chest pain and follows a benign course in 70-85% of cases when promptly recognized. The diagnosis rests on ≥2 of 4 ESC criteria: pleuritic positional chest pain, pericardial friction rub, diffuse ST elevation on ECG, and new pericardial effusion. A dual anti-inflammatory regimen of high-dose NSAIDs plus weight-based colchicine for 3 months cuts recurrence from 37.5% to 16.7% (NNT=5). High-risk features (fever >38°C, tamponade, large effusion) demand hospitalization; for recurrent or corticosteroid-dependent disease, interleukin-1 inhibitors (anakinra, rilonacept) yield profound suppression. Avoiding early high-dose corticosteroids is essential, as they paradoxically fuel recurrence.

Overview and Recommendations

Background

  • •Acute pericarditis accounts for up to 5% of emergency department visits for nonischemic chest pain in North America and Western Europe, with an incidence roughly one-tenth that of non-ST-elevation myocardial infarction. The condition predominantly affects middle-aged men (mean age 52-56 years, male-to-female likelihood ratio 1.85) and exhibits a striking winter peak, a 1.5-fold higher incidence compared with summer, implicating viral respiratory pathogens as major triggers.
  • •Most cases (80-85%) in Western countries are idiopathic or viral, yet pericarditis can herald serious underlying disease: autoimmune conditions (7.3% of identifiable causes), occult malignancy (5.1%, with a 13-fold increased cancer diagnosis rate within 3 months), and tuberculosis in endemic regions. A high index of suspicion is required because untreated purulent or tuberculous pericarditis carries a mortality exceeding 40% and a 50% risk of constrictive pericarditis.
  • •The central pathogenic driver is the NLRP3 inflammasome-IL-1β axis. Inciting injury (viral, post-cardiac surgery, autoimmune) activates the NLRP3 inflammasome in pericardial mesothelial cells, triggering IL-1β cleavage and release. This unleashes a feed-forward inflammatory cascade that produces pleuritic chest pain (via prostaglandin sensitisation of phrenic nerve nociceptors), pericardial effusion (increased vascular permeability), and systemic inflammation (hepatic CRP synthesis). Every effective therapy, NSAIDs, , and , targets a distinct node in this pathway.
  • •The traditional temporal classification, acute (<4-6 weeks), incessant (4-6 weeks to 3 months without a symptom-free interval), recurrent (new episode after a ≥4-6 week symptom-free interval), and chronic (>3 months), dictates therapy duration. An initial episode treated with colchicine for 3 months reduces the 18-month recurrence rate from 37.5% to 16.7% (NNT = 5), while recurrent disease may require 6 months of colchicine and escalation to IL-1 blockade.

Evaluation

  • •Suspect acute pericarditis in any patient presenting with acute, sharp, pleuritic chest pain that characteristically worsens when supine and improves when sitting forward. The pain may radiate to the trapezius ridge (via phrenic nerve irritation), a distinctive feature that helps differentiate it from myocardial ischemia.
  • •Ask about preceding respiratory or gastrointestinal illness (latency 1-2 weeks), fever, dyspnea, and risk factors: recent cardiac surgery or myocardial infarction (post-cardiac injury syndrome), known autoimmune disease (SLE, rheumatoid arthritis), active malignancy, or new medications (immune checkpoint inhibitors, hydralazine).
  • •Examine for a pericardial friction rub, a pathognomonic scratchy sound heard best at the left lower sternal border with the diaphragm of the stethoscope while the patient leans forward and holds expiration. Note that the rub is absent in >70% of cases and may be fleeting; its absence never excludes the diagnosis.
  • •Check for signs of pericardial effusion or tamponade: muffled heart sounds, Ewart’s sign (dullness and tubular breath sounds beneath the left scapula), Beck’s triad (hypotension, muffled heart sounds, distended neck veins), and pulsus paradoxus >10 mmHg. To measure pulsus paradoxus, inflate the cuff above systolic pressure, deflate slowly, and note the first Korotkoff sound that is heard only during expiration; if sounds become audible throughout the cycle only after a drop of >10 mmHg, tamponade is likely.
  • •Obtain a 12-lead ECG immediately. Stage I (acute) findings, present in 25-50% of cases, include diffuse, concave ST-segment elevation in leads I, II, aVL, aVF, V2-V6, and PR-segment depression in II, aVF, V4-V6 (with reciprocal PR elevation in aVR). The absence of reciprocal ST depression differentiates pericarditis from STEMI; concomitant troponin elevation suggests myopericarditis but does not worsen prognosis.
  • •Order laboratory studies: high-sensitivity C-reactive protein (hs-CRP) is elevated in ~78% at presentation and serves as a crucial biomarker for monitoring treatment response. Troponin I or T is elevated in ~30%, indicating myocardial involvement. White blood cell count and ESR are nonspecific and may be normal.
  • •Perform transthoracic echocardiography as the first-line imaging study to detect pericardial effusion (present in ~60%, typically small) and assess for tamponade physiology (right atrial or ventricular diastolic collapse, marked respiratory variation in mitral and tricuspid inflow). Echocardiography also evaluates biventricular function to rule out concomitant myocarditis.
  • •Apply the ESC diagnostic criteria: the diagnosis is confirmed when ≥2 of the following are present: (1) typical pericarditic chest pain, (2) pericardial friction rub, (3) ECG changes characteristic of acute pericarditis, (4) new or worsening pericardial effusion. This clinical constellation is the gold standard.
  • •Stratify risk using validated high-risk markers that mandate hospitalization: fever >38°C (HR 3.56 for specific cause/complication), subacute onset over weeks, large effusion >20 mm on echo, cardiac tamponade, immunosuppression, trauma, oral anticoagulation, and failure to respond to aspirin or NSAID within 7 days. In the absence of these, outpatient management is safe.
  • •Consider cardiac magnetic resonance (CMR) for recurrent, complicated, or diagnostically uncertain cases. Pericardial late gadolinium enhancement and edema on T2-weighted sequences confirm ongoing inflammation and predict recurrence. Chest CT may be used to detect pericardial calcification or lung pathology but lacks CMR’s tissue characterization.
  • •Reserve pericardial biopsy for suspected tuberculosis, malignancy, or refractory effusions when less invasive diagnostics are inconclusive. Routine viral serologies or autoantibody panels are not recommended without specific historical clues.

Management

  • •Initiate NSAID therapy immediately: ibuprofen 600-800 mg PO every 8 hours OR 750-1000 mg PO every 8 hours. Provide proton-pump inhibitor gastroprotection for patients with gastrointestinal risk factors. Indomethacin should be avoided due to a worse GI profile.
  • •Simultaneously start weight-based : 0.5 mg twice daily for patients weighing >70 kg, or 0.5 mg once daily for ≤70 kg. Colchicine must be continued for 3 months after a first episode (6 months after a recurrence), premature discontinuation sharply increases recurrence risk.
  • •Monitor hs-CRP weekly. Continue full-dose NSAID until the patient is pain-free AND hs-CRP has normalised (typically 2-4 weeks). Do not begin tapering NSAIDs while CRP remains elevated, as this predicts therapeutic failure.
  • •Once clinical remission is achieved and CRP is normal, taper the NSAID by reducing the dose by 200-400 mg every 1-2 weeks over 2-4 weeks. An over-rapid taper or abrupt discontinuation is the most common trigger of early recurrence.
  • •Do NOT prescribe high-dose corticosteroids (>0.5 mg/kg/day prednisone equivalent) as initial therapy for uncomplicated idiopathic pericarditis; even a single early course is associated with a 2- to 3-fold increased recurrence risk by interfering with colchicine’s effect and promoting chronicity.
  • •If symptoms or elevated CRP persist despite 1-2 weeks of full-dose NSAID plus colchicine, re-evaluate for high-risk etiologies (purulent, tuberculous, neoplastic). When infection is excluded, a cautious corticosteroid course, 0.2-0.5 mg/kg/day, may be introduced as a second-line therapy, but it must be combined with colchicine and an IL-1 inhibitor if feasible to facilitate subsequent taper.
  • •For patients with ≥2 recurrences or corticosteroid-dependent disease, initiate IL-1 inhibition: 100 mg subcutaneously once daily or 320 mg loading dose followed by 160 mg once weekly. IL-1 blockers rapidly suppress CRP and symptoms, with recurrence rates reduced to ~25% compared with ˜74% on placebo. Continue therapy for 6-12 months, then attempt tapering.
  • •During corticosteroid use, taper extremely slowly: reduce prednisone by 1-2.5 mg every 2-4 weeks only when symptoms are fully resolved and CRP is normal. Any recurrence warrants returning to the last effective dose and an even slower taper.
  • •Hospitalise any patient with high-risk features (fever >38°C, subacute onset, effusion >20 mm, tamponade, immunosuppression, anticoagulation, NSAID failure within 7 days) for targeted investigation and monitoring. These patients require exclusion of bacterial, tuberculous, and neoplastic causes.
  • •Recognize and treat cardiac tamponade emergently: urgent ultrasound-guided pericardiocentesis is indicated for Beck’s triad or pulsus paradoxus >10 mmHg with hemodynamic compromise. Avoid positive-pressure ventilation prior to drainage if possible, as it may precipitate cardiovascular collapse.
  • •Manage myopericarditis conservatively: continue NSAIDs and colchicine, ensure rest, and avoid intense physical activity. Elevated troponin alone does not alter anti-inflammatory therapy nor worsen prognosis if ventricular function is preserved.
  • •For post-cardiac injury syndromes (e.g., following ablation, pacemaker implantation, or post-MI), initiate the same NSAID-colchicine protocol. Consider prophylactic colchicine started 7 days before extensive left atrial ablation to reduce pericarditis incidence (absolute risk reduction from 10.3% to 3.8%).
  • •Avoid non-dihydropyridine calcium-channel blockers (diltiazem, verapamil) not because they are specifically contraindicated but they are not part of pericarditis management; beta-blockers can be used for rate control if atrial fibrillation occurs (4-5% of cases). Routine anticoagulation is not indicated for AF in pericarditis unless CHA2DS2-VASc score warrants.
  • •Counsel patients on activity restriction: athletes must refrain from competitive sports for ≥3 months and require re-evaluation with ECG and echocardiography before clearance. For non-athletes, a gradual return to activity after symptom resolution and CRP normalisation is safe.
  • •Schedule follow-up at 3 months to assess remission, check CRP if symptoms recurred, and consider discontinuation of colchicine. Recurrent symptoms after colchicine cessation may necessitate a 6-month colchicine course or escalation to IL-1 inhibitors.

Board Review — High Yield

  • •Pericardial friction rub, pathognomonic but heard in <30% of cases; best auscultated at left lower sternal border with patient sitting forward and holding expiration.
  • •Diffuse concave ST elevation + PR depression, classic ECG finding; absence of reciprocal ST depression differentiates from STEMI.
  • •Colchicine, weight-based (0.5 mg BID >70 kg, QD ≤70 kg) for 3 months (first episode) reduces recurrence from 37.5% to 16.7% (ICAP trial, NNT 5).
  • •High-risk features, fever >38°C, subacute onset, effusion >20 mm, tamponade, immunosuppression, trauma, anticoagulation, NSAID failure, mandate hospitalization.
  • •hs-CRP, elevated in 78%, normalisation required before tapering NSAID; persistent elevation predicts recurrence.
  • •IL-1 inhibitors, anakinra or rilonacept for ≥2 recurrences or corticosteroid-dependent cases; reduces recurrence rate by ~70%.
  • •Beck’s triad, hypotension, muffled heart sounds, distended neck veins, indicates cardiac tamponade requiring immediate pericardiocentesis.
  • •Pulsus paradoxus, inspiratory drop in systolic BP >10 mmHg; measure by slow cuff deflation and noting first Korotkoff sound only during expiration.
  • •Trapezius ridge pain, referred pain via phrenic nerve; highly specific for pericardial inflammation.
  • •Constrictive pericarditis, complicates <0.5% of idiopathic cases but up to 33% of tuberculous/neoplastic; presents with right heart failure, Kussmaul sign, and pericardial knock.

Deep Dive — Evidence Details

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