Pericarditis

Definition & Epidemiology

Pericarditis is inflammation of the pericardium — the fibroserous sac surrounding the heart — caused by granulocytic and lymphocytic infiltration. It is the most common pericardial disease encountered clinically, accounting for approximately 5% of all non-ischemic chest pain presentations. Incidence is roughly 27.7 cases/100,000 population/year, with men aged 16–65 at higher risk (RR ~2.0 vs. women).

Etiology

Category	Examples
Idiopathic/Viral (most common in developed world, 80–90%)	Coxsackievirus B, echovirus, EBV, CMV, HIV, influenza
Bacterial	TB (most common cause in developing countries), Staphylococcus, Streptococcus
Autoimmune/Connective tissue disease	SLE, RA, systemic sclerosis
Post-cardiac injury	Dressler syndrome (post-MI, weeks later), post-pericardiotomy
Early post-MI pericarditis	2–4 days after transmural MI (~20%)
Uremia	Most common systemic disorder associated
Malignancy	Metastatic (lung, breast, lymphoma), primary
Radiation	Mediastinal irradiation
Drugs	Hydralazine, procainamide, isoniazid, clozapine
Other	Sarcoidosis, amyloidosis, aortic dissection

In SLE, pericarditis associates with disease flare and polyserositis; clinically significant pericarditis develops in <30% overall, but necropsy studies show involvement in 40–80% of SLE patients. — Braunwald's Heart Disease

Pathology

Acute: Fibrinous exudate gives the pericardial surface a characteristic shaggy, "bread-and-butter" appearance. Bacterial infection produces fibrinopurulent (suppurative) exudate; TB may show caseation; malignancy produces hemorrhagic effusion.

Chronic/Constrictive: Healing with fibrosis and scar formation can obliterate the pericardial space. In extreme cases, dense encasement prevents normal diastolic expansion — constrictive pericarditis.

Fig. Acute suppurative (purulent) pericarditis — Robbins & Kumar Basic Pathology

Clinical Features

Symptoms

Chest pain: Sharp, pleuritic; relieved by sitting forward, worsened by lying supine, deep inspiration, or swallowing. Radiates to trapezius ridge or shoulder (pathognomonic of diaphragmatic pleural involvement via phrenic nerve).
Fever (usually low-grade <38°C), myalgias, malaise
Dyspnea if effusion is present

Signs

Pericardial friction rub — pathognomonic; heard in ~1/3 of cases. Best heard at the lower left sternal border with the patient leaning forward in full expiration. Classic rub has 3 components: ventricular systole, early diastole, and atrial contraction. Evanescent and migratory — requires repeated auscultation.
Sinus tachycardia
Atrial fibrillation in ~5% of cases

ECG Changes (4 Stages)

Stage	Findings
Stage I	Diffuse concave ("saddle-shaped") ST elevation in most leads; PR depression (except aVR, which shows PR elevation); Spodick's sign (downsloping TP segment)
Stage II	ST returns to baseline; T waves flatten
Stage III	T-wave inversions
Stage IV	ECG normalizes

Key differentiator from STEMI: diffuse ST elevation across multiple vascular territories (not localized), concave morphology, PR depression, no reciprocal changes (except aVR).

ECG in acute pericarditis showing diffuse ST elevation and PR depression

12-lead ECG: diffuse concave ST elevation in leads I, II, aVF, V2–V6; PR depression in II; PR elevation and ST depression in aVR — classic pericarditis pattern

Diagnosis

Diagnostic criteria — at least 2 of 4 required:

Pericarditic chest pain
Pericardial friction rub
New widespread ST elevation or PR depression on ECG
New or worsening pericardial effusion

Investigations

Test	Findings
ECG	Diffuse ST elevation, PR depression (Stage I)
CRP/ESR/WBC	Elevated (CRP used to monitor treatment response and guide tapering)
Troponin	Elevated in ~30% (myopericarditis)
Echocardiography	Pericardial effusion; rule out tamponade; baseline recommended
CXR	Enlarged cardiac silhouette if effusion >250 mL ("water-bottle" heart)
CT/CMR	Pericardial thickening, enhancement; CMR best for myocardial involvement

High-Risk Features (Warrant Hospitalization)

Fever >38°C
Subacute onset
Large effusion
Cardiac tamponade
Failure of initial NSAID treatment
Immunosuppressed state
Trauma
Anticoagulant therapy

Treatment

First-Line (Acute Idiopathic/Viral)

Drug	Dose	Duration	Taper
Aspirin	750–1000 mg q8h	1–2 weeks	Decrease every 1–2 weeks over 2–3 weeks
Ibuprofen	600–800 mg q8h	1–2 weeks	Decrease every week for 2–3 weeks
Colchicine (adjunct — reduces recurrences by ~50%)	0.5 mg once daily (<70 kg) or 0.5 mg bid (≥70 kg)	3 months	Taper not usually required
Gastroprotection (PPI)	With all NSAID regimens	—	—

CRP-guided duration: taper once patient is asymptomatic and CRP normalized
Corticosteroids: reserved for cases refractory to NSAIDs + colchicine, or when NSAIDs are contraindicated (e.g., pregnancy); avoid as first-line — associated with higher recurrence rates

Recurrent Pericarditis

Repeat NSAIDs + colchicine
Corticosteroids if refractory (low-dose prednisone, slow taper)
Anakinra (IL-1β receptor antagonist): promising for colchicine-refractory cases
Pericardiectomy: last resort

A 2024 meta-analysis confirmed efficacy and safety of IL-1 inhibitors (including anakinra and rilonacept) in recurrent pericarditis management [PMID: 38809412].

Specific Etiologies

Uremia: Intensive dialysis + NSAIDs (indomethacin 25 mg TID); pericardial window if refractory
Bacterial/TB: Pathogen-specific antibiotics; TB requires full anti-tuberculous therapy
Post-MI (Dressler): NSAIDs or aspirin; avoid NSAIDs in early post-MI (impair healing)
Autoimmune: Treat underlying disease; hydroxychloroquine for SLE

Complications

Complication	Features
Pericardial effusion	Variable size; assess hemodynamic significance
Cardiac tamponade	Beck's triad: hypotension, JVD, muffled heart sounds; pulsus paradoxus >10 mmHg; requires urgent pericardiocentesis
Constrictive pericarditis	Late sequela; right-sided venous congestion + low CO; similar to restrictive cardiomyopathy; definitive Rx = pericardiectomy
Recurrence	Up to 30% of patients; risk factors: fever, large effusion, subacute course, initial NSAID failure

Prognosis & Disposition

60% full recovery within 1 week; ~80% within 3 weeks
Up to 30% recurrence rate
Nonviral/non-idiopathic cases have higher rates of progression to constrictive pericarditis
Athletes should avoid competitive sports until asymptomatic (expert consensus)
Outpatient management is appropriate for low-risk, uncomplicated cases; hospitalization for high-risk features

Sources: Braunwald's Heart Disease (11e), Rosen's Emergency Medicine, Robbins & Kumar Basic Pathology

Recent evidence note: A 2024 systematic review/meta-analysis [PMID: 38809412] supports IL-1 inhibitors (anakinra, rilonacept) as effective and safe in recurrent pericarditis refractory to conventional therapy. A 2026 systematic review [PMID: 41276190] catalogued drug-induced pericarditis cases — clozapine, hydralazine, and procainamide among the most frequently implicated agents.

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