Pericarditis means inflammation of the pericardium, the thin, two-layered sac that surrounds your heart. The irritated layers can rub against each other and the chest wall, which often causes sharp, stabbing chest pain that may feel worse when you take a deep breath or lie flat, and better when you sit up and lean forward. The swollen pericardium can also hold extra fluid (a pericardial effusion), which in severe cases can press on the heart and make it hard to pump. Pericarditis can last days to weeks; some people have repeated episodes. Mayo Clinic

Pericarditis means irritation and inflammation of the pericardium—the thin, double-layered sac that surrounds your heart. When this sac becomes inflamed, it can cause sharp, pleuritic chest pain (worse with deep breathing), often relieved by sitting up and leaning forward, and you might hear a scratchy pericardial friction rub with a stethoscope. Doctors diagnose it when typical chest pain is present with supportive signs like a new pericardial effusion (fluid around the heart), or ECG changes such as widespread ST-segment elevation and PR-segment depression, and blood tests showing inflammation (CRP/ESR) or heart irritation (troponin). Most cases are viral/idiopathic and get better with anti-inflammatory therapy and rest; a minority can recur or progress to tamponade (dangerous pressure from fluid) or constriction (a stiff, scarred pericardium). NCBI+2Life in the Fast Lane • LITFL+2

Other names

People may say pericardial inflammation or acute pericarditis for a sudden episode. When it keeps coming back, it’s called recurrent pericarditis. If fluid around the heart builds up and squeezes it, that’s cardiac tamponade, a medical emergency. If the pericardial sac becomes thick and stiff and limits the heart’s filling over time, doctors call it constrictive pericarditis. A special post-heart-injury form after a heart attack or heart surgery is post-myocardial infarction syndrome (Dressler’s syndrome), which is an autoimmune pericarditis. European Society of Cardiology+1

Types

1) Acute pericarditis.
Symptoms start suddenly and usually last under 4–6 weeks. The classic story is sharp, pleuritic chest pain plus a “friction rub”—a scratchy sound a clinician hears with a stethoscope as the inflamed heart covering rubs with each heartbeat. Doctors diagnose acute pericarditis when at least two of these are present: typical chest pain, a pericardial rub, new widespread ST-segment elevation or PR-segment depression on ECG, or a new/worsening pericardial effusion.

2) Incessant and chronic pericarditis.
If symptoms persist beyond 4–6 weeks but resolve by 3 months, it’s called incessant pericarditis. If they last more than 3 months, it’s chronic pericarditis. Some people have long symptom-free periods with later flares; that pattern is called recurrent pericarditis (see below). NCBI

3) Recurrent pericarditis.
This means a new bout of pericarditis after a symptom-free gap of about 4–6 weeks following an initial episode. Recurrences are fairly common in idiopathic/viral cases unless effective anti-inflammatory therapy is used to full resolution. NCBI

4) Pericardial effusion and cardiac tamponade.
Inflammation can lead to fluid build-up between the pericardial layers (effusion). If fluid accumulates quickly or in large amounts, it can compress the heart and cause tamponade, with low blood pressure, fast heartbeat, and shortness of breath—this needs urgent drainage. European Society of Cardiology

5) Constrictive pericarditis (and effusive-constrictive disease).
With long-standing inflammation, the pericardium can scar and stiffen, preventing the heart from filling normally. People may develop leg swelling, belly swelling, and breathlessness on exertion; some have both fluid around the heart and a stiff sac (effusive-constrictive pericarditis). NCBI

Common causes

1) Idiopathic (unknown).
In many cases, doctors cannot find a single clear cause. In high-income countries, most “idiopathic” cases are believed to be viral infections that the body has already cleared by the time symptoms appear. The outlook is usually good, but recurrences can happen.

2) Viral infections (e.g., coxsackie/enteroviruses, adenovirus, influenza).
Viruses can inflame the pericardial lining after a cold or stomach bug. People often report a recent fever, sore throat, or cough before the chest pain starts.

3) COVID-19.
SARS-CoV-2 can trigger pericardial inflammation during or after infection. Chest pain and shortness of breath may appear even as other symptoms improve.

4) HIV infection.
HIV itself and related infections (like tuberculosis) raise the risk of pericarditis, especially when immunity is low.

5) Bacterial infections (including tuberculosis).
Bacteria can infect the pericardium directly—from pneumonia, bloodstream infections, or after chest surgery. Tuberculous pericarditis remains a major cause in many parts of the world.

6) Fungal infections.
More rare, but fungi such as Histoplasma or Aspergillus can involve the pericardium, mainly in people with weakened immune systems.

7) Parasitic infections.
Parasites like Echinococcus (hydatid disease) or Toxoplasma can affect the pericardium, though this is uncommon and more likely in specific regions.

8) Post-myocardial infarction pericarditis (early).
Inflammation can occur in the first few days after a heart attack due to irritation from the damaged heart muscle next to the pericardium.

9) Dressler syndrome (late post-MI or post-cardiac injury).
Weeks after a heart attack, heart surgery, or chest trauma, the immune system can overreact to heart tissue, causing fever, chest pain, and effusion.

10) Post-pericardiotomy syndrome.
After heart surgery, the pericardium can become inflamed as part of the same “post-injury” immune reaction, leading to chest pain and fevers.

11) Aortic dissection.
A tear in the aorta can leak blood into the pericardial sac, causing sudden pericarditis symptoms and possibly tamponade—this is an emergency.

12) Uremia (advanced kidney failure).
Waste products that build up when kidneys fail can irritate the pericardium. Modern dialysis has made classic uremic pericarditis less common, but it still occurs.

13) Autoimmune diseases (e.g., lupus, rheumatoid arthritis, Sjögren’s, vasculitis).
The immune system can mistakenly attack the pericardium, leading to recurrent inflammation and sometimes significant effusions.

14) Autoinflammatory syndromes (e.g., Familial Mediterranean Fever).
Genetic conditions that cause repeated “sterile” inflammation can trigger periodic pericarditis attacks.

15) Hypothyroidism (low thyroid).
Severe, long-standing low thyroid function can cause cholesterol-rich pericardial effusions and chest discomfort.

16) Malignancy (cancer).
Cancers—especially lung, breast, lymphoma, leukemia, or spread from elsewhere—can involve the pericardium, often causing large, sometimes bloody, effusions.

17) Radiation therapy to the chest.
Past radiation for cancers (like lymphoma or breast cancer) can later scar or inflame the pericardium, leading to effusion or constriction.

18) Medications (drug-induced).
Certain drugs (for example hydralazine, isoniazid, procainamide, methyldopa, clozapine, some chemo agents) can trigger pericarditis, often through immune reactions.

19) Trauma or procedures.
Blunt chest injury or invasive heart procedures (catheters, pacemaker/defibrillator leads) can provoke pericardial irritation or bleeding into the sac.

20) Inflammatory bowel disease and other systemic conditions.
Diseases that cause body-wide inflammation can occasionally involve the pericardium, leading to chest pain and effusion.

Sources for causes: comprehensive reviews and guidelines describe infectious (viral most common in high-income settings; TB common in many regions), autoimmune/iatrogenic, post-MI/post-pericardiotomy, metabolic (uremia, hypothyroid), and neoplastic causes. European Society of Cardiology+2Cleveland Clinic+2

Common symptoms and bedside signs

1) Sharp, “stabbing” chest pain.
Often in the center or left chest, can spread to the shoulder or back. It is classically worse with deep breaths, coughing, or lying flat, and better when sitting up and leaning forward because that position reduces rubbing of the inflamed pericardial layers. European Society of Cardiology

2) Pericardial friction rub.
A clinician may hear a scratchy, squeaky, triphasic sound with a stethoscope, best along the left chest while you lean forward and exhale. It’s highly specific for pericarditis, though it can come and go. NCBI

3) Low-grade fever and feeling unwell.
Many people describe fever, fatigue, and malaise, sometimes after a recent cold or flu-like illness, which fits with viral causes. European Society of Cardiology

4) Shortness of breath, worse when lying down.
Breathing may feel hard because painful breathing makes you take shallow breaths, and fluid around the heart or lungs can limit expansion. Symptoms often ease when you sit up. Mayo Clinic

5) Palpitations or fast heartbeat.
You may feel your heart racing. True dangerous rhythm problems are uncommon in pure pericarditis; if present, doctors consider associated myocarditis.

6) Cough or chest tightness.
Irritation near the lungs can trigger a dry cough or a sensation of pressure in the chest, sometimes mimicking other lung problems. Mayo Clinic

7) Pain with swallowing (odynophagia) or hoarseness.
A large inflamed pericardial sac can press on the esophagus or recurrent laryngeal nerve, causing discomfort when swallowing or a hoarse voice. NCBI

8) Shoulder or trapezius pain.
Irritation of the phrenic nerve that runs near the pericardium can send pain to the left shoulder or neck (trapezius ridge). NCBI

9) Night sweats and weight loss.
These “systemic” symptoms raise concern for infections like tuberculosis or cancers when they occur with pericarditis. European Society of Cardiology

10) Leg swelling and belly swelling.
With constrictive pericarditis or tamponade, blood backs up, causing ankle edema and abdominal fluid (ascites). NCBI

11) Lightheadedness or fainting.
If tamponade develops, the heart cannot fill well, blood pressure drops, and people may feel dizzy or pass out—this is an emergency. European Society of Cardiology

12) Chest wall tenderness (often not pericarditis).
If pressing on the ribs reproduces the pain, it often points to musculoskeletal pain rather than true pericarditis; this helps doctors sort out causes. AAFP

13) Hiccups.
Irritation of the diaphragm from an inflamed pericardium can trigger hiccups in some cases. European Society of Cardiology

14) Reduced exercise tolerance.
Because the inflamed or constricted pericardium can limit heart filling and output, you may tire easily with activities you usually tolerate. NCBI

15) Anxiety or a sense of impending doom.
Sharp chest pain can be frightening and may cause anxiety; doctors must also rule out heart attack, which can feel similar early on. NCBI

Diagnostic tests

A) Physical exam (what the clinician checks at the bedside)

1) Heart sound: pericardial friction rub.
A scratchy, “leather-on-leather” sound heard best with the diaphragm at the left sternal border, often when you lean forward. It strongly supports pericarditis. European Society of Cardiology

2) Vital signs (fever, pulse, blood pressure).
Low-grade fever suggests inflammation or infection; a fast heart rate is common with pain or effusion; low blood pressure can signal tamponade and requires urgent care. AAFP

3) Jugular venous pressure (JVP).
A visibly raised neck vein pressure can indicate impaired heart filling from effusion/tamponade or constriction; doctors assess the height and respiratory changes in JVP. European Society of Cardiology

4) Pulsus paradoxus (manual blood-pressure test).
This is a larger-than-normal drop in systolic BP (>10 mmHg) when you breathe in. It suggests cardiac tamponade or severe airway disease and is checked with a cuff while you inhale and exhale. European Society of Cardiology

5) Kussmaul sign.
Instead of falling, the neck veins rise with inspiration. This points to constrictive pericarditis or other causes of poor right-heart filling. ScienceDirect

6) Pericardial “knock.”
A sharp early diastolic sound from a stiff pericardium in constrictive pericarditis, sometimes heard shortly after the normal first heart sound. NCBI

7) Lung exam.
Dullness at the bases and reduced breath sounds may suggest pleural effusions, which can accompany pericarditis, especially with inflammation or heart failure. European Society of Cardiology

8) Peripheral edema and hepatomegaly.
Swelling of the legs and an enlarged, tender liver can appear with right-sided pressure overload from constriction or tamponade. NCBI

9) Chest wall palpation.
Tenderness over the ribs or cartilage supports a muscle/joint source (costochondritis) rather than pericardial inflammation, helping avoid misdiagnosis. AAFP

10) Respiratory/positional provocation.
Clinicians may ask you to sit up and lean forward or take a deep breath to see if pain changes—a classic pattern in pericarditis. European Society of Cardiology

B) Electrodiagnostic tests (electrical tracings of the heart)

11) 12-lead ECG (electrocardiogram).
Typical early finding is diffuse, concave (“saddle-shaped”) ST-segment elevation with PR-segment depression in many leads and PR elevation in aVR—different from a heart-attack pattern, which is usually localized with reciprocal changes. These ECG changes evolve over four stages from ST elevation to T-wave inversion and later normalization. European Society of Cardiology

12) Serial ECGs over time.
Repeating ECGs can show the evolution of stages (from early ST elevation to later T-wave inversion), which supports pericarditis rather than a single-territory heart attack. NCBI

13) Spodick sign.
A down-sloping TP segment on ECG, best seen in leads II, V4–V6, is an early supportive clue and appears in a meaningful fraction of acute cases. Life in the Fast Lane • LITFL

14) Low QRS voltage or electrical alternans.
Very large effusions can cause small-amplitude QRS complexes and beat-to-beat alternation in QRS height (electrical alternans), suggesting swinging of the heart in fluid and possible tamponade. Life in the Fast Lane • LITFL

C) Laboratory & pathological tests (blood and fluid studies)

15) Inflammatory markers (CRP, ESR, WBC).
Raised C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and white blood cell count support active inflammation and help track recovery as levels fall with treatment. European Society of Cardiology

16) Cardiac enzymes (troponin, CK-MB).
These may be mildly elevated if the heart muscle is also irritated (so-called myopericarditis). Troponin helps rule out a heart attack but, when elevated with pericarditis symptoms, points to combined involvement.

17) Kidney function tests (BUN, creatinine).
High levels suggest uremia, a known cause of pericarditis in advanced kidney disease, and guide the need for dialysis-related care. NCBI

18) Thyroid tests (TSH).
Low thyroid function can be linked to pericardial effusion; checking TSH helps find a treatable cause. European Society of Cardiology

19) Autoimmune panels (ANA, anti-dsDNA, RF/anti-CCP, ANCA).
These blood tests look for lupus, rheumatoid arthritis, vasculitis and other immune causes when symptoms or exam suggest them. European Society of Cardiology

20) Infection testing (blood cultures, TB tests, HIV/hepatitis tests).
Cultures and IGRA/PPD for tuberculosis and relevant viral tests (e.g., HIV, hepatitis) are used when infection is suspected. Pericardial fluid—if drained—can be sent for cell count, protein/LDH (exudate), Gram stain/culture, cytology, and PCR for TB/viruses.

D) Imaging & hemodynamic studies

21) Chest X-ray.
Often normal in uncomplicated acute pericarditis. If the effusion is large, the heart may look enlarged (“water-bottle” shape), and there may be small pleural effusions. European Society of Cardiology

22) Transthoracic echocardiogram (heart ultrasound).
First-line test. It shows fluid around the heart, its amount, and whether there are signs of tamponade (e.g., right-sided chamber collapse, very full IVC, abnormal flow with breathing). Ultrasound also helps guide safe fluid drainage.

23) Doppler echocardiography for constriction.
Doppler patterns (like respirophasic variation in mitral/tricuspid inflow and abnormal septal motion) help tell constrictive pericarditis from restrictive cardiomyopathy.

24) Cardiac CT.
CT can show pericardial thickening, calcification, or large effusions and identify problems in nearby structures (e.g., aortic disease) that could trigger pericarditis. European Society of Cardiology

25) Cardiac MRI (CMR).
CMR can display inflammation and scarring in the pericardium (and heart muscle) using late gadolinium enhancement and edema-sensitive sequences. It helps confirm myopericarditis or constrictive pericarditis.

26) Cardiac catheterization (hemodynamics) for tricky cases.
If constrictive pericarditis is suspected and noninvasive tests are unclear, pressure measurements in the heart can show diastolic pressure equalization and discordant ventricular pressure changes with breathing—patterns that support constriction.

27) Pericardiocentesis (diagnostic and therapeutic).
Removing fluid with a needle can relieve tamponade and allows lab testing of the fluid (infection, cancer cells, TB). In suspected infectious or malignant causes, doctors may drain even small effusions to obtain a diagnosis.

28) Bedside ultrasound in the emergency department.
Point-of-care echo quickly checks for effusion and signs of tamponade in people with unstable blood pressure or severe chest symptoms. European Society of Cardiology

29) Observation/telemetry for rhythm issues.
Continuous heart-rhythm monitoring can catch transient arrhythmias; these are not common in isolated pericarditis, but monitoring is considered when symptoms are severe or myocarditis is suspected. NCBI

30) Follow-up CRP or imaging to confirm resolution.
Doctors often repeat CRP or echocardiography to be sure the inflammation and any effusion are settling, which helps guide when it’s safe to return to normal activity.

Non-Pharmacological Treatments

1. Relative rest & activity restriction (2–4 weeks) — Gentle daily living only until pain, CRP, and ECG normalize; prevents mechanical irritation and reduces recurrence risk. Purpose: reduce inflammation load. Mechanism: less pericardial shear stress while healing. PubMed

2. Sleep with head elevated — Propping up reduces pleuritic pain and breathlessness from effusion. Purpose: symptom relief. Mechanism: positional reduction of pericardial pressure on adjacent structures. PubMed

3. Graduated return to exercise — After symptom and CRP resolution, increase activity slowly to avoid flares. Purpose: safe conditioning. Mechanism: avoids re-triggering inflammation during healing. PubMed

4. Cold/warm compresses — Local chest wall comfort for pain. Purpose: non-drug analgesia. Mechanism: thermal modulation of superficial nociceptors (symptom-level). (Supportive only.) PubMed

5. Breathing exercises — Pursed-lip/diaphragmatic breathing may ease pleuritic discomfort and anxiety. Purpose: comfort and relaxation. Mechanism: lowers sympathetic tone and perceived pain. PubMed

6. Stress reduction (mindfulness, CBT, gentle yoga) — Calms pain-anxiety cycle and improves adherence to rest. Purpose: quality-of-life support. Mechanism: reduces adrenergic arousal that can amplify pain perception. (Adjunct only.) PubMed

7. Hydration and small meals — Avoid large meals that worsen chest pressure; keep bowels regular while on high-dose NSAIDs/colchicine. Purpose: comfort and GI protection. Mechanism: minimizes reflux/straining. PubMed

8. Avoid alcohol during recovery — Alcohol can aggravate gastritis and interact with NSAIDs. Purpose: reduce GI bleeding risk. Mechanism: less mucosal injury while on NSAIDs. FDA Access Data

9. Avoid smoking — Smoking worsens overall cardiovascular health and healing. Purpose: heart protection. Mechanism: reduces systemic inflammation and vascular stress. PubMed

10. Vaccinations as indicated (e.g., influenza) — Reduces infection-triggered relapses. Purpose: prevent infectious triggers. Mechanism: lower viral illnesses that can precipitate pericarditis. PubMed

11. Salt moderation — If there’s effusion or borderline heart function, excess sodium may worsen fluid retention. Purpose: reduce fluid symptoms. Mechanism: neurohormonal/sodium-water balance. PubMed

12. Gastroprotection habits — Take NSAIDs with food; consider PPI per clinician advice. Purpose: prevent ulcers/bleeding. Mechanism: food buffers acid; PPIs reduce gastric acid secretion. FDA Access Data

13. Follow inflammatory markers (CRP) with your clinician — Guides when to stop therapy to reduce relapse. Purpose: tailor duration. Mechanism: treat until biochemical quiescence. PubMed

14. Education on red-flag symptoms — Knowing signs of tamponade prompts urgent care. Purpose: safety. Mechanism: early recognition prevents shock. PMC

15. Nutrition pattern (Mediterranean-style) — Emphasizes anti-inflammatory foods while you recover. Purpose: overall risk reduction. Mechanism: shifts eicosanoid milieu and antioxidants. (Adjunctive only.) Office of Dietary Supplements

16. Limit strenuous isometric activities — Heavy lifting temporarily avoided to reduce pain spikes. Purpose: avoid flares. Mechanism: prevents abrupt intrathoracic pressure changes. PubMed

17. Sleep hygiene — Good sleep lowers pain sensitivity and aids healing. Purpose: comfort and recovery. Mechanism: normalizes neuro-immune responses. PubMed

18. Adherence check-ins — Regular follow-up optimizes tapering and relapse prevention. Purpose: outcomes. Mechanism: early dose adjustments. PubMed

19. Comorbidity control — Treat thyroid, autoimmune, renal, or TB disease to prevent ongoing triggers. Purpose: address root cause. Mechanism: removes inflammatory drivers. PubMed

20. Family/work pacing plan — Temporary adjustments reduce stress and allow recovery. Purpose: practical healing. Mechanism: lowers psychological stress load. PubMed

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Drug Treatments

Treatment strategy note: Most acute cases use a high-dose NSAID plus colchicine; refractory or recurrent cases may need steroid-sparing agents and, now, rilonacept (the only FDA-approved therapy for recurrent pericarditis). Always pair NSAIDs with GI protection as appropriate. PubMed+1

1. Aspirin (NSAID) — Common first-line after MI or when aspirin is preferred. Typical pericarditis regimens use high doses (e.g., 650–1000 mg every 6–8 hours) then taper as pain/CRP improve; dosing is individualized and must consider bleeding risk. FDA labeling warns about GI bleeding and Reye’s in children and gives product-specific strengths. Purpose: reduce pain/inflammation. Mechanism: COX-1/COX-2 inhibition lowering prostaglandins. Side effects: GI upset/ulcer, bleeding risk. (Pericarditis use off-label; dose/safety from aspirin labels.) FDA Access Data+1

2. Ibuprofen (NSAID) — A frequent first-line choice (e.g., 600–800 mg three to four times daily in adults initially; then taper). Rx labels cap total daily dose (≤3,200 mg/day) and warn about CV and GI risks; OTC labels cap lower. Purpose: symptom control + inflammation reduction. Mechanism: reversible COX inhibition. Side effects: dyspepsia, edema, renal effects, rare CV events; use gastroprotection if risk is high. (Pericarditis use off-label.) FDA Access Data+2FDA Access Data+2

3. Indomethacin (NSAID) — Potent NSAID sometimes used when others fail. Labels emphasize GI/CV warnings and lowest effective dose for shortest duration. Purpose: anti-inflammatory pain relief. Mechanism: COX inhibition. Side effects: GI toxicity, CNS effects (headache, dizziness). (Off-label for pericarditis.) FDA Access Data+1

4. Naproxen (NSAID) — Longer half-life; regimens often 500 mg twice daily initially, then taper with symptom control. Labels highlight GI/CV warnings and specific strengths. Purpose: reduce pain/inflammation. Mechanism: COX inhibition. Side effects: GI upset/bleeding, renal effects; consider PPI. (Off-label for pericarditis.) FDA Access Data+1

5. Colchicine — Guideline cornerstone for acute and recurrent pericarditis (but in the U.S. it’s FDA-approved for gout/FM F, not pericarditis). Typical adult dose commonly used in guidelines: 0.5–0.6 mg once or twice daily (weight-adjusted), for 3 months (acute) or 6–12 months (recurrent), adjusted for renal/hepatic function and interactions. Purpose: halves recurrence risk when added to NSAIDs. Mechanism: microtubule disruption reduces neutrophil chemotaxis/inflammasome activity. Side effects: GI upset, cytopenias with interacting drugs. (Dosing/safety from FDA labels.) FDA Access Data+2FDA Access Data+2

6. Prednisone/Prednisolone (corticosteroid) — Reserved for specific causes or NSAID/colchicine intolerance; use lowest effective dose with slow taper to limit recurrences. Purpose: anti-inflammatory immunosuppression. Mechanism: broad cytokine suppression. Side effects: hyperglycemia, weight gain, infection risk, relapse on rapid taper. (Label safety/dosing info.) FDA Access Data+1

7. Rilonacept (ARCALYST) — First and only FDA-approved therapy for recurrent pericarditis and to reduce recurrence risk (≥12 years). Label dosing commonly: 320 mg SC loading, then 160 mg weekly (adult); pediatric weight-based. Purpose: rapidly controls pain and prevents relapse. Mechanism: IL-1α/β “trap” that neutralizes the cytokine driver. Side effects: injection-site reactions, URIs; monitor for infections. ARCALYST HCP+2FDA Access Data+2

8. Anakinra (KINERET) — IL-1 receptor antagonist used off-label for colchicine-resistant, steroid-dependent recurrent pericarditis (supported by AIRTRIP trial/observational data). Label dosing for approved conditions is 100 mg SC daily (adjust per renal function). Purpose: reduce inflammation and recurrences when standard therapy fails. Mechanism: blocks IL-1 signaling. Side effects: infections, neutropenia, injection reactions. (Use off-label for pericarditis; label provides safety framework.) FDA Access Data+2FDA Access Data+2

9. Azathioprine — Steroid-sparing immunomodulator off-label in recurrent autoimmune-driven cases. Purpose: allow steroid taper and reduce flares. Mechanism: purine synthesis inhibition dampening lymphocyte proliferation. Side effects: leukopenia, liver injury; TPMT/NUDT15 considerations. (Use safety from FDA labeling.)

10. Methotrexate — Another off-label steroid-sparing option in refractory autoimmune pericarditis. Purpose: maintain remission. Mechanism: anti-folate effects reduce immune activation; weekly dosing. Side effects: cytopenias, liver toxicity; folate supplement helps. (Use safety from FDA labeling.)

11. Mycophenolate mofetil — Off-label immunosuppressant sometimes used when others fail. Purpose: steroid-sparing. Mechanism: inosine monophosphate dehydrogenase inhibition → less lymphocyte proliferation. Side effects: GI upset, infections, leukopenia. (Use safety from FDA labeling.)

12. Intravenous immune globulin (IVIG) — Off-label rescue in immune-mediated or refractory cases. Purpose: immunomodulation during severe flares. Mechanism: Fc-mediated immune regulation. Side effects: headache, aseptic meningitis, thrombosis risk; requires specialist supervision.

13. Tocilizumab — Off-label IL-6 pathway blocker in selected refractory overlaps. Purpose: steroid-sparing symptom control. Mechanism: IL-6 receptor blockade. Side effects: infection risk, liver enzyme rise; lab monitoring needed.

14. Proton pump inhibitor (e.g., omeprazole) — For gastroprotection during high-dose NSAID therapy. Purpose: cut ulcer/bleeding risk. Mechanism: H+/K+ ATPase inhibition reduces acid. Side effects: headache, diarrhea; drug interactions possible. (Label-based safety.)

15. H2-blocker + ibuprofen combination (DUEXIS®) — Combines ibuprofen with famotidine to reduce NSAID GI risk where appropriate. Purpose: maintain NSAID effect with gastric protection. Mechanism: COX inhibition + H2 blockade. Side effects: those of NSAIDs plus H2 blocker effects. FDA Access Data

16. Acetaminophen (paracetamol) — Adjunct for pain/fever when NSAID doses are being tapered or contraindicated (note: not anti-inflammatory). Purpose: analgesic/antipyretic. Mechanism: central COX effects. Side effects: hepatotoxicity at high doses. (Label-based safety.)

17. Isoniazid (when TB pericarditis is proven/suspected; part of multi-drug regimen per TB protocols). Purpose: treat the cause. Mechanism: mycolic acid synthesis inhibition. Side effects: hepatitis, neuropathy—give pyridoxine. (Label-based safety; use under specialist TB care.)

18. Rifampin (as part of TB regimen). Purpose/Mechanism: bactericidal RNA polymerase inhibition. Side effects: drug interactions, hepatitis; orange secretions. (Label-based safety.)

19. Low-dose aspirin for post-MI cases — Preferred anti-inflammatory in post-MI pericarditis because other NSAIDs may interfere with myocardial healing/antiplatelet therapy. Purpose: pain/inflammation with cardiac safety context. Mechanism/side effects: as above.

20. Corticosteroid pulse (e.g., IV methylprednisolone) — For selected severe autoimmune or incessant flares under specialist care, then slow taper to avoid relapse. Purpose: rapid inflammation control. Mechanism/side effects: potent glucocorticoid effects; infection risk. (Label-based safety.)

Key drug references used above include FDA labels for aspirin, ibuprofen, indomethacin, naproxen, colchicine, rilonacept, anakinra, and combination products; see citations. FDA Access Data+8FDA Access Data+8FDA Access Data+8

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Dietary Molecular Supplements

Important: No supplement cures pericarditis. Discuss each with your clinician for safety and interactions.

1. Omega-3 fatty acids (EPA/DHA) — 1–2 g/day of combined EPA/DHA from diet/supplements is commonly used for general anti-inflammatory support. They shift eicosanoids toward less inflammatory mediators, which might modestly aid symptom control alongside standard therapy. Watch for bleeding risk at high doses, especially with anticoagulants. Office of Dietary Supplements

2. Curcumin (turmeric extract) — Typical research doses 500–1000 mg/day of standardized curcuminoids; bioavailability-enhanced forms are often needed. Curcumin inhibits multiple inflammatory signaling pathways; early data suggest pain/inflammation benefits in other conditions, but pericarditis-specific trials are lacking. GI upset and drug interactions can occur. NCCIH+1

3. Vitamin D3 — Correcting deficiency (dose individualized; many adults need 1000–2000 IU/day, but test-based plans are best) supports normal immune function. Vitamin D modulates innate/adaptive immunity and antimicrobial peptides; aim for clinician-guided repletion, not megadoses. Office of Dietary Supplements+1

4. Magnesium — If dietary intake is low, supplementing 100–200 mg/day (elemental) may support heart rhythm and blood pressure modestly; avoid in significant kidney disease. Evidence for BP effect is small; too much causes diarrhea. Office of Dietary Supplements+1

5. Coenzyme Q10 — Typical 100–200 mg/day with fat-containing meals; supports mitochondrial energy pathways. Evidence for cardiac outcomes is mixed; consider only as supportive with clinician input. NCCIH+1

6. Ginger extract — 500–1000 mg/day is often used for anti-inflammatory/anti-nausea effects; may help NSAID-related dyspepsia but can increase bleeding risk with anticoagulants. Evidence in pericarditis is absent.

7. Quercetin — 250–500 mg/day used in studies for general anti-inflammatory effects; theoretical benefits via antioxidant pathways, but data are limited and interactions exist.

8. Selenium (for deficiency) — 50–100 mcg/day repletion in low-selenium states supports antioxidant enzymes; chronic high doses are toxic. No pericarditis-specific data.

9. Vitamin C — 250–500 mg/day as general antioxidant support; high doses can cause GI upset and kidney stones in predisposed people.

10. Boswellia serrata — Standardized extracts (e.g., 300–500 mg 2–3 times daily) have anti-inflammatory triterpenes; pericarditis evidence is lacking, so treat as experimental adjunct only.

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Immune-Modulating / Regenerative Therapies

There are no approved stem-cell drugs for pericarditis and no proven “immunity boosters” that treat it. In difficult, recurrent cases, clinicians may use immune-modulating therapy:

1. Rilonacept — Weekly IL-1 inhibitor with rapid pain relief and markedly reduced recurrence risk in recurrent pericarditis (FDA-approved for this use). Dose and safety as above; monitor for infections. FDA Access Data+1

2. Anakinra — Daily IL-1 receptor antagonist used off-label for steroid-dependent, colchicine-resistant disease; adjust for renal function and monitor neutrophils/infections. FDA Access Data

3. Azathioprine — Steroid-sparing oral immunosuppressant in autoimmune-associated pericarditis; requires CBC/LFT monitoring.

4. Methotrexate — Weekly oral or subcutaneous dosing with folate; monitor CBC/LFTs and avoid in pregnancy.

5. Mycophenolate mofetil — Oral agent that reduces lymphocyte proliferation; GI and infection risks; specialist oversight.

6. IVIG — In hospital/infusion center for selected immune-mediated flares; monitor for thrombosis, renal effects, and aseptic meningitis.

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Procedures / Surgeries

1. Pericardiocentesis (needle drainage) — A catheter is guided into the pericardial space to remove fluid urgently if cardiac tamponade is present, or diagnostically for suspected infection/malignancy. It rapidly relieves pressure so the heart fills normally again and often yields fluid for testing. European Society of Cardiology+1

2. Pericardial window (surgical drainage) — A small piece of pericardium is removed via subxiphoid/VATS approach to create a permanent drainage path into the chest or abdomen, used for recurrent/loculated effusions or malignant effusions that re-accumulate after taps. Medscape+1

3. Pericardiectomy (partial/total removal) — For constrictive pericarditis or highly refractory recurrent disease, surgeons remove most or all of the pericardium to restore cardiac filling; complete pericardiectomy is associated with better outcomes when feasible. PMC+1

4. Percutaneous balloon pericardiotomy — A catheter-based technique that opens a controlled window between pericardium and pleura, used in selected recurrent effusions (especially malignant). revespcardiol.org

5. Catheter-guided pericardial biopsy — Performed when TB or malignancy is strongly suspected and fluid cytology is nondiagnostic; helps direct causal therapy. European Society of Cardiology

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Preventions

1. Treat infections promptly and complete prescribed courses.

2. Follow NSAID + colchicine plans and tapers exactly; do not stop early when pain fades.

3. Avoid strenuous exercise until symptoms, ECG, and CRP normalize.

4. Use gastroprotection with high-dose NSAIDs when appropriate.

5. Keep vaccinations current (e.g., influenza) to reduce viral triggers.

6. Manage autoimmune, thyroid, kidney disease to prevent ongoing inflammation.

7. For TB risk, ensure evaluation and therapy if indicated.

8. Limit alcohol and avoid smoking.

9. Maintain a heart-healthy, anti-inflammatory diet pattern. 10) Keep scheduled follow-ups for monitoring CRP and adjusting therapy. PubMed

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When to See a Doctor Urgently

Seek immediate care for severe or worsening chest pain, fainting, marked shortness of breath, new confusion, very low blood pressure, or signs of tamponade (extreme breathlessness, lightheadedness, or collapse). Call your clinician promptly if pain returns during taper, fever persists >72 hours on treatment, or new swelling/rapid weight gain occurs. These red flags are emphasized in cardiology guidance because tamponade can be rapidly life-threatening without drainage. PMC

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What to Eat and What to Avoid

1. Do eat: fish (salmon/sardines) for omega-3s 2–3×/week

2. Do eat: mixed vegetables, berries, whole grains, legumes, nuts.

3. Do eat: olive oil in place of saturated fats.

4. Do hydrate: water, not sugary drinks.

5. Do moderate salt if there’s fluid/effusion.

6. Avoid: heavy alcohol while on NSAIDs/steroids.

7. Avoid: very spicy/acidic meals if you have reflux on NSAIDs.

8. Avoid: energy drinks/high caffeine if palpitations worsen.

9. Caution: grapefruit with certain immunosuppressants—ask your doctor.

10. Check: supplement–drug interactions before starting anything new. (Dietary points reflect anti-inflammatory and GI-safety principles; supplements are adjuncts only.) Office of Dietary Supplements

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FAQs

1) Is pericarditis the same as a heart attack?
No. Both cause chest pain, but pericarditis pain is sharp/pleuritic and position-dependent; ECG shows diffuse ST elevation/PR depression rather than localized MI patterns. Troponin can be mildly elevated in myopericarditis, but coronary arteries are not blocked. Life in the Fast Lane • LITFL

2) How do doctors confirm the diagnosis?
Typical chest pain plus at least one of: pericardial rub, new widespread ST elevation or PR depression on ECG, or new/worsening pericardial effusion on echo; labs (CRP) support the diagnosis. PubMed

3) Why is colchicine recommended so often?
When added to NSAIDs, colchicine reduces pain and roughly halves the risk of recurrence; in the U.S. this is an off-label use (colchicine is labeled for gout and FMF), but it is a guideline mainstay worldwide. PubMed+1

4) What if my pericarditis keeps coming back?
Now we have rilonacept, the only FDA-approved treatment that both treats recurrent pericarditis and reduces recurrences; some centers also use anakinra off-label. A steroid-sparing plan (e.g., azathioprine, methotrexate) may be used. American College of Cardiology+1

5) How long should I rest?
Most people reduce activity for a few weeks and resume gradually once pain resolves and CRP/ECG normalize—your clinician individualizes this. Too-early exertion can trigger relapse. PubMed

6) Do I always need procedures?
No. Procedures are for complications: tamponade needs urgent pericardiocentesis; constriction may need pericardiectomy; recurrent malignant effusions may need a window. European Society of Cardiology+1

7) Are steroids bad for pericarditis?
They’re effective but can increase relapse if used early/high without a careful, slow taper. They’re reserved for specific situations or intolerance to NSAIDs/colchicine. PubMed

8) How long does it last?
Acute cases usually improve in days and resolve over weeks; 15–30% can recur, especially if treatment is too short or causes persist. ScienceDirect

9) Can pericarditis damage my heart?
Most recover fully. A small fraction progress to constriction (scarred pericardium) requiring surgery; early identification and treatment reduce this risk. European Society of Cardiology

10) What about exercise and sports?
Avoid competitive sports until symptom-free with normalized tests; then return under guidance to reduce recurrences. PubMed

11) Can I travel?
Once stable and pain-controlled, yes. Avoid high exertion and keep medicines handy; seek care immediately if severe chest pain or breathlessness occurs. PubMed

12) Which pain reliever is “best”?
Choice depends on your health profile; ibuprofen, naproxen, or aspirin are common, paired with colchicine. Use the lowest effective dose and gastroprotection when needed. FDA Access Data+1

13) Do supplements help?
They may offer adjunct anti-inflammatory support (e.g., omega-3s), but none replace standard therapy. Discuss safety and interactions first. Office of Dietary Supplements

14) When should I worry about tamponade?
Red flags are worsening breathlessness, fainting, profound weakness, or very low BP; this is an emergency requiring drainage. PMC

15) Are IL-1 inhibitors lifelong?
Duration is individualized; trials show strong recurrence prevention while on therapy. Clinicians may attempt cautious taper after sustained remission. AHA Journals

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: November 09, 2025.

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