What does pericarditis chest pain feel like and how is it different from a heart attack?

Pericarditis pain is typically sharp and pleuritic — worse with deep breathing, coughing, or lying flat, and relieved by sitting forward. It often radiates to the trapezius or left shoulder. Heart attack pain is usually pressure-like or crushing, radiates to the jaw or arm, and is not position-dependent. The ECG is key: pericarditis produces diffuse concave-upward ST elevation across most leads plus PR depression, rather than the regional ST changes of a heart attack. Your GP or emergency department will use ECG, troponin, and sometimes imaging to tell them apart.

What is colchicine and why is it used for pericarditis?

Colchicine is an anti-inflammatory agent (originally derived from the crocus plant, used in gout) that targets the NALP3 inflammasome pathway driving pericardial inflammation. Three landmark trials — COPE, CORP, and ICAP — showed that adding colchicine 0.5 mg twice daily for three months to standard NSAID therapy reduced pericarditis recurrence by roughly 50%. It is now first-line alongside NSAIDs for acute pericarditis. Common side effects are gastrointestinal (nausea, diarrhoea); dose adjustment is needed in kidney or liver disease.

What is myocarditis and who is at risk?

Myocarditis is inflammation of the heart muscle itself, most commonly triggered by a viral illness (Coxsackie B, parvovirus B19, adenovirus, SARS-CoV-2). It can also result from autoimmune disease, certain medications (immune checkpoint inhibitors, clozapine), or rarely mRNA COVID-19 vaccination in young males. The clinical range is wide — many cases are mild and self-limiting, but some cause dangerous arrhythmias, reduced heart function, or sudden cardiac death, particularly in young athletes. A preceding flu-like or gastrointestinal illness one to four weeks before symptoms is a common pattern.

Why is exercise restriction so important after myocarditis?

Inflamed heart muscle is vulnerable to arrhythmia under the physical demands of exercise. Vigorous or competitive sport in the setting of active myocarditis has been associated with sudden cardiac death in young people. Australian and international cardiology guidelines recommend avoiding competitive and vigorous exercise for three to six months following confirmed myocarditis. Return to sport requires cardiology assessment, normal cardiac MRI findings, normal troponin, and satisfactory exercise stress testing. This restriction is precautionary — the vast majority of people with myocarditis recover well.

What should I know about mRNA COVID-19 vaccines and myocarditis?

A rare association between mRNA COVID-19 vaccines and myocarditis has been established, predominantly affecting males aged 12 to 29, most commonly after the second dose. Rates are estimated at roughly one to ten cases per 100,000 doses. The vast majority of cases are mild and self-limiting with supportive care. ATAGI guidance recommends that people who experienced vaccine-associated myocarditis consider a non-mRNA alternative (Novavax protein-based vaccine) for future doses. For young males more broadly, Comirnaty (Pfizer) carries a lower myocarditis rate than Spikevax (Moderna). Any suspected case should be reported to TGA's DAEN system.

What is cardiac tamponade and what are the warning signs?

Cardiac tamponade is a life-threatening emergency where fluid accumulates rapidly in the pericardial sac, compressing the heart and preventing it from filling properly. The classic warning signs are Beck's triad — low blood pressure, raised jugular venous pressure (distended neck veins), and muffled or distant heart sounds — plus pulsus paradoxus (a drop of 10 mmHg or more in blood pressure on breathing in). Prompt echocardiography confirms the diagnosis; emergency drainage of the fluid (pericardiocentesis) is life-saving. Call 000 immediately for collapse, severe breathlessness, or haemodynamic instability.

Pericarditis and myocarditis

Pericarditis and myocarditis: recognition and GP management

By Dr HB Lo, FACRRM Reviewed 12 July 2026 9 min read

Pericarditis is inflammation of the sac surrounding the heart; myocarditis affects the heart muscle. Both most often follow a viral illness, presenting with chest pain, ECG changes, and sometimes a raised troponin.

Acute pericarditis is typically benign and self-limiting. First-line treatment is an NSAID plus colchicine for three months, which roughly halves the risk of recurrence. Exercise restriction until CRP normalises is essential.

Myocarditis ranges from mild and self-limiting to life-threatening arrhythmia or heart failure. Cardiac MRI confirms the diagnosis. Exercise restriction for three to six months is required after confirmed myocarditis.

Sharp chest pain in a young person following a viral illness is one of the more distinctive presentations in general practice. It may represent pericarditis — inflammation of the fibrous sac surrounding the heart — or, more worryingly, myocarditis: inflammation of the heart muscle itself. The two conditions overlap, can coexist (myopericarditis or perimyocarditis), and share a common aetiological trigger in viral infection.

Both conditions are important not to miss: pericarditis because the pain is alarming and can mimic acute coronary syndrome, and myocarditis because the minority of severe cases carries risk of arrhythmia, heart failure, or sudden cardiac death. The Cardiac Society of Australia and New Zealand (CSANZ) and international guidelines have clear frameworks for assessment and management.

A. Core clinical — the AU general-practice framework

Pericarditis

Classic presentation. Sharp, pleuritic chest pain is the hallmark of pericarditis — pain that worsens with inspiration, coughing, and swallowing, is at its worst lying flat, and characteristically eases when the patient sits upright and leans forward. Radiation to the trapezius ridge or left shoulder is distinctive and reflects pericardial contact with the diaphragmatic nerve supply. A low-grade fever, malaise, and myalgia from viral prodrome are common accompaniments.

Physical examination. A pericardial friction rub — a scratchy, triphasic sound best heard at the left lower sternal edge with the patient sitting forward and breath held in expiration — is pathognomonic when present, but is intermittent and often missed. Distant heart sounds suggest an effusion. Beck’s triad (hypotension, raised JVP, muffled heart sounds) signals tamponade and is an emergency.

ECG changes. Therapeutic Guidelines describe four classic ECG stages in pericarditis:

Diffuse concave-upward (“saddle-shaped”) ST elevation across most leads except V1 and aVR, with reciprocal ST depression in aVR; PR depression (especially in II and aVF) with PR elevation in aVR.
ST normalisation with T-wave flattening.
Diffuse T-wave inversion.
ECG normalisation over weeks.

The diffuse distribution (not regional), absence of Q waves, and PR depression distinguish pericarditis from myocardial infarction. Pericarditis ECG changes are not always present or may be subtle.

Causes. In high-income countries such as Australia, approximately 80–90% of pericarditis is idiopathic or presumed viral. Identifiable causes include Coxsackievirus, EBV, CMV, influenza, SARS-CoV-2, bacterial infection (uncommon; consider TB in people born overseas or immunocompromised), autoimmune disease (SLE, rheumatoid arthritis, scleroderma), uraemia, malignancy, drug reactions, post-cardiac surgery (post-pericardiotomy syndrome), and post-myocardial infarction (Dressler’s syndrome, 2–8 weeks post-infarction).

Diagnosis criteria. The ESC 2015 pericardial disease guidelines require two of four criteria for clinical diagnosis: (1) typical chest pain; (2) pericardial friction rub; (3) new ST elevation or PR depression on ECG; (4) new or worsening pericardial effusion.

Investigations. Standard workup includes ECG, troponin, CRP/ESR, FBE, and transthoracic echocardiogram. Troponin is normally negative in pure pericarditis — elevation implies myocardial involvement (myopericarditis) and warrants cardiology referral. CRP guides treatment duration; a falling CRP indicates settling inflammation. Selective additional testing (ANA, RF, HIV, TB quantiFERON/IGRA, blood cultures) is directed by clinical features rather than routine.

Myocarditis

Presentation. Myocarditis spans a spectrum from entirely asymptomatic (found incidentally on cardiac MRI after viral illness) to fulminant with arrhythmia, heart failure, or cardiogenic shock. Common presentations include chest pain (often indistinguishable from pericarditis when pericardial inflammation coexists), dyspnoea, palpitations, fatigue, and syncope. Tachycardia disproportionate to fever is a useful sign. A preceding viral upper respiratory or gastrointestinal illness one to four weeks earlier is common. The most feared outcome — sudden cardiac death in young athletes — is rare overall but elevates the importance of the diagnosis in active young people.

ECG and investigations. ECG findings in myocarditis are non-specific: ST-T changes, T-wave inversion, Q waves, AV block, ventricular ectopy, and sustained ventricular arrhythmia. Troponin is typically elevated. BNP or NT-proBNP rises with heart failure. Echocardiogram may show regional or global hypokinesis and reduced left ventricular ejection fraction. Cardiac MRI using Lake Louise criteria — T1 mapping, T2 mapping, and late gadolinium enhancement — is the gold standard for non-invasive diagnosis, demonstrating myocardial oedema and inflammation with a characteristic mid-wall or subepicardial (not subendocardial) distribution distinct from ischaemic injury. Coronary angiography is performed in adults with troponin elevation to exclude acute coronary syndrome before attributing the rise to myocarditis.

B. Treatment evidence — NSAID, colchicine, and when to avoid steroids

Acute idiopathic pericarditis — first-line treatment. Per eTG Cardiovascular and AMH, the combination of an NSAID plus colchicine for three months is first-line:

NSAID: ibuprofen 600 mg three times daily, or aspirin 750–1000 mg three times daily (preferred if recent myocardial infarction, given antiplatelet benefit). Naproxen is an alternative. Continue until symptoms resolve and CRP normalises, then taper over 1–2 weeks. Prescribe PPI cover.
Colchicine 0.5 mg twice daily for three months — the COPE, CORP, and ICAP trials (NEJM 2013) consistently showed ~50% reduction in recurrence compared with NSAID alone. Side effects are predominantly gastrointestinal (diarrhoea, nausea); dose reduction to 0.5 mg once daily is appropriate for those weighing under 70 kg or with renal/hepatic impairment.
Exercise restriction — until symptom resolution, CRP normalisation, and ECG resolution. Athletes require ≥3 months of restriction even for a first uncomplicated episode.

Corticosteroids: avoid as first-line. Despite their intuitive appeal as anti-inflammatory agents, corticosteroids are associated with higher rates of pericarditis recurrence and should not be used first-line in acute pericarditis. They are reserved for genuine NSAID contraindication, autoimmune aetiology, or refractory/recurrent disease.

Recurrent pericarditis. About 15–30% of patients experience recurrence within 18 months. Management involves prolonged colchicine (6+ months), and if NSAID plus colchicine fails, low-dose prednisolone with slow taper. Anakinra (an IL-1 inhibitor) is reserved for corticosteroid-dependent recurrent pericarditis and requires specialist authorisation via TGA Special Access Scheme.

Myocarditis: supportive management. There is no proven anti-inflammatory therapy for acute viral myocarditis (immunosuppression is reserved for specific autoimmune subtypes such as giant cell myocarditis and sarcoid myocarditis). Management is supportive: admission, monitoring, and guideline-directed heart failure therapy (beta-blocker, ACE inhibitor or ARNI, mineralocorticoid receptor antagonist, SGLT2 inhibitor, diuretics) where ventricular dysfunction develops. Arrhythmia management follows standard protocols. Coronary intervention is performed if ischaemia is identified. Mechanical circulatory support (IABP, ECMO) may be required in fulminant cases. Endomyocardial biopsy is reserved for fulminant presentations and situations where specific histology would alter management (giant cell, sarcoid, eosinophilic myocarditis).

C. Cardiac tamponade and constrictive pericarditis

Tamponade occurs when pericardial fluid accumulates rapidly enough to compress cardiac filling. Beck’s triad — hypotension, raised JVP, and muffled heart sounds — combined with pulsus paradoxus (systolic blood pressure fall ≥10 mmHg on inspiration) should prompt immediate echocardiography. Diastolic right ventricular collapse on echo confirms haemodynamic compromise. Pericardiocentesis (emergency pericardial drainage) is life-saving; this is a hospital procedure requiring cardiology or cardiothoracic surgery. Call 000 for any suspected tamponade.

Constrictive pericarditis is a late complication where the pericardium becomes fibrosed and calcified, preventing diastolic cardiac filling. It presents with right-sided heart failure features — peripheral oedema, ascites, raised JVP, and the characteristic Kussmaul’s sign (paradoxical JVP rise on inspiration). TB is the leading worldwide cause; idiopathic, post-surgical, and post-radiation causes are also important in Australia. Pericardiectomy is the definitive treatment and is a major surgical procedure.

D. Australian operations

Pharmacotherapy (PBS). Aspirin, ibuprofen, and naproxen are PBS general benefit. Colchicine (0.5 mg) is PBS general benefit. PPI gastric protection is PBS general benefit. Prednisolone is PBS general benefit. Anakinra (Kineret) for refractory recurrent pericarditis requires TGA Special Access Scheme or Authorised Prescriber arrangement and is not PBS-funded. Heart failure medications — ACE inhibitors, ARNIs, beta-blockers, MRAs, SGLT2 inhibitors — are PBS-subsidised per the chronic heart failure indications.

MBS items. Standard general practice consultation items (23/36/44) cover assessment. The GP Chronic Condition Management Plan items (965/967, replacing 721/723/732 from 1 July 2025 per MBS Online) are appropriate for recurrent or post-myocarditis chronic management, including allied health referral. Echocardiography (item 55113) and cardiac MRI are Medicare-rebatable for appropriate indications with specialist referral. The Heart Health Check (item 699, ≥30 years) provides a structured cardiovascular risk framework for longer-term follow-up.

Specialist referral. Cardiology referral is indicated for any troponin-positive pericarditis (myopericarditis), suspected myocarditis, large effusion or haemodynamic compromise, refractory or recurrent pericarditis, suspected constrictive pericarditis, and return-to-sport assessment post-myocarditis. CSANZ and the Heart Foundation Australia provide clinician resources and specialist directories. Telehealth cardiology improves access in regional and rural settings.

Vaccination. Annual influenza vaccination is recommended in people with established cardiac disease. Pneumococcal Prevenar 20 is recommended ≥70 years and for at-risk groups. COVID-19 boosters follow ATAGI guidance. Regarding mRNA COVID-19 vaccines: for those who experienced vaccine-associated myocarditis, ATAGI recommends considering Novavax (NVX-CoV2373, protein-based) for future doses. Any suspected adverse event should be reported to the TGA DAEN system.

Driving. Austroads Assessing Fitness to Drive 2022 applies to post-myocarditis patients with high-risk arrhythmia or significant ventricular dysfunction. Document and discuss driving fitness at follow-up.

E. Special populations

Young athletes. Myocarditis is a leading cardiovascular cause of sudden cardiac death in young athletes. The threshold for investigation is low in this population. Return to competitive sport requires cardiology clearance, normal cardiac MRI, normal troponin, absence of arrhythmia on exercise stress testing, and a minimum of three to six months from the acute illness. Pre-participation cardiac screening in athletes is not universally mandated in Australia but is an area of active clinical debate (CSANZ).

Young males and mRNA vaccination. As outlined in the FAQ above, rare vaccine-associated myocarditis clusters in males 12–29 years, most often after the second mRNA dose. The condition is typically mild and self-limiting, and benefit-risk remains clearly favourable at the population level. Clinicians should be aware of the pattern, counsel at-risk groups, and report suspected cases to TGA.

Pregnancy. Autoimmune pericarditis (lupus-related) may flare peri-partum. Colchicine is generally avoided in pregnancy (limited safety data); NSAID use is restricted after 20 weeks gestation (fetal ductus arteriosus risk). Specialist obstetric and cardiology co-management is appropriate for pericarditis or myocarditis complicating pregnancy.

Older adults. TB pericarditis, uraemic pericarditis (CKD on dialysis), malignant pericardial disease, and post-cardiac surgery pericarditis are relatively more common in older patients. A broader initial differential and aetiological workup is warranted.

Immunocompromised. Bacterial, fungal, and mycobacterial pericarditis — including TB — are important considerations. Sputum AFB, IGRA/quantiFERON, blood cultures, and pericardial fluid analysis (cytology, microscopy, AFB culture) guide management in this group.

When to escalate

Arrange urgent hospital assessment for:

Haemodynamic instability — suspected tamponade (Beck’s triad, pulsus paradoxus, hypotension) — this is an emergency, call 000.
Elevated troponin with pericarditis features (myopericarditis).
Any clinical suspicion of myocarditis in a young person — especially an athlete.
Fever over 38°C, large effusion, immunocompromised state, or failure to respond to NSAID + colchicine within a week.
Arrhythmia, syncope, or signs of heart failure.
Suspected malignant or TB pericarditis.

Refer to cardiology (non-urgent) for:

Recurrent pericarditis not controlled with NSAID + colchicine.
Post-myocarditis follow-up including cardiac MRI review and return-to-sport clearance.
Suspected constrictive pericarditis.

What this article is and is not

This is general health information based on current Australian cardiovascular guidelines — Therapeutic Guidelines (eTG), AMH, CSANZ, Heart Foundation Australia, ATAGI — and major pericarditis and myocarditis trials. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about your specific situation, including investigations and treatment, are made with your GP and treating clinicians.

For acute symptoms of chest pain, difficulty breathing, or collapse: call 000. For Australian consumer resources: HealthDirect — Pericarditis, HealthDirect — Myocarditis, Heart Foundation Australia.

Sources cited

Frequently asked questions

What does pericarditis chest pain feel like and how is it different from a heart attack?

Pericarditis pain is typically sharp and pleuritic — worse with deep breathing, coughing, or lying flat, and relieved by sitting forward. It often radiates to the trapezius or left shoulder. Heart attack pain is usually pressure-like or crushing, radiates to the jaw or arm, and is not position-dependent. The ECG is key: pericarditis produces diffuse concave-upward ST elevation across most leads plus PR depression, rather than the regional ST changes of a heart attack. Your GP or emergency department will use ECG, troponin, and sometimes imaging to tell them apart.
What is colchicine and why is it used for pericarditis?

Colchicine is an anti-inflammatory agent (originally derived from the crocus plant, used in gout) that targets the NALP3 inflammasome pathway driving pericardial inflammation. Three landmark trials — COPE, CORP, and ICAP — showed that adding colchicine 0.5 mg twice daily for three months to standard NSAID therapy reduced pericarditis recurrence by roughly 50%. It is now first-line alongside NSAIDs for acute pericarditis. Common side effects are gastrointestinal (nausea, diarrhoea); dose adjustment is needed in kidney or liver disease.
What is myocarditis and who is at risk?

Myocarditis is inflammation of the heart muscle itself, most commonly triggered by a viral illness (Coxsackie B, parvovirus B19, adenovirus, SARS-CoV-2). It can also result from autoimmune disease, certain medications (immune checkpoint inhibitors, clozapine), or rarely mRNA COVID-19 vaccination in young males. The clinical range is wide — many cases are mild and self-limiting, but some cause dangerous arrhythmias, reduced heart function, or sudden cardiac death, particularly in young athletes. A preceding flu-like or gastrointestinal illness one to four weeks before symptoms is a common pattern.
Why is exercise restriction so important after myocarditis?

Inflamed heart muscle is vulnerable to arrhythmia under the physical demands of exercise. Vigorous or competitive sport in the setting of active myocarditis has been associated with sudden cardiac death in young people. Australian and international cardiology guidelines recommend avoiding competitive and vigorous exercise for three to six months following confirmed myocarditis. Return to sport requires cardiology assessment, normal cardiac MRI findings, normal troponin, and satisfactory exercise stress testing. This restriction is precautionary — the vast majority of people with myocarditis recover well.
What should I know about mRNA COVID-19 vaccines and myocarditis?

A rare association between mRNA COVID-19 vaccines and myocarditis has been established, predominantly affecting males aged 12 to 29, most commonly after the second dose. Rates are estimated at roughly one to ten cases per 100,000 doses. The vast majority of cases are mild and self-limiting with supportive care. ATAGI guidance recommends that people who experienced vaccine-associated myocarditis consider a non-mRNA alternative (Novavax protein-based vaccine) for future doses. For young males more broadly, Comirnaty (Pfizer) carries a lower myocarditis rate than Spikevax (Moderna). Any suspected case should be reported to TGA's DAEN system.
What is cardiac tamponade and what are the warning signs?

Cardiac tamponade is a life-threatening emergency where fluid accumulates rapidly in the pericardial sac, compressing the heart and preventing it from filling properly. The classic warning signs are Beck's triad — low blood pressure, raised jugular venous pressure (distended neck veins), and muffled or distant heart sounds — plus pulsus paradoxus (a drop of 10 mmHg or more in blood pressure on breathing in). Prompt echocardiography confirms the diagnosis; emergency drainage of the fluid (pericardiocentesis) is life-saving. Call 000 immediately for collapse, severe breathlessness, or haemodynamic instability.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.