Cardiology: Pericarditis Myocarditis Endocarditis (Complete)

• Pericardial disease: The Pericardium | Acute Pericarditis | Treating Pericarditis | Recurrent Pericarditis | Myopericarditis | Pericardial Effusion | Constrictive Pericarditis | Specific Causes of Pericardial Disease
• Infective endocarditis: What Is Infective Endocarditis? | Organisms | Clinical Features | Diagnosis | Antibiotic Treatment | Surgery | Complications | Special Situations | Prevention and Prophylaxis
• Rheumatic disease: Acute Rheumatic Fever | Rheumatic Heart Disease
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🛡️ Pericardial disease, endocarditis and rheumatic fever are inflammatory and infective conditions of the heart's lining and covering. Pericarditis is common and usually benign, but can recur, constrict the heart or cause tamponade. Infective endocarditis is less common but kills about 1 in 4 patients within a year, and needs a team approach. Rheumatic fever is now rare in the UK but still causes much of the world's valve disease.
Your four questions for every patient: Is this inflammation, infection or something else (MI, dissection)? Is there an effusion, and is it compressing the heart? Could this be endocarditis - have blood cultures been taken before antibiotics? Does the patient need a surgeon?

The Pericardium

• Structure: A two-layered sac around the heart - a thin inner (visceral) layer stuck to the heart, and a tough outer (parietal) layer. Between them is normally 15–50 mL of fluid, which lets the heart move smoothly.
• What can go wrong:
  • Inflammation (pericarditis) - chest pain, rub.
  • Fluid build-up (pericardial effusion) - which can compress the heart (tamponade).
  • Scarring and thickening (constrictive pericarditis) - which stops the heart filling.
• Why the speed matters: The pericardium can stretch slowly. A litre can collect over months without symptoms, but 150 mL of sudden bleeding can cause tamponade.

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Acute Pericarditis

Causes:

• Idiopathic or viral - about 80–90% in developed countries (coxsackie, echovirus, adenovirus, influenza, SARS-CoV-2).
• Bacterial - TB (common worldwide and in people from high-incidence countries); purulent pericarditis (staphylococci, streptococci).
• After cardiac injury - after MI (early or Dressler's), cardiac surgery, PCI, ablation, pacemaker insertion, trauma.
• Autoimmune - SLE, rheumatoid arthritis, systemic sclerosis, vasculitis, familial Mediterranean fever.
• Cancer - lung, breast, lymphoma, leukaemia, melanoma.
• Metabolic - uraemia, hypothyroidism.
• Drugs and radiation - hydralazine, procainamide, isoniazid (drug-induced lupus), immune checkpoint inhibitors, chest radiotherapy; some vaccines (mRNA COVID-19, rarely).

Clinical pattern:

• Sharp central chest pain - worse lying flat and on breathing in, eased by sitting forward. Often radiates to the trapezius ridge.
• Often follows a viral illness.
• Pericardial friction rub - a scratchy, "squeaky leather" sound, best heard leaning forward. It comes and goes.
• Fever.

ECG:

• Widespread, saddle-shaped ST elevation across many leads (not matching one coronary territory).
• PR depression (and PR elevation in aVR).
• No reciprocal ST depression (except aVR and V1).
• Later, T waves invert after the ST segments normalise.

Diagnosis (ESC) - at least 2 of:

• Pericardial chest pain.
• Friction rub.
• New widespread ST elevation or PR depression.
• New or worsening pericardial effusion.

Supported by raised CRP and pericardial inflammation on imaging (cardiac MRI).

Tests:

• ECG; CRP; FBC.
• Troponin - if raised, think myopericarditis.
• U&E (uraemia); chest X-ray.
• Echo in everyone (effusion, LV function).
• TB tests, autoimmune screen, TFTs and others guided by history.

High-risk features - admit and investigate:

• Fever above 38°C.
• Subacute onset over days or weeks.
• Large effusion (over 20 mm) or tamponade.
• No response to NSAIDs within a week.
• Myopericarditis.
• Immunosuppression; trauma; oral anticoagulants.

Low-risk patients can be treated as outpatients.

💡 Clinical Pearl: Pericarditis versus STEMI: pericarditis has widespread concave ST elevation without reciprocal depression, PR depression, pain that changes with position and breathing, and often a younger patient after a virus. If in doubt, treat as ACS and get an urgent echo and senior opinion.

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Treating Pericarditis

• Anti-inflammatory drug plus gastroprotection (PPI), continued until symptoms and CRP settle, then tapered:
  • NSAID - e.g. ibuprofen 600 mg three times daily for 1–2 weeks - or high-dose aspirin (750–1,000 mg three times daily).
  • Aspirin is preferred after MI, or if already on antiplatelets. Avoid NSAIDs early after MI.
• Plus colchicine - reduces recurrences by about half:
  • 500 micrograms once daily (under 70 kg) or twice daily (70 kg or more), for 3 months.
  • Side effects: diarrhoea.
  • Interactions: Clarithromycin, statins (myopathy). Reduce the dose in renal impairment.
• Exercise: Avoid strenuous exercise until symptoms, CRP and ECG have settled. Athletes usually need longer before returning to competition, guided by tests (ESC 2025 takes an individualised approach).
• Steroids (low to moderate dose prednisolone) are second-line - only if NSAIDs and aspirin are contraindicated or ineffective, or for autoimmune causes and pregnancy. Early steroid use increases recurrences. Exclude TB and bacterial infection first.
• Treat the cause - dialysis for uraemia; antibiotics and drainage for purulent pericarditis; TB treatment.

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Recurrent Pericarditis

• Definition: A new episode after a symptom-free interval of 4–6 weeks or more. It affects about 1 in 3 people not given colchicine.
• Mechanism: Often autoinflammatory (interleukin-1 driven) rather than ongoing infection.
• Treatment:
  • NSAID or aspirin plus colchicine for at least 6 months.
  • Taper slowly, guided by symptoms and CRP.
  • Low-dose steroids if needed, tapered very slowly.
• Steroid-dependent, colchicine-resistant disease (specialist): Interleukin-1 blockers (anakinra, rilonacept) are very effective. Azathioprine or IV immunoglobulin are alternatives.
• Look again for a cause - autoimmune disease, TB, cancer, familial Mediterranean fever.
• Pericardiectomy as a last resort.

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Myopericarditis

• What it is: Pericarditis with heart muscle involvement - a raised troponin with normal or near-normal LV function.
• ESC 2025: Myocarditis and pericarditis are now seen as one spectrum - "inflammatory myopericardial syndrome" - with the same urgency of assessment, imaging and follow-up.
• Investigations:
  • Coronary assessment (often CT coronary angiography) to exclude ACS when there is doubt.
  • Cardiac MRI to show inflammation (oedema, late gadolinium enhancement).
• Treatment:
  • Anti-inflammatory treatment at lower NSAID doses, plus colchicine.
  • Avoid strenuous exercise for at least 3–6 months - exercise during myocarditis can trigger arrhythmias and sudden death. Return is guided by MRI, ECG and Holter monitoring.
• Predominant myocarditis (reduced EF, arrhythmia, heart failure): See the Cardiomyopathy chapter.

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Pericardial Effusion

• Causes:
  • As for pericarditis.
  • Malignancy - the commonest cause of large symptomatic effusions.
  • Hypothyroidism.
  • Uraemia.
  • Heart failure; post-cardiac surgery.
  • Drugs (minoxidil).
• Severity on echo:
  • Small: under 10 mm.
  • Moderate: 10–20 mm.
  • Large: over 20 mm.
• Clinical pattern:
  • Often none.
  • Breathlessness, chest fullness, cough, hiccups, hoarseness, dysphagia.
  • Quiet heart sounds.
  • ECG: Small complexes; electrical alternans (beat-to-beat change in QRS height) in large effusions.
  • Chest X-ray: A large "globular" heart.
• Management:
  • Tamponade: Urgent drainage (see the Cardiac Emergencies chapter).
  • Suspected bacterial, TB or malignant effusion: Diagnostic pericardiocentesis - send fluid for cell count, culture, AFB, cytology and biochemistry.
  • Large effusion without tamponade: Treat the cause; drain if symptomatic or not resolving. Recurrent malignant effusions may need a pericardial window or instilled treatment.
  • Small, asymptomatic effusion with normal CRP: Find the cause; monitor.

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Constrictive Pericarditis

Mechanism: The pericardium becomes thick, scarred and stiff (sometimes calcified), encasing the heart like a rigid shell. The heart fills briefly in early diastole, then stops suddenly. Pressures rise behind the heart, causing mainly right-sided congestion.

Causes:

• Idiopathic or viral pericarditis.
• Previous cardiac surgery.
• Chest radiotherapy (e.g. lymphoma, breast).
• TB - the commonest cause worldwide.
• Connective tissue disease; uraemia; asbestos.

Clinical pattern:

• Slowly progressive right heart failure - fatigue, oedema, ascites, hepatomegaly. Often mistaken for liver disease.
• Raised JVP with a sharp y descent; Kussmaul's sign (JVP rises on inspiration).
• Pericardial knock (early diastolic sound).
• Pulsus paradoxus (less common than in tamponade).
• AF.

Constriction or restrictive cardiomyopathy?

Investigations:

• Echo.
• CT (calcification) and cardiac MRI (thickening, inflammation).
• Cardiac catheterisation showing equal pressures in all chambers and "dip and plateau" pressure traces.

Treatment:

• Surgical pericardiectomy for chronic constriction.
• Transient constriction (with active inflammation on MRI) may respond to anti-inflammatory drugs.
• Diuretics for symptoms.
• TB treatment for tuberculous constriction.

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Specific Causes of Pericardial Disease

• Tuberculous pericarditis:
  • Subacute fever, weight loss and effusion - often in people from high-incidence countries and people with HIV.
  • Exudative, lymphocytic fluid; high adenosine deaminase.
  • Standard TB treatment. Steroids may reduce constriction in some patients.
  • High risk of constriction.
• Purulent pericarditis:
  • Bacterial - from pneumonia, empyema, surgery or bacteraemia.
  • Very ill and septic, often with tamponade.
  • Urgent drainage plus IV antibiotics. High mortality.
• Uraemic and dialysis pericarditis: Often without typical ECG changes. Intensify dialysis.
• Malignant pericardial disease: Lung, breast, lymphoma - usually advanced disease. Drain; consider a pericardial window; treat the cancer.
• Post-cardiac injury syndromes:
  • Dressler's syndrome (weeks after MI) and post-pericardiotomy syndrome (after cardiac surgery).
  • An immune reaction - fever, pericarditis, pleurisy, effusions.
  • NSAIDs or aspirin plus colchicine.
• Early post-MI pericarditis (days 1–3): Over a transmural infarct. Treat with aspirin rather than NSAIDs.
• Radiation-induced: Acute pericarditis, or constriction years later.
• Hypothyroidism: Slowly accumulating effusion, rarely tamponade - resolves with levothyroxine.
• Autoimmune - SLE, rheumatoid arthritis: treat the underlying disease.
• Haemopericardium: Trauma, aortic dissection, free wall rupture after MI, procedures, anticoagulation - a surgical emergency.

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What Is Infective Endocarditis?

Mechanism:

• Damaged or abnormal heart lining - valves, prosthetic material, wires - attracts platelets and fibrin.
• Bacteria in the blood (from teeth, skin, lines, injecting, gut or urinary tract) stick there and multiply, forming vegetations.
• These destroy valves, form abscesses, break off as emboli, and trigger immune complex disease.

Who is at risk:

• Highest risk:
  • Prosthetic valves (including TAVI and valve repairs with prosthetic material).
  • Previous endocarditis.
  • Some congenital heart disease (cyanotic disease, or repairs with prosthetic material).
• Others:
  • People who inject drugs.
  • Cardiac devices (pacemakers, ICDs).
  • Haemodialysis and long-term IV lines.
  • Degenerative valve disease in older people; mitral valve prolapse with regurgitation.
  • Rheumatic heart disease; HCM.
  • Diabetes; immunosuppression.

Changing picture: Infective endocarditis is now commoner in older people and is often healthcare-associated (lines, devices, procedures). Staphylococcus aureus is now the commonest cause. Mortality is about 20% in hospital and about 30% at 1 year.

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Organisms

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Clinical Features

Suspect endocarditis in anyone with fever plus a new murmur, or fever with risk factors, embolic events or unexplained heart failure.

• General:
  • Fever (about 90%) - may be absent in older or immunosuppressed people.
  • Night sweats, weight loss, fatigue, aches.
• Heart:
  • New or changed murmur (regurgitant).
  • Heart failure from valve destruction.
  • Heart block (aortic root abscess).
• Emboli (in about a third):
  • Stroke or TIA.
  • Limb ischaemia.
  • Splenic or renal infarcts.
  • Septic pulmonary emboli (right-sided endocarditis).
  • Mycotic aneurysms.
• Immune and vascular signs (less common now, as diagnosis is earlier):
  • Splinter haemorrhages (nail beds).
  • Janeway lesions - painless palm and sole macules (embolic).
  • Osler's nodes - painful fingertip nodules (immune).
  • Roth spots - retinal haemorrhages with pale centres.
  • Conjunctival petechiae.
  • Haematuria (glomerulonephritis).
  • Splenomegaly.
  • Clubbing (long-standing subacute disease).
• Bloods: Raised CRP and ESR, anaemia, raised WCC, haematuria, AKI.

⚠️ Safety Pearl: Every patient with Staphylococcus aureus bacteraemia needs an echo (and often TOE) to look for endocarditis, plus an infection specialist review. S. aureus in the blood is never "just a contaminant".

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Diagnosis

• Blood cultures - before antibiotics:
  • Three sets, from separate venepunctures (ideally at least 30 minutes apart, or over 1 hour).
  • In severe sepsis, take 2 sets within an hour and start antibiotics without delay.
  • Continuous bacteraemia (all sets positive) is typical.
• Echocardiography:
  • Transthoracic echo (TTE) first.
  • Transoesophageal echo (TOE) if TTE is negative but suspicion remains, with prosthetic valves or devices, or to look for complications (abscess, perforation) before surgery.
  • Repeat echo if the patient deteriorates or the initial echo is negative but suspicion is high (vegetations can appear later).
• Other imaging:
  • Cardiac CT - abscesses, pseudoaneurysms.
  • FDG-PET/CT - very useful in prosthetic valve and device infection.
  • Brain MRI and body CT for emboli.
• Modified Duke criteria (updated by ESC 2023 and Duke-ISCVID 2023):
  • Major criteria:
    • Positive blood cultures with a typical organism (or persistent bacteraemia).
    • Imaging evidence - vegetation, abscess, new prosthetic valve leak, or positive PET/CT.
  • Minor criteria:
    • Predisposing heart condition or injecting drug use.
    • Fever above 38°C.
    • Vascular phenomena (emboli, mycotic aneurysm, Janeway lesions).
    • Immunological phenomena (Osler's nodes, Roth spots, glomerulonephritis).
    • Microbiology that does not meet the major criterion.
  • "Definite" endocarditis: 2 major, or 1 major plus 3 minor, or 5 minor.
• Culture-negative endocarditis: Serology (Coxiella, Bartonella, Brucella), and PCR and culture of any removed valve tissue.

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Antibiotic Treatment

Principles:

• High-dose, bactericidal IV antibiotics for a long time - usually 4–6 weeks.
• Bacteria in vegetations are hard to reach.
• Managed by the endocarditis team - cardiology, cardiac surgery, microbiology or infectious diseases.

Empirical treatment (while awaiting cultures - follow local and BSAC guidance), for example:

• Native valve, subacute: Amoxicillin (with or without gentamicin).
• Native valve, severe sepsis or S. aureus risk: Vancomycin (plus gentamicin, or broader Gram-negative cover per local policy).
• Prosthetic valve: Vancomycin plus gentamicin plus rifampicin.

Targeted treatment once the organism is known (typical courses):

• Streptococci (penicillin-sensitive): Benzylpenicillin or ceftriaxone for 4 weeks (2 weeks with gentamicin in selected uncomplicated cases). 6 weeks for prosthetic valves.
• S. aureus (MSSA): Flucloxacillin for 4–6 weeks. Add rifampicin (with or without gentamicin) for prosthetic valves.
• MRSA: Vancomycin or daptomycin, with rifampicin for prosthetic material.
• Enterococci: Amoxicillin plus gentamicin, or amoxicillin plus ceftriaxone (which avoids gentamicin kidney toxicity), for 6 weeks.
• HACEK: Ceftriaxone for 4 weeks.
• Fungal: Amphotericin or echinocandin, plus surgery, then long-term azole suppression.

Oral step-down: Selected stable patients with left-sided endocarditis caused by streptococci, S. aureus or enterococci, who are responding well, can switch to oral antibiotics after at least 10 days of IV treatment (POET trial; ESC 2023). Outpatient IV therapy (OPAT) is another option.

Monitoring:

• Temperature, CRP, repeat blood cultures (until negative).
• Drug levels - vancomycin, gentamicin.
• Renal function; hearing (gentamicin).
• ECG for new heart block.

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Surgery

About half of patients with left-sided endocarditis need surgery. The three main reasons (ESC 2023):

• Heart failure - severe acute regurgitation, valve obstruction or fistula causing heart failure or shock. This is the commonest indication, and the most urgent (emergency surgery if shocked).
• Uncontrolled infection:
  • Abscess, pseudoaneurysm, fistula, enlarging vegetation.
  • Persistent bacteraemia despite appropriate antibiotics (e.g. beyond 7 days).
  • Fungal or multidrug-resistant organisms.
  • Most prosthetic valve endocarditis caused by S. aureus.
• Prevention of embolism:
  • Large vegetations (10 mm or more) with a previous embolic event.
  • Or very large vegetations (above 30 mm), especially on the mitral valve.

After a stroke: Surgery is usually still possible after an ischaemic stroke without major haemorrhage. It is often delayed after intracranial haemorrhage - a specialist team decision.

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Complications

• Heart:
  • Valve destruction and heart failure.
  • Perivalvular abscess - new heart block (lengthening PR interval, especially with aortic valve endocarditis).
  • Fistulas; pericarditis.
  • MI from coronary emboli.
• Nervous system (about a quarter):
  • Embolic stroke.
  • Brain abscess; meningitis.
  • Mycotic aneurysm - can rupture, causing intracranial haemorrhage.
  • Encephalopathy.
• Kidneys:
  • Immune complex glomerulonephritis.
  • Renal infarcts.
  • Drug toxicity (gentamicin, vancomycin).
  • Sepsis-related AKI.
• Others:
  • Splenic infarction or abscess.
  • Septic arthritis, discitis or vertebral osteomyelitis.
  • Peripheral mycotic aneurysms.
  • Septic pulmonary emboli (right-sided disease).
• Anticoagulation:
  • Do not start antiplatelets or anticoagulants to prevent emboli - they increase bleeding without benefit.
  • Patients already on anticoagulation (e.g. mechanical valves) usually switch to heparin.
  • Stop anticoagulation temporarily after an intracranial bleed.

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Special Situations

• People who inject drugs:
  • Often right-sided (tricuspid) endocarditis with S. aureus.
  • Fever, cough, pleuritic pain and septic pulmonary emboli (multiple cavitating lung nodules); sometimes no murmur.
  • Generally a better prognosis than left-sided disease.
  • Address the addiction (opioid substitution, harm reduction) as part of treatment - it reduces reinfection.
• Prosthetic valve endocarditis:
  • Early (within 1 year) - often staphylococci from surgery.
  • Late - like native valve endocarditis.
  • Echo is harder; TOE and PET/CT help.
  • Higher mortality; surgery is more often needed.
• Cardiac device infection (pacemaker, ICD):
  • Pocket infection or lead endocarditis.
  • Needs complete removal of the device and leads, plus antibiotics.
  • Reimplant on the other side once infection has cleared, if still needed.
• Older people: Atypical - confusion, falls, no fever. Often enterococcal or S. gallolyticus; look for bowel cancer.
• Haemodialysis: Staphylococci from lines; high mortality.
• After TAVI: Increasingly common; mostly managed medically because surgical risk is high.

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Prevention and Prophylaxis

• Antibiotic prophylaxis for dental procedures:
  • NICE CG64 says antibiotic prophylaxis is not routinely recommended for dental or other procedures, but that it may be appropriate for individual high-risk patients.
  • ESC 2023 recommends prophylaxis (e.g. a single dose of amoxicillin before treatment) for high-risk patients - prosthetic valves, previous endocarditis, some congenital heart disease, ventricular assist devices - having dental procedures that involve the gums or root canals.
  • UK dental guidance (SDCEP) supports considering prophylaxis for these high-risk groups after discussion with the patient and their cardiologist.
• For everyone at risk:
  • Good dental hygiene and regular dental check-ups - daily bacteraemia from teeth matters more than occasional procedures.
  • Avoid tattoos and body piercing.
  • Prompt treatment of skin and other infections.
  • Careful IV line care in hospital; remove lines that are not needed.
  • Patient education - seek medical advice for unexplained fever, and ask for blood cultures before antibiotics.

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Acute Rheumatic Fever

Mechanism: An immune reaction 2–4 weeks after a group A streptococcal throat infection. Antibodies against the streptococcus cross-react with heart, joint, brain and skin tissue ("molecular mimicry"). It is now rare in the UK, but common in low-income countries, Indigenous populations and areas of overcrowding.

Diagnosis - revised Jones criteria: Evidence of a recent streptococcal infection (raised ASO titre or anti-DNase B, positive throat culture), plus either 2 major criteria, or 1 major and 2 minor.

• Major criteria:
  • Carditis - pancarditis; usually mitral regurgitation; may be found only on echo.
  • Polyarthritis - migratory, large joints, very responsive to aspirin.
  • Sydenham's chorea - involuntary jerky movements, emotional lability; may occur months later.
  • Erythema marginatum - pink rings on the trunk.
  • Subcutaneous nodules - over bony prominences.
• Minor criteria:
  • Fever.
  • Arthralgia.
  • Raised ESR or CRP.
  • Prolonged PR interval.

Treatment:

• Penicillin to eradicate the streptococcus.
• Aspirin or NSAIDs for arthritis.
• Steroids for severe carditis (sometimes).
• Heart failure treatment.
• Treatment for chorea if severe.

Secondary prevention: Long-term benzathine penicillin injections every 3–4 weeks (or oral penicillin) to prevent recurrences. Continue for years - typically at least until age 21, or 10 years after the last episode, and longer if there is carditis.

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Rheumatic Heart Disease

• What it is: Chronic valve damage - thickening, fusion and scarring - after one or more attacks of rheumatic fever. It is the commonest acquired heart disease in young people worldwide.
• Valves affected:
  • Mitral valve (most common) - mitral stenosis and regurgitation.
  • Then the aortic valve.
  • Multiple valves often involved.
• In the UK: Mostly seen in older people, or people who grew up in countries where rheumatic fever is common. Mitral stenosis often presents with breathlessness and AF, especially in pregnancy.
• Management:
  • See the Valvular Heart Disease chapter (mitral stenosis - balloon valvotomy, valve surgery).
  • Anticoagulation with warfarin (not DOACs) for AF with moderate to severe mitral stenosis.
  • Secondary prophylaxis with penicillin.
  • Dental care and endocarditis awareness.

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Drug Reference Table

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Spot the Diagnosis

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Exam-style Scenarios