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PH-CV14

Infective and non-infective endocarditis

How damaged valves gather sterile clots that bacteria in the blood colonise, why acute and subacute endocarditis differ, and how vegetations destroy valves, embolise and seed immune complexes to cause the classic signs.

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  • 6 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Explain why a normal valve resists infection, and how endothelial damage, a sterile platelet–fibrin deposit and bacteraemia combine to start endocarditis.
  • Contrast acute (Staphylococcus aureus) with subacute (viridans streptococcal) endocarditis, and explain right-sided endocarditis in people who inject drugs.
  • Explain how vegetations destroy valves and spread, and relate emboli and immune complexes to Osler nodes, Janeway lesions, splinter haemorrhages, Roth spots and glomerulonephritis.
  • Distinguish non-bacterial thrombotic (marantic) and Libman–Sacks endocarditis from infective endocarditis.
  • Apply the modified Duke criteria, recognise the classic appearances and tests, and explain how bactericidal antibiotics, surgery and anticoagulation act on the mechanism.

What it is

Endocarditis is inflammation of the endocardium, almost always of the heart valves, marked by vegetations: masses of platelets and fibrin on the valve surface. In infective endocarditis, micro-organisms, usually bacteria, grow within the vegetations; in non-infective endocarditis the vegetations are sterile, as in non-bacterial thrombotic (marantic) endocarditis and the Libman–Sacks endocarditis of lupus.

5 types to tell apart
Acute infective endocarditis
A virulent organism, most often Staphylococcus aureus, attacks normal or abnormal valves and destroys them over days.
Subacute infective endocarditis
A less virulent organism, classically a viridans streptococcus from the mouth, settles on an already abnormal valve and smoulders for weeks to months.
Prosthetic valve and device endocarditis
Infection of an artificial valve, its sewing ring or pacemaker leads: early cases come from contamination at surgery, later ones from bacteraemia.
Right-sided endocarditis
Usually of the tricuspid valve, mostly in people who inject drugs; it sends septic emboli to the lungs.
Non-infective endocarditis
Sterile vegetations: marantic endocarditis in cancer and other hypercoagulable or wasting states, and Libman–Sacks endocarditis in lupus and antiphospholipid syndrome.

US spelling: sulphate → sulfate.

Normal function

A smooth lining that blood cannot stick to

The endocardium lines every chamber and covers both surfaces of the valves: a single layer of endothelial cells on a thin bed of connective tissue. The valve leaflets beneath have almost no blood vessels. They are nourished by the blood flowing over them, and immune cells reach them mainly from that surface.

Healthy endothelium resists clotting and adhesion. It releases nitric oxide and prostacyclin, which keep platelets inactive, and carries thrombomodulin and heparan sulphate, which damp thrombin. Fast, smooth flow over the , , and valves sweeps away anything that might settle, so bacteria that enter the blood briefly, as they do after chewing or brushing the teeth, pass by without lodging.

Each valve closes against a pressure difference. Blood leaking through a faulty valve, or squeezed through a narrow one, forms a fast jet that runs from high to low pressure: from ventricle to atrium through a leaking mitral or tricuspid valve, and from aorta to ventricle through a leaking aortic valve.

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