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PA26.{5,7} | Rheumatic Heart Disease & Infective Endocarditis — SDL Guide (Part 3)

Complications of Chronic Rheumatic Heart Disease

A multi-panel diagram shows chronic rheumatic mitral valve disease leading to atrial fibrillation, thromboembolism, pulmonary hypertension, right heart failure, infective endocarditis, and multivalvular involvement. — **Panel A:** Thickened scarred mitral valve, mitral stenosis, left atrial dilatation, pulmonary venous hypertension, pulmonary arterial hypertension, right ventricular pressure overload. **Panel B:** Dilated left atrium, atrial fibrillation electrical waves, left atrial appendage, left atrial thrombus, irregularly irregular ECG rhythm. **Panel C:** Systemic embolus, aorta, cerebral embolism causing stroke, renal infarct, limb ischaemia. **Panel D:** Pulmonary oedema, haemosiderin-laden macrophages or heart failure cells, pulmonary arteriole medial hypertrophy, raised JVP, hepatomegaly, peripheral oedema. **Panel E:** Scarred mitral valve, scarred aortic valve, bacterial vegetations, infective endocarditis, multivalvular involvement summary.

CRHD and its haemodynamic consequences lead to a cascade of complications:

Cardiac complications:
• Atrial fibrillation (AF): Left atrial dilatation from chronic pressure overload → electrical remodelling → AF. Occurs in ~40% of mitral stenosis patients. AF dramatically worsens haemodynamics (loss of atrial kick + fast rate).
• Right heart failure: Progressive pulmonary hypertension → right ventricular pressure overload → right heart failure (raised JVP, hepatomegaly, peripheral oedema)

Thromboembolic complications:
• Left atrial thrombus (especially in the left atrial appendage) in AF → systemic embolism → stroke, renal infarct, limb ischaemia
• Risk especially high when AF is present

Infective complications:
• Damaged, scarred valves provide a substrate for bacterial colonisation → infective endocarditis (IE) superimposed on CRHD — covered in the second half of this module

Lung complications:
• Pulmonary venous hypertension → pulmonary oedema (acute) and pulmonary haemosiderosis (chronic — 'heart failure cells' — haemosiderin-laden macrophages in sputum)
• Pulmonary arterial changes — medial hypertrophy → fixed pulmonary hypertension

Other valves:
• Mitral + aortic involvement in ~40%; pure mitral stenosis ~25%; pure mitral regurgitation ~10%; tricuspid and pulmonary rarely isolated

SELF-CHECK

A 38-year-old woman with known rheumatic mitral stenosis presents with sudden onset right-sided weakness and dysphasia. Her pulse is irregularly irregular. Which mechanism best explains her neurological deficit?

A. Embolic stroke from left atrial thrombus in the context of atrial fibrillation

B. Haemorrhagic stroke due to pulmonary hypertension

C. Septic embolism from infective endocarditis vegetations

D. Vasospasm from elevated left atrial pressure

Reveal Answer

Answer: A. Embolic stroke from left atrial thrombus in the context of atrial fibrillation

The irregularly irregular pulse indicates atrial fibrillation, a direct complication of chronic mitral stenosis from left atrial dilatation. AF causes stasis of blood in the left atrial appendage → thrombus formation → systemic thromboembolism — in this case, a cardioembolic stroke. Septic embolism (option C) would require features of infective endocarditis (fever, new murmur change, positive blood cultures) — not mentioned here.

Infective Endocarditis — Classification and Etiology

A three-panel medical diagram compares acute and subacute infective endocarditis, showing valve vegetations, affected valve substrates, and typical causative organisms. — **Panel A:** Anterior cutaway heart showing cardiac endocardium, mitral valve, aortic valve, valve vegetations, leaflet destruction, and embolic fragments.. **Panel B:** Comparison of acute IE caused commonly by Staphylococcus aureus on previously normal valves versus subacute IE caused by Streptococcus viridans, Enterococcus, or HACEK organisms on damaged valves.. **Panel C:** Predisposing substrates and typical organisms: rheumatic heart disease, early prosthetic valve, late prosthetic valve, and IV drug use with associated valve targets and pathogens..

Infective endocarditis (IE) is an infection of the cardiac endocardium, predominantly affecting heart valves. It is classified by clinical course and causative organism:

Acute IE (AIE):
• Caused by highly virulent organisms — Staphylococcus aureus most common (~50% of all IE)
• Attacks previously normal valves — does not need prior damage
• Rapid, destructive course — days to weeks
• Produces large, bulky, friable, destructive vegetations
• High mortality without rapid treatment

Subacute IE (SIE):
• Caused by low-virulence organisms — Streptococcus viridans (oral flora, ~30% of IE), Enterococcus, HACEK organisms
• Almost always attacks previously damaged or abnormal valves (RHD, bicuspid aortic valve, prosthetic valve, congenital defects)
• Indolent course — weeks to months; constitutional symptoms dominate early
• Produces smaller, less destructive vegetations but with equal embolism risk

Predisposing conditions:

Substrate	Typical organism
Rheumatic heart disease (mitral/aortic)	S. viridans, S. aureus
Prosthetic valve (early <60 days)	S. epidermidis, S. aureus, gram-negatives
Prosthetic valve (late >60 days)	S. viridans, S. epidermidis
IV drug use	S. aureus → right-sided, tricuspid valve
Congenital heart disease	S. viridans, S. aureus
No predisposing cause	S. aureus (community-acquired)

Pathology of Infective Endocarditis — Vegetations

Diagram showing infective endocarditis vegetations on the mitral valve, their stepwise formation, and comparison of acute, subacute, and rheumatic valve lesions. — **Panel A:** Gross mitral valve view with vegetation, fibrin-platelet-bacteria mass, leaflet destruction, perforation, chordae tendineae, and atrial surface of mitral valve.. **Panel B:** Sequential formation stages: endothelial damage, platelet-fibrin thrombus, transient bacteraemia, bacterial adhesion and colonisation, layered infected vegetation.. **Panel C:** Comparison of acute IE due to S. aureus, subacute IE due to S. viridans, rheumatic verruca along closure line, and low-pressure-side valve locations..

The hallmark lesion of IE is the vegetation — a mass of thrombotic material colonised by microorganisms on the valve surface.

How vegetations form:
1. Turbulent flow or direct injury creates a focus of endothelial damage
2. Platelet-fibrin thrombus forms on the denuded surface (as in NBTE)
3. Transient bacteraemia delivers organisms to the thrombus
4. Bacteria adhere, colonise, and proliferate within the fibrin-platelet matrix
5. Further layers of fibrin and platelets deposit over the infected nidus
6. Result: a complex mass of fibrin, platelets, bacteria, inflammatory cells, and necrotic debris

Gross features of IE vegetations:
• Acute IE (S. aureus): Large (up to several cm), irregular, bulky, friable, destructive — erode into the valve leaflet, cause perforation and rupture; may extend into surrounding structures (annulus, myocardium, conduction system)
• Subacute IE (S. viridans): Smaller, 'wart-like', less destructive — but still friable and prone to embolism
• Location: Most commonly on the atrial surface of the mitral/tricuspid valve and the ventricular surface of the aortic/pulmonary valve (i.e., at the low-pressure side of the jet stream)

Diagram comparing large irregular infective endocarditis vegetations on the mitral valve with small regular rheumatic verrucae along the closure line. — **Panel A:** Opened mitral valve showing large irregular vegetation, leaflet destruction, mitral valve leaflet, and chordae tendineae.. **Panel B:** Rheumatic verrucae shown as small regular bead-like lesions along the mitral valve line of closure.. **Panel C:** Direct size and surface comparison between large friable infective endocarditis vegetation and small regular rheumatic verruca..