Difference in vegetation of infection endocarditis, rheumatic heart disease, NBTEnd Libmann sacks endocarditis in tabulat form 2nd mbbs pathology
comparison of vegetations in rheumatic heart disease infective endocarditis NBTE Libman-Sacks endocarditis valve
| Feature | Infective Endocarditis (IE) | Rheumatic Heart Disease (RHD) | Nonbacterial Thrombotic Endocarditis (NBTE) | Libman-Sacks Endocarditis (LSE) |
|---|---|---|---|---|
| Size | Large | Small | Small to medium | Small to medium |
| Number | Single or multiple | Multiple, small, warty | Single or multiple | Single or multiple |
| Character/Texture | Bulky, friable, soft | Small, warty (verrucae) | Bland (non-inflammatory) | Inflammatory |
| Destructiveness | Irregular, destructive - can extend onto chordae or myocardium, erode into underlying tissue (ring abscess) | Minimal destruction acutely; causes fibrous thickening/scarring over time | Non-destructive; local effect on valve usually trivial | Non-destructive locally, but heals with scarring |
| Composition | Fibrin, inflammatory cells, and organisms (bacteria/fungi) | Fibrin deposits along inflamed valve tissue (no organisms) | Fibrin and platelets (bland thrombus, virtually no inflammation) | Fibrin, immune complexes, inflammatory cells (no organisms) |
| Location on valve | Anywhere on leaflets, can extend to chordae/myocardium | Along the line of closure of the leaflet | Along the line of closure of the valve | Attached on either side of the valve leaflet (both atrial and ventricular surfaces) - a distinguishing feature |
| Underlying valve | Often previously damaged/abnormal valve (or normal in virulent organisms) | Follows acute rheumatic fever (post-streptococcal, Group A strep cross-reactive antibodies) | Usually previously normal valves | Occurs in setting of SLE (with or without antiphospholipid antibodies) |
| Etiology/Association | Bacteremia/fungemia (S. viridans - subacute; S. aureus - acute) | Acute rheumatic fever (immune cross-reaction to strep M protein) | Hypercoagulable states - malignancy (mucinous adenocarcinoma), DIC, hyperestrogenic states, catheter trauma | Systemic lupus erythematosus (immune complex deposition, fibrinoid necrosis) |
| Inflammation | Marked, with organisms present | Present (Aschoff bodies, Anitschkow cells in myocardium) | Absent/minimal - purely thrombotic | Present - immune-mediated with fibrinoid necrosis |
| Embolic risk | High (friable, organism-laden emboli -> septic infarcts, mycotic aneurysms) | Low | High (loosely attached, easily dislodged -> bland infarcts in brain, heart, other organs) | Can embolize but historically considered less common; associated with cerebral events in APS |
| Healing | Fibrosis, calcification if healed | Fibrous thickening, commissural fusion, chordal shortening (chronic RHD) | Minimal residual change | Fibrosis and valve deformity (can resemble chronic RHD) |