Features | DIVHD | Rheumatic VHD | Primary Calcific VHD | Libman-Sacks endocarditis30 |
---|---|---|---|---|
Mechanism | 5-HT2B agonist | Microbial agents as trigger | Multifactorial atherosclerosis-like | Antiphospholipid Syndrome-deposition immune complexes |
Age | Young and old depending on type drug | Younger | Older | Younger and middle aged (women) |
Localisation | Left > right | Left > right | Left | Left ≫ right |
Valvular thickening | Yes ++(+) | Yes +++ | Yes + | Yes++, but also valvular masses |
Histopathology | Myxoid plaques on the valve with conserved architecture | Neovascularisation, inflammation and calcification | Predominant annular or valvular body leaflets calcifications | Diffuse thickening ± sterile fibrofibrinous vegetations, sometimes small calcifications |
Calcification | No | Yes + | Yes ++ | Sometimes |
Commissural fusion | No | Yes++ (MV >AV) | Yes + (AV >MV) | Rare (MV) |
Restrictive motion and Increased tenting | Yes ++(+) | Yes +++ | Yes + | Yes+ if thickening is predominant feature |
Functional effect (stenosis/regurgitation) | Regurgitation | Stenosis and regurgitation | Stenosis and regurgitation | Regurgitation (stenosis); systemic embolisation (mass) |
Subvalvular apparatus | Thickened and shortened | Thickened, calcified and shortened | Less affected | Not affected |
In some cases different diseases might be present in the same patient complicating the diagnosis.