Table 1.
Pathophysiological classification of tricuspid regurgitation (23).
| Leaflet morphology | Pathophysiology | Etiology | Imaging | |
|---|---|---|---|---|
| Primary | Abnormal | Loss of leaflet coaptation due to intrinsic changes, excessive mobility, or perforation | Myxomatous disease Endocarditis Trauma Carcinoid Rheumatic Iatrogenic (biopsy) Congenital |
According to the etiology Description of the etiology, lesions and dysfunction |
| Secondary: Atrial | Normal | RA enlargement and dysfunction leading to TA dilation, conical remodeling of the RV | Atrial fibrillation | Severe RA remodeling RV basal diameter may be enlarged despite usually normal RV volume Leaflet tethering is absent or limited |
| Secondary: Ventricular | Considered normal | RV enlargement and/or dysfunction leading to significant leaflet tethering and TA dilation | Pulmonary hypertension RV cardiomyopathy RV infarction |
Dominant mechanism is leaflet tethering ± TA dilation |
| CIED-related: Primary |
Abnormal | Leaflet impingement Leaflet/chordal entanglement Leaflet adherence Leaflet laceration/perforation Leaflet avulsion (post lead extraction) |
Pacemaker Implantable cardiac defibrillator Cardiac resynchronization therapy |
3D echocardiograhy (±color) is mandatory for reliable diagnosis |
| CIED-related: Secondary | Normal | RV enlargement and/or dyssynchrony/dysfunction due to pace-maker stimulation and leading to significant leaflet tethering and TA dilation | Pacemaker rhythm | Dominant mechanism is leaflet tethering ± TA dilation |
RA, right atrial; TA, tricuspid annulus; RV, right ventricle; CIED, cardiac implantable electronic device; 3D, Three dimensional.