Causes of Tricuspid Regurgitation with Normal Leaflets
Tricuspid regurgitation with structurally normal leaflets is most commonly secondary (functional) TR, caused by right ventricular dysfunction and/or tricuspid annular dilatation in response to pressure or volume overload, rather than primary valve pathology. 1
Primary Mechanism: Functional (Secondary) TR
The fundamental pathophysiology involves three interconnected processes: 1
- Tricuspid annular dilatation - The annulus loses its normal saddle-shaped configuration, becoming flat, planar, and distorted with diastolic diameter >21 mm/m² (>35 mm absolute) 1
- Leaflet tethering - Progressive RV remodeling causes papillary muscle displacement and apical displacement of leaflets, preventing proper coaptation 1
- Loss of annular contraction - Normal 25% systolic contraction of the annulus is impaired 1
Key Quantitative Markers of Functional TR:
- Tenting area >1 cm² indicates severe functional TR 1
- Coaptation distance (distance from annular plane to coaptation point) >0.76 cm predicts persistent TR 1
Underlying Causes of RV Dysfunction Leading to Functional TR
Pressure Overload Conditions 1
- Pulmonary hypertension (any etiology) - Systolic PA pressures >55 mm Hg commonly cause TR with anatomically normal valves 1
- Left-sided valve disease - Particularly mitral stenosis or mitral regurgitation causing elevated pulmonary pressures 1
- Pulmonic valve stenosis 1
- Pulmonary embolism (acute or chronic thromboembolic) 2
Volume Overload Conditions 1
Atrial Factors 3, 4
- Chronic atrial fibrillation - Causes isolated annular dilatation even without other cardiac abnormalities 3, 4
- Right atrial enlargement - Creates progressive annular dilatation 1
Iatrogenic Causes 1
- Intra-annular RV pacemaker or ICD leads - Can cause functional TR through mechanical interference 1
- Post-cardiac transplant (biopsy-related trauma) 1
The Self-Perpetuating Cycle
Critical concept: TR itself creates a vicious cycle where regurgitation leads to further RV dilation, which causes more annular dilatation and leaflet tethering, worsening the TR 1. This explains why:
- TR may not resolve after correcting the initial cause (e.g., mitral valve surgery) 3
- Late TR can appear years after initial cardiac surgery 3
- Isolated tricuspid surgery has poor outcomes once RV dysfunction is established 3, 4
Ventricular Interdependence Effects
With severe RV dilation, the interventricular septum shifts toward the LV, causing: 1, 2
- Reduced LV cavity size and restricted LV filling 1
- Increased LV diastolic pressure 1
- Biventricular diastolic dysfunction 2
Clinical Pitfall
**The most common error is assuming TR <40 mm Hg PA pressure indicates primary valve pathology** - while this correlation exists, functional TR can occur at lower pressures if significant annular dilatation is present (>35 mm or >21 mm/m²) 1. Always measure annular dimensions directly rather than relying solely on PA pressure estimates.
Approximately 80% of Significant TR Cases
Functional TR accounts for approximately 80% of all significant tricuspid regurgitation cases, with the remaining 20% due to primary valve abnormalities (endocarditis, rheumatic disease, carcinoid, trauma, congenital anomalies, etc.) 1.