Mechanisms of Pulmonary Hypertension-Induced Valvular Regurgitation
Tricuspid Regurgitation
Pulmonary hypertension causes tricuspid regurgitation primarily through right ventricular systolic pressure elevation leading to RV cavity enlargement, tricuspid annular dilatation, and papillary muscle displacement with leaflet tethering—all occurring with structurally normal valve leaflets. 1
Primary Pathophysiologic Mechanisms
RV pressure overload from elevated pulmonary artery pressures directly increases RV systolic pressure, which initiates a cascade of structural changes even when the tricuspid valve itself is anatomically normal 1
Progressive RV remodeling occurs as the ventricle dilates in response to chronic pressure overload, with the cavity enlargement causing geometric distortion of the subvalvular apparatus 1, 2
Tricuspid annular dilatation develops as the RV enlarges, with the annulus losing its normal saddle shape and becoming flat, planar, and distorted—this is considered the most important factor in functional TR development 1
Papillary muscle displacement occurs with RV dilatation, causing leaflet tethering that prevents adequate coaptation during systole 1, 3
Hemodynamic Thresholds
Systolic pulmonary artery pressures exceeding 55 mm Hg are likely to cause TR with anatomically normal tricuspid valves, whereas TR occurring with systolic pulmonary artery pressures below 40 mm Hg typically reflects structural valve abnormalities 1
The severity of TR correlates directly with the degree of pulmonary hypertension, with severe TR associated with higher right atrial pressures (mean 15 mm Hg vs 10 mm Hg) and lower cardiac index (2.2 L/min/m² vs 2.8 L/min/m²) 4
Self-Perpetuating Cycle
TR itself worsens RV function by creating volume overload superimposed on the existing pressure overload, leading to further RV dilatation, more annular dilatation and tethering, and progressively worsening TR 1
Right atrial enlargement accompanies this process, with 91% of patients with severe TR demonstrating right atrial dilatation compared to 47% in those with mild or no TR 4
Ventricular interdependence develops in advanced cases, where the dilated RV shifts the interventricular septum toward the left ventricle, potentially reducing LV cavity size and causing restricted LV filling with increased LV diastolic and pulmonary artery pressures 1
Clinical Implications
Severe TR is strongly predictive of mortality in pulmonary hypertension, with an adjusted hazard ratio of 1.83 for 5-year mortality risk even after controlling for age, functional class, and pulmonary vascular resistance 4
The presence of a pansystolic murmur of tricuspid regurgitation reflects elevated right ventricular pressures and is a key physical examination finding in pulmonary arterial hypertension 5
Mitral Regurgitation
Pulmonary hypertension causes mitral regurgitation through an indirect mechanism involving left ventricular dysfunction from ventricular interdependence, though this is far less common than tricuspid regurgitation and typically occurs only in advanced disease with severe RV failure.
Mechanism of Ventricular Interdependence
Septal shift occurs when the dilated, failing RV causes the interventricular septum to bow toward the left ventricle during diastole, reducing LV cavity size and altering LV geometry 1
This geometric distortion can affect mitral valve apparatus geometry, potentially causing functional mitral regurgitation through altered papillary muscle position and leaflet coaptation 1
Important Clinical Distinction
Mitral regurgitation in the context of pulmonary hypertension is more commonly the primary pathology causing secondary pulmonary hypertension, rather than pulmonary hypertension causing mitral regurgitation 6
In patients with rheumatic mitral valve disease and secondary pulmonary hypertension, functional tricuspid regurgitation is far more common than any worsening of the primary mitral pathology 6
Prognosis After Mitral Intervention
When mitral regurgitation is the primary lesion causing pulmonary hypertension, the concomitant tricuspid regurgitation may improve after mitral valve repair if pulmonary hypertension is severe and the tricuspid valve anatomy is not grossly distorted 7
However, improvement is less likely when significant tricuspid annular dilatation has already occurred, and functional tricuspid regurgitation persists or progresses in patients with advanced right ventricular dysfunction despite successful mitral valve replacement 7, 6
Functional tricuspid regurgitation regressed in 38 of 42 survivors with severe pulmonary hypertension after mitral valve replacement, but persisted or progressed in 22 of 34 survivors with impaired right ventricular function 6
Key Pitfall to Avoid
- Do not assume mitral regurgitation will automatically improve pulmonary hypertension-related tricuspid regurgitation—patients with moderate or greater TR at the time of mitral surgery should be considered for concomitant tricuspid intervention, especially if tricuspid annular dilatation is present 2