How can a shunt cause tricuspid regurgitation?

How a Shunt Causes Tricuspid Regurgitation

A shunt causes tricuspid regurgitation primarily through right ventricular volume overload leading to RV dilation, tricuspid annular dilatation, and papillary muscle displacement—mechanisms that occur even with structurally normal tricuspid valve leaflets.

Primary Pathophysiologic Mechanisms

Volume Overload Pathway

Left-to-right shunts (such as atrial septal defects) cause tricuspid regurgitation by creating chronic RV volume overload, which progressively dilates the right ventricle and secondarily stretches the tricuspid annulus. 1, 2 This volume loading effect has been directly demonstrated in surgical studies where shunt procedures worsen tricuspid regurgitation scores, while volume-reducing interventions improve them. 3

• Atrial septal defects specifically cause RV volume overload through continuous left-to-right shunting, resulting in pulmonary overcirculation and progressive RV enlargement. 1, 2
• The chronic volume load causes the tricuspid annulus to lose its normal saddle-shaped geometry, becoming flat and planar—this annular dilatation is the most critical factor in functional tricuspid regurgitation development. 4
• Papillary muscle displacement occurs as the RV cavity enlarges, creating leaflet tethering that prevents proper coaptation during systole. 4

Pressure Overload Contribution

When shunts lead to pulmonary hypertension (as can occur with large, long-standing left-to-right shunts), a secondary pressure overload mechanism compounds the volume overload effects. 1, 4

• Elevated pulmonary artery pressures increase RV systolic pressure, which accelerates RV remodeling and further worsens tricuspid annular dilatation. 4
• Systolic pulmonary artery pressures exceeding 55 mmHg are likely to cause tricuspid regurgitation even with anatomically normal valves. 4
• The combination of volume and pressure overload creates a vicious cycle where tricuspid regurgitation itself adds additional volume load to the already stressed RV. 4

Specific Shunt-Related Scenarios

TIPS (Transjugular Intrahepatic Portosystemic Shunt)

TIPS acutely increases right atrial pressure by 3-5 mmHg, which can precipitate or worsen tricuspid regurgitation through volume overload and elevated right-sided pressures. 1

• The sudden increase in venous return to the right heart creates acute RV volume loading. 1
• Pre-existing chronic volume overload from portal hypertension may have already caused RV dysfunction and tricuspid annular dilatation, making these patients particularly vulnerable. 1
• Right atrial pressures exceeding 14.5 mmHg pre-TIPS or 21.5 mmHg post-TIPS are associated with increased mortality, highlighting the importance of assessing baseline tricuspid regurgitation severity before TIPS creation. 1

Surgical Shunts in Congenital Heart Disease

Blalock-Taussig shunts significantly worsen tricuspid regurgitation, with studies showing tricuspid regurgitation scores increasing from 0.7 ± 0.5 preoperatively to 1.4 ± 0.6 postoperatively. 3

• This contrasts sharply with pulmonary artery banding (which reduces volume load), where tricuspid regurgitation scores decrease from 1.7 ± 0.8 to 0.9 ± 0.6. 3
• The mechanism is pure RV volume loading from the systemic-to-pulmonary arterial shunt. 3

Paradoxical Right-to-Left Shunting

Severe tricuspid regurgitation can itself create or unmask right-to-left shunting through a patent foramen ovale by causing right atrial pressure elevation and "ventricularization" of right atrial pressures. 5, 6, 7

• The tricuspid regurgitant jet, when oriented toward the interatrial septum, can force blood through a patent foramen ovale during late systole to mid-diastole. 5
• Right atrial dilatation from severe tricuspid regurgitation mechanically reopens the foramen ovale. 7
• This creates systemic hypoxemia and cyanosis, which may require emergent surgical intervention. 6

Critical Clinical Implications

Pre-Procedural Assessment

Before TIPS creation, careful assessment of tricuspid regurgitation etiology is mandatory—when volume overload is suspected, volume optimization should be attempted before reassessment. 1

• Chronic volume overload resulting in RV dysfunction and persistent moderate-to-severe functional tricuspid regurgitation can be prohibitive of TIPS. 1
• Echocardiographic surveillance is warranted in high-risk patients at 3 months post-TIPS, when hemodynamic changes peak. 1

Surgical Considerations

Unrecognized patent foramen ovales or atrial septal defects should be investigated before VAD implantation or intraoperatively, with repair performed during the procedure to prevent paradoxical emboli and hypoxemia from right-to-left shunting. 1

• Severe tricuspid insufficiency should be repaired at the time of LVAD implantation to prevent RV failure. 1
• The enlarged right atrium from chronic shunt-related volume overload creates hemodynamic complications and predisposes to thrombus formation, particularly with atrial fibrillation. 2

Common Pitfall

The most critical pitfall is failing to recognize that structurally normal tricuspid valves can develop severe regurgitation purely from hemodynamic forces created by shunts—this is functional, not organic, valve disease. 4, 3 Addressing the underlying shunt and volume load is essential, as isolated tricuspid valve intervention without correcting the hemodynamic abnormality will likely fail.