Can obesity cause tricuspid regurgitation?

Can Obesity Cause Tricuspid Regurgitation?

Obesity does not directly cause tricuspid regurgitation through primary valve damage, but it creates multiple pathophysiologic mechanisms that lead to functional (secondary) TR, including pulmonary hypertension, right ventricular dysfunction, and increased fluid volume overload.

Mechanisms Linking Obesity to Tricuspid Regurgitation

Pulmonary Hypertension Pathway

• Obesity causes obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS), which lead to episodes of oxygen desaturation, transient increases in pulmonary artery pressures, and eventually permanent pulmonary hypertension 1
• Over time, these repeated hypoxemic episodes result in right ventricular hypertrophy and dysfunction 1
• Pulmonary hypertension with systolic PA pressures exceeding 55 mm Hg causes TR even with anatomically normal tricuspid valve leaflets through RV cavity enlargement, tricuspid annular dilatation, and papillary muscle displacement 2, 3

Volume Overload Mechanism

• Obesity increases plasma volume and cardiac output through activation of both the sympathetic nervous system and renin-angiotensin-aldosterone system 1
• This increased fluid retention creates volume overload on the right ventricle, contributing to RV remodeling and subsequent functional TR 1
• The mechanical effects of excess abdominal fat mass increase intrathoracic pressure, further compromising right-sided cardiac function 1

Right Ventricular Remodeling

• Obesity causes RV dilation independent of other factors, with obese patients demonstrating significantly larger RV end-diastolic and end-systolic areas compared to normal-weight patients with TR 4
• Tricuspid annular dilatation (>35 mm absolute or >21 mm/m²) develops as the RV enlarges, causing the annulus to lose its normal saddle shape and become flat and planar 3
• Leaflet tethering occurs from papillary muscle displacement, preventing proper leaflet coaptation despite structurally normal valve tissue 3

Clinical Context and Caveats

The Obesity Paradox

• Despite causing more RV remodeling, overweight and obese patients with established significant TR demonstrate better long-term survival compared to normal-weight patients (5-year survival 65-67% vs 58%, p<0.001) 4
• This obesity paradox means that while obesity contributes to TR development, once TR is present, higher BMI is independently associated with lower all-cause mortality (HR 0.628 for overweight, HR 0.573 for obese) 4
• This does not negate obesity's role in TR causation but highlights the complex relationship between body weight and outcomes in established valvular disease 4

Distinguishing Functional from Primary TR

• Functional TR accounts for approximately 80% of all significant TR cases, with obesity-related mechanisms falling into this category 3
• A common pitfall is assuming TR with PA pressures <40 mm Hg indicates primary valve pathology—functional TR can occur at lower pressures if significant annular dilatation is present (>35 mm or >21 mm/m²) 3
• Quantitative markers of functional TR include tenting area >1 cm² and coaptation distance >0.76 cm 3

Additional Obesity-Related Cardiovascular Effects

• Obesity causes cardiac autonomic neuropathy with parasympathetic withdrawal and sympathetic predominance, increasing risk of atrial and ventricular dysrhythmias that can worsen TR 1
• Obesity is associated with diastolic and systolic ventricular dysfunction, left ventricular hypertrophy, and congestive heart failure—all of which can contribute to elevated pulmonary pressures and secondary TR 1
• Increased inflammatory cytokines (CRP, IL-6, IL-18) associated with obesity may contribute to progressive cardiac remodeling 1

Clinical Implications

Progressive Nature

• Once TR develops, it creates a vicious cycle: TR itself worsens RV function through volume overload superimposed on existing pressure overload, leading to further RV dilatation, more annular dilatation, and progressively worsening TR 2
• In advanced cases, ventricular interdependence develops where the dilated RV shifts the interventricular septum toward the LV, reducing LV cavity size and causing restricted LV filling 2, 3

Management Considerations

• Weight loss in obese patients can improve diastolic function and modify cardiovascular risk factors, though specific data on TR reversal with weight loss are limited 1
• Addressing underlying obesity-related conditions (OSA, pulmonary hypertension, volume overload) is essential to prevent TR progression 1
• Patients with obesity and higher systolic blood pressure warrant special attention as these factors predict significant TR development 5