Echocardiographic markers of severe tricuspid regurgitation associated with right-sided congestive heart failure

Background and aim of the study: Severe tricuspid regurgitation (TR), diagnosed with echocardiography, is not necessarily symptomatic. The study aim was to identify echocardiographic markers associated with right-sided congestive heart failure (RCHF) in patients with severe TR. Methods: Ninety-six patients (30 males, 66 females; mean age 67 ± 11 years) with echocardiographic findings of severe TR were followed clinically and with transthoracic echocardiography (TTE). Clinical data were collected on heavy diuretic consumption and signs of volume overload (neck vein congestion, lower-limb edema, ascites). TTE included evaluation of the right heart chamber dimensions, systolic function, pulmonary pressure and change in inferior vena cava. (IVC) diameter during respiration. Patients were subdivided according to the presence (group A, n = 52) or absence (group B, n = 44) of signs of RCHF that included volume overload and heavy diuretic consumption (i.e. ≥80 mg furosemide/day or combined furosemide/spironolactone at any dosage). Results: Among the patients, 52 (54.2%) had RCHF and 44 (45.8%) did not. Atrial fibrillation was present in 88% of group A and 76% of group B (p = NS). Group A patients had a significantly larger right ventricular area, right atrial area and IVC diameter than group B patients, but a significantly smaller variation in IVC diameter during respiration (11.2 ± 8.5% versus 24.3 ± 14.1%, p = 0.001). Right ventricular systolic function and systolic pulmonary pressure were similar in the two groups. On multivariate analysis, respiratory-related variation in IVC diameter (p <0.001) and systolic pulmonary artery pressure (p = 0.04) were the only independent echocardiographic markers of RCHF. Conclusion: Diminished respiratory variation in IVC diameter and systolic pulmonary artery pressure are independent markers of volume overload in patients with severe TR. These findings may reflect exhaustion of IVC capacitance due to markedly increased right heart filling pressures, though intrinsic changes in IVC tonus may also be involved.