Cardiac remodelling in secondary tricuspid regurgitation: Should we look beyond the tricuspid annulus diameter?

BACKGROUND

A better understanding of the mechanism of tricuspid regurgitation severity would help to improve the management of this disease.

AIM

We sought to characterize the determinants of isolated secondary tricuspid regurgitation severity in patients with preserved left ventricular ejection fraction.

METHODS

This was a prospective observational multicentre study. Patients with severe tricuspid regurgitation were asked to participate in a registry that required a control echocardiogram after optimization of medical treatment and a follow-up. Patients had to have at least mild secondary tricuspid regurgitation when clinically stable, and were classified according to five grades of tricuspid regurgitation severity, based on effective regurgitant orifice area.

RESULTS

One hundred patients with tricuspid regurgitation (12 mild, 31 moderate, 18 severe, 17 massive and 22 torrential) were enrolled. Right atrial indexed volume and tethering area were statistically associated with the degree of tricuspid regurgitation (P<0.001 and P=0.005, respectively). When the tricuspid annular diameter was≥50mm, the probability of having severe tricuspid regurgitation or a higher grade was>70%. For an increase of 10mL/m in right atrial volume, the effective regurgitant orifice area increased by 4.2mm, and for an increase of 0.1cm in the tethering area, the effective regurgitant orifice area increased by 2.35mm. The degree of right ventricular dilation and changes in tricuspid morphology were significantly related to tricuspid regurgitation severity class (P<0.001). No significant difference in right ventricular function variables was observed between the tricuspid regurgitation classes.

CONCLUSIONS

For tricuspid regurgitation to be severe or torrential, both right atrial dilatation and leaflet tethering are needed. Interestingly, right cavities dilated progressively with tricuspid regurgitation severity, without joint degradation of right ventricular systolic function variables.