Transcatheter tricuspid valve repair and pulmonary hypertension: navigating through troubled waters

This commentary refers to ‘Clinical characteristics, diagnosis, and risk stratification of pulmonary hypertension in severe tricuspid regurgitation and implications for transcatheter tricuspid valve repair’ by P. Lurz et al., on page 2785.

We thank Dr D’Alto and Naeije¹ for their interest in our work regarding transcatheter tricuspid valve repair (TTVR) and pulmonary hypertension (PHT).²

We agree that our PHT definition differs from the current recommendations regarding invasive PHT diagnosis. However, systolic pulmonary artery pressure (sPAP) 50 mmHg was used as PHT criterion in previous reports in the field,³ the criterion is highly comparable between echocardiography and right heart catheterization and sensitivity analysis demonstrated a youden index optimized predictive value close to the literature based cut-off for sPAP at 49 mmHg.

Although our manuscript relates non-invasive and invasive PHT assessment, our goal was clinical risk stratification according to PHT categories rather than the analysis of the agreement between modalities. Evaluating the reasons for echocardiographic sPAP underestimation, we found that echocardiography underestimated right atrial pressure (RAP), especially in the highest RAP levels. Additionally, the discordant PHT group (echo/invasive PHT−/+) demonstrated the most severe tricuspid regurgitation (TR) grades and more frequently a v-wave cut-off sign, suggesting a systematic underestimation of the right ventricular (RV)–right atrial (RA) gradient due to limitations of the Bernoulli equation in this group.

The tricuspid annular plane systolic excursion (TAPSE)/sPAP ratio has recently been suggested as a surrogate of right ventricle-to-pulmonary circulation coupling.⁴ Risk stratification in our cohort was based on the median ratio in PHT patients (0.29). This value also corresponded to the maximized younden index on receiver operating statistics for the prediction of the combined endpoint in our cohort.

We agree that evidence of precapillary PHT might serve as an important risk marker in TTVR patients. In our analysis, an elevated transpulmonary gradient (TPG) was prognostically unfavourable. Interestingly, TPG but not an elevated pulmonary vascular resistance was predictive of the combined endpoint and TPG risk stratified better within PHT patients.

Although we believe that our manuscript adds an important, clinically applicable risk parameter (discordant PHT diagnosis as by sPAP) in the TTVR population, a significant number of questions regarding the predictive value of invasive haemodynamic parameters and their specific cut-off values within TTVR patients remain to be addressed in order to create informed decision trees as suggested by Dr D’Alto.

As for now, we would refrain from a priori excluding PHT patients from TTVR. In the light of a symptomatic benefit in all patient groups and the absence of a control group in our analysis, the lack of randomized data and a treatment benefit of TTVR in a variety of subgroups (including echocardiographic PHT patients) in comparison to propensity matched controls,³ it is currently unclear whether TTVR should be considered futile in any subgroup of PHT patients.

Conflict of interest: P.L. is a consultant to Abbott, Edwards and Medtronic. K.P.R. has nothing to declare.

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