Tricuspid regurgitation improvement in relation to the amount of pulmonary artery pressure reduction.

I was interested in the study conducted by Dr. Zoroufian et al.,1 in which they conclude, “the improvement in tricuspid regurgitation (TR) severity is directly correlated with the amount of pulmonary artery systolic pressure (PAPs) reduction after mitral balloon valvotomy (MBV)” and propose a moderately sensitive and specific cut-off point for PAPs change in the prediction of TR improvement. This conclusion is based on the post-MBV result, in which patients with TR severity improvement showed a greater decrease in PAPs following MBV than did those with unchanged or worsened TR grade (p value < 0.034).

I believe the conclusion is not properly substantiated because there is a great mismatch between the groups and the paper fails to consider the possible influence of confounders. Based on their findings, the ejection fraction (EF) was significantly lower in patients who showed a worsening in the TR grade after intervention. Likewise, as it is accurately noticed in the discussion, right ventricular dilation is a common cause of functional TR,2, 3 and mitral stenosis (MS) severity4 has been indicated as a significant different variable in the comparison of patients with and without TR improvement following MBV. A comparison of the demographic data, which are highly associated with PAPs,5 is also ignored in the current study. Taken together, I think there is a need to a comprehensive comparison of the demographic variables and echocardiographic measurements between the patients according to the TR change; and thereafter, all the significant variables in the univariate comparison (such as primary/secondary or/and changes in PAPs, right ventricular dimension [RVD], EF level, and possibly some demographic variables) along with the other possible confounders (initial MS grade or mitral valve area [MVA], MS severity change, or MVA increase) should be entered into the multivariable logistic model to identify the independent predictors of TR improvement. Finally, the associations of the independent predictors with TR improvement in the final model should be expressed as odds ratios (OR) with 95% CIs.

Furthermore, although PAPs > 35 and PAPs ≥ 25 are mentioned as the definitions for pulmonary artery hypertension (PAH) according to the referred citations,6–8 it is not definitely obvious what criteria are employed by the authors to define PAH. As I looked through the references, I did not find PAPs > 35 as a definition for PAH. It was just mentioned that the upper limit value of PAPs in a normal population is 30mmHg. Accordingly, 28% of the normal population had PAPs > 30 mmHg in a study conducted by Berndan et al.5 Moreover, even 37 ≤ PAPs ≤ 50 mmHg is considered a suggestive but not definite criterion for the presence of PAH.7 Based on the current guidelines, mean PAP ≥ 25 mmHg (but not mean PAPs as it is written in the paper) at rest as assessed by right heart catheterization (RHC) is mentioned as a diagnostic criterion for PAH6, 7 After all, in regard to the aim of the study, it seems there is no need to use such a definition, and the use of PAPs as a quantitative variable for the subsequent analysis would lead to more accurate results.

The purpose of this letter is to point out some pitfalls which are generally ignored by the investigators and weaken the final conclusion. I hope it may be helpful.