Comment on: “Echocardiography-Derived Exercise Pulmonary Hypertension and Longitudinal Changes in Pulmonary Artery Pressures in Systemic Sclerosis”

Alexandra Mihai

https://doi.org/10.1002/pul2.70291 

Dear Editor,
Early identification of pulmonary vascular disease remains a major unmet need in systemic sclerosis. In this context, the study by Kagami and colleagues provides important insights into the role of exercise stress echocardiography in detecting early hemodynamic abnormalities [1].

In this study, the presence of EIPH was associated with a greater longitudinal increase in resting systolic pulmonary artery pressure (sPAP). However, the magnitude of the observed change in the overall cohort appears relatively modest (+1.2 mmHg vs. −1.0 mmHg over a median follow-up of 2.4 years). Considering the known variability of Doppler-derived pulmonary artery pressure estimates, such small differences may fall within expected measurement variability and are therefore difficult to interpret as clinically meaningful progression [2, 3]. This also highlights the intrinsic limitations of relying solely on isolated, flow-dependent variables like sPAP. Evaluating the multipoint pressure–flow relationship (e.g., mPAP/CO slope) during ESE represents a more robust physiological marker to distinguish true pulmonary vascular remodeling from high-flow states. Nevertheless, we acknowledge the authors' insightful sensitivity analysis excluding patients who initiated pulmonary vasodilators or heart failure medications, which revealed a more pronounced divergence (+2.2 mmHg vs. −1.6 mmHg). This suggests that early targeted treatments may indeed mask the natural progression of pulmonary vascular disease in these individuals.

The authors carefully adjusted their analyses for several potential confounders. Yet, baseline differences between groups and the relatively limited sample size may still leave room for residual confounding. In addition, control patients were selected among individuals who did not undergo ESE, potentially reflecting a different level of clinical suspicion for pulmonary vascular disease and introducing a selection bias.

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