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

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.

Interestingly, among patients with normal baseline mean PAP (mPAP), the proportion developing an mPAP > 20 mmHg at follow‐up was substantially higher in the EIPH group (37%) than in non‐EIPH patients (11%) and controls (7%). This finding strongly supports the hypothesis that EIPH identifies individuals at an early stage of pulmonary vascular disease. Due to the remarkable reserve capacity of the pulmonary circulation, pulmonary artery pressures and pulmonary vascular resistance may remain normal at rest. ESE may therefore help unmask early abnormalities before overt resting pulmonary hypertension becomes evident.

Notably, the study found greater longitudinal sPAP progression in men and in patients with diffuse cutaneous SSc. These findings suggest that ESE might be particularly valuable for risk stratification targeting these specific higher‐risk subpopulations [4, 5].

In conclusion, considering the poor prognosis associated with delayed diagnosis of pulmonary arterial hypertension in SSc, the ability of ESE to unmask early pulmonary vascular disease carries important clinical implications. Identifying an early pulmonary vascular phenotype via ESE may support a shift toward a more proactive approach, enabling closer hemodynamic monitoring and informing future strategies aimed at earlier therapeutic intervention. Prospective studies are warranted to validate these noninvasive parameters against invasive right heart catheterization and to better define their therapeutic implications. In this context, ESE emerges as a promising tool to refine current screening algorithms in this high‐risk population.

Author Contributions

The author was responsible for the conception, drafting, and revision of the manuscript and approved the final version.

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