Reply To: “Pulmonary Artery Dilatation in Different Causes of Pulmonary Hypertension”

We read with great interest the recent article by Xi et al. entitled “Pulmonary artery dilatation in different causes of pulmonary hypertension.” The authors provide a comprehensive evaluation of more than one thousand patients with different subtypes of pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH), showing that pulmonary artery (PA) dilatation is a common finding but does not independently predict survival. Their conclusion that only the 6-min walk distance serves as an independent prognostic marker highlights the complexity of interpreting PA size in clinical practice. Several previous studies support and expand these observations. Badagliacca et al. [1] demonstrated in a cohort of patients with severe PH that although PA dilatation was present in more than 75% of cases, it had no prognostic impact, with outcomes instead determined by functional class and disease etiology. Similarly, Duijnhouwer et al. [2] confirmed that PA diameter measured at diagnosis did not independently predict mortality in PAH or CTEPH when established prognostic factors such as NYHA class, 6-min walk distance, and NT-proBNP were considered. Nevertheless, other reports suggest that in selected contexts, PA enlargement may carry prognostic weight. Żyłkowska et al. [3] found that PA dilatation ≥ 48 mm was independently associated with unexpected death in PAH and CTEPH, raising concern for catastrophic complications such as rupture, dissection, or coronary artery compression. In connective tissue disease–associated PAH, Li et al. [4] showed that a main PA diameter ≥ 37.7 mm predicted poor long-term survival, identifying vascular enlargement as a risk marker in this subgroup. Finally, a systematic review and meta-analysis by Badea et al. [5] emphasized the potential clinical consequences of extreme PA dilatation, highlighting its association with left main coronary artery compression, with thresholds between 40 and 44 mm providing optimal accuracy for screening. Taken together, these studies, along with the findings of Xi et al., suggest that while PA dilatation is highly prevalent across PH subtypes and correlates with several hemodynamic and anatomical features, its prognostic significance is heterogeneous. PA size alone is not a reliable predictor of outcome in most patients, but in specific scenarios—such as CTD-PAH, marked enlargement beyond 40–48 mm, or when complications like coronary artery compression are suspected—its measurement may have important clinical implications. Could serial assessments of PA diameter over time, rather than a single baseline measurement, provide additional information on disease progression and therapeutic response? Could the integration of PA diameter with functional markers (e.g., 6MWD, NT-proBNP, functional imaging, RV-PA coupling) improve prognostic models compared with each parameter considered in isolation? Are the observed associations specific to PH pathophysiology, or does PA dilatation represent a more general vascular response to pressure/flow overload conditions? In cases of severe dilatation, could early or interventional treatment (e.g., coronary stenting in the case of LMCA compression) modify prognosis? Future prospective, multicenter studies addressing these aspects may help delineate the true clinical significance of PA dilatation and refine its role in prognostic models for PAH. Dr. Annalisa Caputo and Dr. Gianmarco Scoccia conceived and drafted the manuscript. All authors critically revised t The authors declare no conflicts of interest.he content and approved the final version. The authors have nothing to report. The authors have nothing to report. The authors declare no conflicts of interest. Dr. Annalisa Caputo.