C66-21 Correlation of Computed Tomography-Derived Pulmonary Artery Diameter With Hemodynamic and Functional Parameters in Interstitial Lung Disease-Associated Pulmonary Hypertension

Abstract Rationale Computed tomography (CT)-based pulmonary artery (PA) enlargement has been associated with elevated mean pulmonary artery pressure (mPAP) across several pulmonary hypertension (PH) subtypes. However, most prior studies included heterogeneous or COPD-predominant populations, limiting their relevance to PH associated with interstitial lung disease (PH-ILD). In this phenotype, fibrosis-induced tractional dilation, loss of alveolar-capillary surface area, and impaired lung compliance alter vascular geometry and may confound imaging-based estimation of pulmonary vascular load. Understanding whether PA diameter maintains a meaningful relationship with hemodynamics and right ventricular function in PH-ILD could refine noninvasive disease assessment. This study examines correlations between CT-measured PA diameter and both invasive (mPAP, PVR) and physiologic (TAPSE, DLCO) indices in a well-characterized PH-ILD cohort. Methods Adults with ILD who underwent both high-resolution CT and right heart catheterization within six months were retrospectively analyzed. Echocardiographic (TAPSE) and physiologic (DLCO) data were extracted from corresponding evaluations. Correlations between PA diameter and each variable were assessed using Spearman’s rho. Results Eighty patients met inclusion criteria. Correlations between PA diameter and physiologic measures were as outlined in the table below. PA diameter demonstrated only a borderline correlation with mPAP and minimal association with other parameters. Conclusions In PH-ILD, pulmonary artery enlargement on CT demonstrates only a subtle association with hemodynamic severity, suggesting that vascular dilation reflects a complex interplay of both fibrotic and vascular remodeling rather than pressure load alone. These findings highlight the limits of relying solely on PA diameter as a surrogate for pulmonary vascular disease and emphasize the need for integrated imaging-hemodynamic models that account for the unique structural distortion inherent to fibrotic lung disease. This abstract is funded by: None