Pulmonary vascular and airway changes in previously hospitalised COVID-19 patients: Long-term functional respiratory imaging findings correlate with reduced DLCO

Abstract

Background Persistent respiratory symptoms in COVID-19 patients have raised concerns about structural remodelling in the lung. We assessed structural changes and their correlation with reduced DLCO, eight months after discharge, in previously hospitalised COVID-19 patients. Materials and Methods An exploratory observational study was conducted on 26 male patients (mean age: 60 years, range: 50–69) previously hospitalised for COVID-19. CT scans, performed eight months post-discharge, were analysed using functional respiratory imaging (FRI) to assess lung structure and function. Analyses were made based on diffusion capacity for carbon monoxide (DLCO). Results Patients with low DLCO (≤75%; n=9) exhibited a significantly lower proportion of small blood vessels with a cross-sectional area<5 mm2 compared to patients with normal DLCO (>75%; n=17) (median (IQR) 56 (51–59) % vs. 60 (56–64) %, p=0.008), as well as a reduced absolute volume of small vessels with a cross-sectional area<5 mm2 (129 (121–151) ml vs. 155 (132–175) ml, p=0.025). Bronchial dilatation was more evident in the low DLCO group, with a higher ratio of airway volume to lobar volume (siVaw) (149 (138–165) % vs. 117 (93–132) %, p=0.002). SiVaw showed a significant inverse relationship with DLCO (r=–0.56, p=0.004, R2=0.31). Lobar volumes were reduced in both DLCO groups, and more pronounced in the low DLCO group (72 (65–81) % vs. 90 (79–95) %, p=0.001), as was total lung capacity (TLC) (73 (64–85) % vs. 92 (85–98) % of predicted, p=0.003). FEV1/FVC ratios were elevated in both groups, with a potential difference observed between the low and normal DLCO groups (110 (103–118) % vs. 105 (95–113) %, p=0.074). Conclusions We demonstrate long-term vascular and airway remodelling detected with FRI in previously hospitalised COVID-19 patients and highlight potential mechanisms underlying persistent pulmonary dysfunction and emphasise the need to investigate the underlying pathophysiology to identify potential individualised treatment strategies for this patient group.