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RationaleThe impact of COVID-19 on patients with Interstitial Lung Disease (ILD) has not been established. ObjectivesTo assess outcomes following COVID-19 in patients with ILD versus those without in a contemporaneous age, sex and comorbidity matched population. MethodsAn international multicentre audit of patients with a prior diagnosis of ILD admitted to hospital with COVID-19 between 1 March and 1 May 2020 was undertaken and compared with patients, without ILD obtained from the ISARIC 4C cohort, admitted with COVID-19 over the same period. The primary outcome was survival. Secondary analysis distinguished IPF from non-IPF ILD and used lung function to determine the greatest risks of death. Measurements and Main ResultsData from 349 patients with ILD across Europe were included, of whom 161 were admitted to hospital with laboratory or clinical evidence of COVID-19 and eligible for propensity-score matching. Overall mortality was 49% (79/161) in patients with ILD with COVID-19. After matching ILD patients with COVID-19 had higher mortality (HR 1.60, Confidence Intervals 1.17-2.18 p=0.003) compared with age, sex and comorbidity matched controls without ILD. Patients with a Forced Vital Capacity (FVC) of <80% had an increased risk of death versus patients with FVC [≥]80% (HR 1.72, 1.05-2.83). Furthermore, obese patients with ILD had an elevated risk of death (HR 1.98, 1.13-3.46). ConclusionsPatients with ILD are at increased risk of death from COVID-19, particularly those with poor lung function and obesity. Stringent precautions should be taken to avoid COVID-19 in patients with ILD.
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In contrast to early reports of conventional acute respiratory distress syndrome (ARDS) as the underlying pathophysiology of hypoxemic respiratory failure observed in patients with severe COVID-19, more recent findings implicate direct involvement of the pulmonary vasculature in giving rise to these symptoms. In earlier research, we demonstrated that patients with COVID-19 showed markedly reduced pulmonary blood volumes in pulmonary vessels <5 mm2 in cross-sectional area visible on imaging (termed "BV5"), with attendant dilation of larger, more proximal vessels. Here, we present preliminary results in which reduced BV5 is shown to correlate significantly with increased need for supplemental oxygen and abnormal arterial blood gas measurements in hospitalized COVID-19 patients. We suggest a potential mechanistic link between observed clinical, pathological, and imaging findings, and outline how these may be helpful in clinical assessment as well as the development of novel therapies.
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BackgroundMounting evidence supports the role of pulmonary hemodynamic alternations in the pathogenesis of COVID-19. Previous studies have demonstrated that changes in pulmonary blood volumes measured on CT are associated with histopathological markers of pulmonary vascular pruning, suggesting that quantitative HRCT analysis may eventually be useful in the assessment pulmonary vascular dysfunction more broadly. MethodsBuilding upon previous work, automated HRCT measures of small blood vessel volume and pulmonary vascular density were developed. Scans from 103 COVID-19 patients and 108 healthy volunteers were analyzed and their results compared, with comparisons made both on lobar and global levels. ResultsCompared to healthy volunteers, COVID-19 patients showed significant reduction in BV5 (pulmonary blood volume contained in blood vessels of <5 mm2) expressed as BV5/(Total pulmonary blood volume) (p<0.0001), and significant increases in BV5_10 and BV 10 (pulmonary blood volumes contained in vessels between 5 and 10 mm2 and above 10 mm2, respectively) (p<0.0001). These changes were consistent across lobes. ConclusionsCOVID-19 patients display striking anomalies in the distribution of blood volume within the pulmonary vascular tree, consistent with increased pulmonary vasculature resistance in the pulmonary vessels below the resolution of HRCT.
