Influenza and COVID-19 pneumonia: the difference is pulmonary hypertension

ABSTRACT

PurposeTo describe the incidence of pulmonary artery thrombosis in COVID-19 versus influenza pneumonia using CT angiography and to assess whether it may increase the risk of pulmonary hypertension.Materials and MethodsSingle and dual energy CT pulmonary angiography of age- and gender-matched patients with influenza and COVID-19 pneumonia, referred for extra-corporeal membrane oxygenation (ECMO) and/or mechanical ventilation from January 2016 to January 2021, were retrospectively evaluated. Two independent observers qualitatively and quantitively assessed clot burden and Qanadli CT Obstruction Index. Two consensus observers calculated pulmonary artery volume and right to left ventricular diameter ratio (Terarecon, California, USA) to diagnose pulmonary hypertension. Pulmonary infarct volume and perfused blood volume relative enhancement were also calculated (Syngo via, Siemens Healthineers, Forchheim, Germany). All radiologic parameters were correlated with clinical data. To assess if in situ thrombosis could be visualised on CT, isolated segmental and subsegmental filling defects were used as an imaging surrogate. For statistical analyses, Graphpad Prism9 and IBM SPSS v27.0 software were used.ResultsThe incidence of either central PE or DVT was equal between patients with COVID-19 and influenza pneumonia (20%). The incidence of isolated segmental and subsegmental filling defects was higher in COVID-19 but without statistical significance (44% vs 32%;p=0.5607). Right to left ventricular diameter and pulmonary artery to aorta ratios were higher in COVID-19 compared to influenza (1.01 vs 0.866 and 1.04 vs 0.904;p=0.0071 and p=0.0023, respectively).ConclusionIn a comparable group of patients with severe COVID-19 and influenza pneumonia, CT features of pulmonary hypertension are more often present in patients with COVID-19 pneumonia despite an equal clot burden on CT. This is not attributable to pulmonary thrombosis visible on CT and supports the hypothesis that micro- rather than macrovascular obstruction is the cause of severe hypoxia in COVID-19 pneumonia.