Extended Data Fig. 5.

Persisting cardio-renal abnormalities due to COVID-19 infection. A 66-year-old man with history of hypertension was admitted with increasing breathlessness and transient syncope. There was no history of chest pain. The PCR test confirmed SARS-CoV-2 infection and the D-Dimer concentration was 35,656 ng/L. The admission electrocardiogram revealed atrial fibrillation with a rapid ventricular rate requiring electrocardioversion due to haemodynamic compromise (a). The computed tomography (CT) pulmonary angiogram revealed COVID-19 pneumonitis (b) and bilateral pulmonary arterial thrombus involving both central and peripheral branches (c). Treatment dose low molecular weight heparin was initially prescribed followed by directoral anticoagulation. Despite additional treatment with tocilizumab and dexamethasone for covid pneumonitis, intubation and mechanical ventilation were necessary during a 4-day admission to the intensive care unit (ICU). The patient recovered, supported by treatment with inhaled oxygen and a reducing dose of dexamethasone. At visit 2, one month later, the research coronary CT angiogram and FFRct excluded obstructive coronary artery disease (d). Protocoldirected MRI revealed tissue inflammation in the kidney (increased renal T1 (e, cortex 1666ms, medulla 2060 ms), and myocardium (native T1 (f, 1303 ms), and native T2 (g, 49 ms) associated with late gadolinium enhancement localized to the inferior left ventricular wall with a sub-epicardial distribution (h) in keeping with myocardial inflammation. The CT chest scan revealed substantially improvement in the lung parenchyma, and the previously identified pulmonary emboli were no longer evident.