Résumé
Importance: Acute COVID19 related myocardial, pulmonary and vascular pathology, and how these relate to each other, remains unclear. No studies have used complementary imaging techniques, including molecular imaging, to elucidate this. Objective: We used multimodality imaging and biochemical sampling in vivo to identify the pathobiology of acute COVID19. Design, Setting and Participants: Consecutive patients presenting with acute COVID19 were recruited during hospital admission in a prospective cross sectional study. Imaging involved computed tomography coronary angiography (CTCA - identified coronary disease), cardiac 2deoxy2[fluorine18]fluoroDglucose positron emission tomography/computed tomography (18F FDG PET/CT identified vascular, cardiac and pulmonary inflammatory cell infiltration) and cardiac magnetic resonance (CMR identified myocardial disease), alongside biomarker sampling. Results: Of 33 patients (median age 51 years, 94% male), 24 (73%) had respiratory symptoms, with the remainder having non-specific viral symptoms. Nine patients (35%, n=9/25) had CMR defined myocarditis. 53% (n=5/8) of these patients had myocardial inflammatory cell infiltration. Two patients (5%) had elevated troponin levels. Cardiac troponin concentrations were not significantly higher in patients with myocarditis (8.4ng/L [IQR 4.0, 55.3] vs 3.5ng/L [2.5, 5.5], p=0.07) or myocardial cell infiltration (4.4ng/L [3.4, 8.3] vs 3.5ng/L [2.8, 7.2], p=0.89). No patients had obstructive coronary artery disease or vasculitis. Pulmonary inflammation and consolidation (percentage of total lung volume) was 17% (IQR 5, 31%) and 11% (7, 18%) respectively. Neither were associated with presence of myocarditis. Conclusions and relevance: Myocarditis was present in a third patients with acute COVID-19, and the majority had inflammatory cell infiltration. Pneumonitis was ubiquitous, but this inflammation was not associated with myocarditis. The mechanism of cardiac pathology is non-ischaemic, and not due to a vasculitic process.