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438 she had had recurrent infections of the upper respiratory tract and reported loss of taste. She did not complain of chest pain and was hemody‐ namically stable. It could not be clarified wheth‐ er the atrial fibrillation was a new ‐onset pathol‐ ogy or (very likely) a rather long ‐standing dis‐ order. Otherwise, the patient was healthy, she was not hypertensive and did not have diabe‐ tes mellitus or thyroid disorders nor was she obese (body mass index, 25.2 kg/m2). We deter‐ mined D ‐dimer levels for risk stratification of the severity of the disease and found they were elevated at 14 903 μg/l (reference range <230 μg/l). C ‐reactive protein levels were elevated with 95.9 mg/l (reference range <5 mg/l), procal‐ citonin levels were normal. Thus, we performed an unenhanced computed tomography scan of the thorax (Figure 1A) as well as computed tomog‐ raphy pulmonary angiography (Figure 1B). Bipul‐ monary ground‐glass opacities with transition to consolidations compatible with COVID ‐19 Elevated levels of D ‐dimer are discussed as a marker for an unfavorable outcome in severe acute respiratory syndrome coronavirus 2 infec‐ tions. Zhang et al1 reported significantly higher levels of D ‐dimer (as well as C ‐reactive protein and procalcitonin) as associated with a more se‐ vere course of the disease in an analysis of the re‐ cords of 140 hospitalized patients with corona‐ virus disease 2019 (COVID ‐19). The authors dis‐ cussed the elevated D ‐dimer levels as indicative of a sustained inflammatory response and dis‐ turbed coagulation after the infection. Other au‐ thors confirmed that elevated D ‐dimer levels are a negative prognostic factor, for example, Zhou et al2 in a retrospective multicenter cohort study in 191 patients. So far, there is limited data on whether SARS‐ ‐CoV ‐2 infection also favors thromboembolic events. Danzi et al3 recently reported the case of a 75 ‐year ‐old patient (sinus rhythm on electro‐ cardiogram) with a severe bilateral SARS ‐CoV ‐2 pneumonia and concomitant acute pulmonary embolism (no strong predisposing risk factors for venous thromboembolism). Xie et al4 also re‐ ported 2 cases from Wuhan (57‐ and 70 ‐year ‐old men) in which SARS ‐CoV ‐2 pneumonia was com‐ plicated by acute pulmonary embolism. Coro‐ navirus disease 2019 with changes in the lung could theoretically induce a hypercoagulable state. The vascular response to (systemic) hypoxia is controlled by hypoxia ‐inducible transcription fac‐ tors. The target genes of hypoxia ‐inducible tran‐ scription factors include factors regulating throm‐ bus formation.5 We report the case of a 66 ‐year ‐old woman who tested positive for COVID ‐19 one week be‐ fore the admission. She was admitted to our clin‐ ic due to atrial fibrillation and because she felt as if she was about to faint (March 31, 2020). Fur‐ thermore, she complained of a light cough and rhinitis; she had no fever. For about 3 months, CLiNiCAL iMAge

SARS-CoV-2 pneumonia and pulmonary embolism in a 66-year-old female