key: cord-0947731-bskjn78c authors: Nasab, Entezar Mehrabi; Heidarzadeh, Siamak; Athari, Seyyed Shamsadin title: Right Atrial Clot and Pulmonary Embolism in a Patient with COVID-19: A Case Report date: 2021-08-13 journal: Radiol Case Rep DOI: 10.1016/j.radcr.2021.08.015 sha: 434fcd6434e620d98f27d2a9c19f7282a2b479bf doc_id: 947731 cord_uid: bskjn78c The infection caused by the novel coronavirus (COVID-19) immersed the globe into a widespread pandemic. The disease leads to acute respiratory disease syndrome (ARDS), hypercoagulation, and cardio-vascular diseases. In this case report, we presented an 80-year-old man with right atrial clot and acute pulmonary embolism, who was diagnosed with COVID-19. The patient was isolated and transferred to the ICU with a diagnosis of submissive PTE and RA clot following COVID-19 infection. Antibiotics and anticoagulants were administered, and the patient was referred for mechanical thrombectomy. He did not die and after recovery, was discharged with warfarin administration. Preventing thromboembolic events seems to be the first priority in the management of COVID-19 patients. It is necessary to look for strategies to manage and prevent the early occurrence of thromboembolic events in these patients. The virus causing the COVID-19 infection is a single-stranded RNA coronavirus, which led to the recent pandemic in the world. The disease mainly leads to acute respiratory distress syndrome (ARDS) in patients. However, its other complications include endothelial dysfunction, a hyper-coagulation state, thromboembolic events, and vascular diseases (1, 2) . Vascular complications such as myocardial ischemia, ischemic stroke, systemic arterial thrombi, pulmonary thromboembolism, and deep vein thrombosis have been reported (3) (4) (5) . In this report, we described an 80-year-old man with acute pulmonary embolism and right atrial clot, presenting with the signs of the novel coronavirus pneumonia. An 80-year-old Iranian man was admitted to the emergency department of our care center with acute severe dyspnea at rest, dry cough, feeling ill, and fever. The symptoms persisted for the past 10 hours. The patient's past history revealed type 2 diabetes mellitus, chronic renal failure (CRF), and coronary artery disease. Clinical examination and checking his vital signs showed normal blood pressure (BP= 110/75 mmHg), fever (39°C), tachycardia (heart rate= 100), tachypnea (respiratory rate= 24 cycles per minute), and hypoxemia (peripheral O 2 saturation of 85% while breathing into the ambient air). Oxygen saturation improved by administering supplemental oxygen via the nasal cannula. There were bilateral diffuse coarse crackles on auscultation. He was evaluated for the COVID-19 infection by reverse-transcriptase polymerase chain reaction (RT-PCR) test. Also, routine blood tests, pulmonary computed tomography scanning (CT-scan), electrocardiography (ECG), and transthoracic echocardiography (TTE) were performed. The COVID-19 PCR test was positive, and his laboratory findings showed elevated levels of WBC, LDH, and Cr, as well as negative troponin ( Table 1) . The CT scan showed round-glass opacities in both lungs (Fig. 1 ). There were no signs of pericardial or pleural effusion. The ECG showed sinus tachycardia, right axis deviation, right ventricular strain pattern (T wave inversion in the right precordial and inferior leads), the S1Q3T3 pattern, incomplete Right Bundle Branch Block (RBBB), and a dominant R wave in V1 (Fig. 2) . Normal left ventricular size, mild systolic dysfunction (LVEF= 50%), D-shape LV, and paradoxical septal motion were noted in TTE. Moderate right ventricular enlargement and mild to moderate systolic dysfunction were also observed. The left atrium had a normal size. However, the right atrium was dilated and contained a large (20-mm diameter) and highly mobile thrombus extending across the tricuspid valve into the right ventricle. Also, mild mitral regurgitation (MR), moderate tricuspid regurgitation (TR) with pulmonary hypertension (TRG= 45, PAP= 45-50 mmHg), moderate pulmonic regurgitation (PR), and dilated main pulmonary artery were observed (Fig. 3) . Pulmonary CT angiography (PCTA) confirmed pulmonary thromboembolism (PTE). Thrombotic lesions were distributed in the peripheral arteries of both lungs. Doppler ultrasound revealed no deep vein thrombosis (DVT) in lower limbs. The patient was isolated and transferred to the intensive care unit (ICU) with the diagnosis of submissive PTE, RA clot, and coronavirus pneumonia. Antibiotics and anticoagulants were administered. The patient was a surgery candidate and was referred for mechanical thrombectomy. He did not die and survived, after recovery and control of COVID-19, the patient was discharged with warfarin administration. In our patient, the diagnosis of COVID-19 was confirmed by RT-PCR on a nasopharyngeal sample and coronavirus pneumonia suggestive ground-glass opacities on lung CT scan. The clinical presentation of the disease encompasses fever, cough, dyspnea, myalgia, and diarrhea (6, 7) . Our patient presented with fever, illness, and dyspnea. He was hospitalized and diagnosed with COVID-19 pneumonia, PTE, and RA clot. The novel coronavirus seems to increase the risk of thrombotic complications. The pathophysiological mechanisms of thrombosis include immobilization, hypoxia, inflammation, endothelial dysfunction, and a hypercoagulable state. The virus activates the inflammatory response, induces the release of inflammatory factors by the endothelium, and triggers hemostatic systems, resulting in diffuse endothelial inflammation and microvascular dysfunction, which can finally lead to widespread thrombosis (86) . The acute phase of the COVID-19 infection is associated with a cytokine storm that can trigger thromboembolic events in the early stages of the disease. (97) . In our patient, thromboembolism occurred in the acute phase of the COVID-19 infection. At the time of COVID-19 diagnosis, the symptoms of RA clot and PE were also observed. The patient had no recent hospitalization records, immobility, or other acute pulmonary embolism risk factors. Therefore, it seems that the main culprit of the thromboembolic event in our patient was the COVID-19 infection. The diagnosis of the novel coronavirus infection coincided with embolism, making the condition more complicated for administering prophylactic agents for thromboembolism. Klok et al. argued that PTE phenotype in patients with the novel coronavirus infection was different from that of patients without coronavirus infection, noting that thrombotic lesions in COVID-19 patients were distributed in the peripheral arteries of lungs (108) . The results of PCTA in our patient were consistent with the results of the recent report. This involvement pattern is actually strong evidence pointing out the COVID-19 infection as the main etiology of the thromboembolic event in our patient. The occlusion of pulmonary artery circulation aggravates disease course and increases the mortality rate in COVID-19 patients (119). Therefore, preventing thromboembolic events is the first priority in the management of COVID-19 patients. However, the main problem is that there is no specific guideline on how to manage thromboembolism in these patients. Due to the high mortality and morbidity of thromboembolic events, researchers are advised to look for strategies to prevent and manage the early occurrence of thromboembolic events in COVID-19 patients. Chief, -in -Dear Editor Please see our manuscript submitted on the website entitled " onsideration for " for c 19: A Case Report -Pulmonary Embolism in a Patient with COVID In the article, we have tried to provide an . Radiology Case Reports publication in the 19. -field of the COVID extensive literature review, focusing on the recently raised The data for this article was prepared with the help of an expert team of academic researchers by the rigorous investigation of the currently available literature. I am currently tment of the immunology at the the assistant professor of the immunology in the depar , Iran. 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