Background: COVID-19 induces robust systemic inflammation. One of the main complications is the increased coagulation due to endotheliitis. There is an increased incidence of pulmonary embolism (PE) in COVID-19 patients. However, clinical characteristics for a strict analysis are yet to be determined. Aim: We evaluated oxygenation and characteristics in patients with COVID-19 PE (CPE). Material and methods: We evaluated 215 COVID-19 patients from 1 January to 30 April 2021. We found 18 patients affected by PE (CPE, 50.0% males, aged 67.00 ± 10.86 years). As controls, we used data from patients affected by PE evaluated in our ward between 1 January 2015 and 31 December 2019 (64 patients, 53.1% males, aged 70.88 ± 16.44 years). All patients underwent a complete physical examination, pulmonary computerised tomography, laboratory tests, D-dimers and blood gas analysis at the time of diagnosis. Results: There were no differences in laboratory tests nor in D-dimers between the two groups. In the CPE group we found a significantly increased pO2 (92.83 ± 42.52 vs. 76.11 ± 32.58 mmHg; p < 0.05), difference of oxygen between alveoli and arteries (A-aDO2; 169.3 ± 171.9 vs. 52.97 ± 39.65 mmHg; p < 0.05), and oxygen saturation % (97.06 ± 2.59 vs. 93.77 ± 5.53%; p < 0.05) compared to controls. No difference was found in pCO2 and the ratio between pO2 and percentage of inspired oxygen (P/F). Finally, a significantly decreased urate (3.67 ± 1.49 vs. 5.60 ± 2.10; p < 0.05) was found in CPE compared to controls. In CPE, platelets count presents an inverse correlation to P/F (r = −0.389, p = 0.02) but a direct correlation to A-aDO2 (r = 0.699, p = 0.001). No similar findings were present in controls. Discussion: COVID-19 PE appears to have a different clinical setting. Reduced oxygenation described in PE may not to be considered as a sign of disease. The increased A-aDO2 may indicate that COVID-19 PE involved smaller vessels compared to classical PE. A possible diffuse capillary thrombosis could explain these results.

Abstract Background Primary mediastinal B–cell lymphoma (PMBCL) is an aggressive B–cell lymphoma that represents 2–3% of non –Hodgkin lymphoma cases and typically affects young adult Caucasian women. Diagnosis can be difficult and often need a multidisciplinary approach. Case a 75 year old female, with history of hypertension, came to ER for severe dyspnea. She complains also neck and left arm oedema. Blue swelling of face and trunk were described. Heart PoCUS was inconclusive, describing only a hypoechoic dilation of right atrium while the other three heart chambers were reduced in dimensions. Chest TC revealed a huge mediastinal mass next to a thrombosis of superior cava vein and right atrium (7 cm diameter) and a diffuse subsegmental pulmonary embolism. Arm and neck Lymphnodes were also enlarged . Low molecular weight heparin was given twice a day. Due the respiratory failure a high–flow nasal cannula oxygen treatment was performed. PET revealed FDG uptake in antero–superior mediastinum, but there was the same uptake in heart right atrium without a connection with the previous described. Therefore, this was no more considered as thrombus but as mass. The micro–bubble test revealed right to left shunt. She refused heart MRI. The patient was not suitable for an open–surgery biopsy, thus she was scheduled for a TC guided one, in order to obtain a pathological diagnosis for a suspected right atrium sarcoma. Due to the high risk we choose to perform the less invasive as possible way to have a histological sample. Thus, and intravascular biopsy of atrial mass by femoral vein was performed. The patient did not present any sequelae after procedure and she continued anticoagulation. The subsequent histological analysis revealed a PMBCL with a primary localization in Right atrium. Unfortunately, a sepsis by multiple resistant pseudomonas Aeruginosa and Aspergillus spp. arose and the patient died three weeks after biopsy. Conclusion A PMBCL is a rare and aggressive disease. Like in our patient, mediastinal syndrome is often associated to the disease. However, intracardiac localization are even rarer events. In large case series, less than 1% of intracardiac masses were lymphomas. In our patient, open–surgery was not suitable for multiple comorbidities. However, intravascular approach was less aggressive but effective to obtain enough tissue for diagnosis. Unfortunately, the immune suppression related to PMBCL and opportunistic infections drive a mortal sepsis.

BACKGROUND:COVID-19 induces robust systemic inflammation. Patients with cardiovascular disease (CVD) are at an increased risk of death. However, much effort is being spent to identify possible predictors of negative outcomes in order to have a more specific clinical setting. CVD scores are a useful tool in evaluating risk of cardiovascular events.AIM:We evaluated oxygenation and characteristics in COVID-19 patients according to cardiovascular risk stratification performed using the Framingham risk score (FRS) for cardiovascular disease.MATERIALS AND METHODS:We evaluated 155 COVID-19 patients (110 males and 45 females, aged 67.43 ± 14.72 years). All patients underwent a complete physical examination, chest imaging, laboratory tests and blood gas analysis at the time of diagnosis. Seventeen patients died (10 males and 7 females, aged 74.71 ± 7.23 years) while the remaining 138 patients (100 males and 38 females, aged 66.07 ± 15.16 years) were alive at discharge.RESULTS:Deceased patients have an increased FRS compared to those that survived (27.37 ± 5.03 vs. 21.33 ± 9.49, p < 0.05). Compared to survivors, the deceased group presents with a significant increase in white blood cells (p < 0.05) and D-dimers (p < 0.05). There was no difference in pCO2, SO2, and in alveolar arteriolar oxygen difference (A-aDO2). On the contrary, in deceased patients there was an increased pO2 (p < 0.05) and a decreased ratio between oxygen inspired and pO2 (P/F; p < 0.05). FRS shows a negative correlation to P/F (r = 0.42, p < 0.05) in the deceased while no correlation was found in the survivors. No other correlation has been found with blood gas parameters or in the inflammation parameters evaluated in the two groups.DISCUSSION:CVD may be considered as a major risk factor for death in COVID-19 patients. The increased risk relates to a reduced lung capacity but it is not related to blood gas values. Similarly, CV risk score results are independent from the inflammatory status of the patients.