Background Coronavirus disease 2019 (COVID-19) has infected people in many countries worldwide. Discovering an effective treatment for this disease, particularly in severe cases, has become the subject of intense scientific investigation. Therefore, the objective of this study was to evaluate the efficacy of intravenous immunoglobulin (IVIg) in patients with severe COVID-19 infection. Methods This study was conducted as a randomized placebo-controlled double-blind clinical trial. Fifty-nine patients with severe COVID-19 infection who did not respond to initial treatments were randomly assigned into two groups. One group received IVIg (human)—four vials daily for 3 days (in addition to initial treatment), while the other group received a placebo. Patients’ demographic, clinical, and select laboratory test results, as well as the occurrence of in-hospital mortality, were recorded. Results Among total study subjects, 30 patients received IVIg and 29 patients received a placebo. Demographics, clinical characteristics, and laboratory tests were not statistically different (P > 0.05) between the two groups. The in-hospital mortality rate was significantly lower in the IVIg group compared to the control group (6 [20.0%] vs. 14 [48.3%], respectively; P = 0.022). Multivariate regression analysis demonstrated that administration of IVIg did indeed have a significant impact on mortality rate (aOR = 0.003 [95% CI: 0.001–0.815]; P = 0.042). Conclusions Our study demonstrated that the administration of IVIg in patients with severe COVID-19 infection who did not respond to initial treatment could improve their clinical outcome and significantly reduce mortality rate. Further multicenter studies with larger sample sizes are nonetheless required to confirm the appropriateness of this medication as a standard treatment. Trial registration A study protocol was registered at the Iranian Registry of Clinical Trials (www.IRCT.ir), number IRCT20200501047259N1. It was registered retrospectively on May 17th, 2020.

Introduction: Given the role of platelets in thrombus formation, markers of platelet activation may be able to predict outcomes in patients with acute pulmonary thromboembolism (PTE). Methods: In a prospective cohort study, 492 patients with acute PTE were enrolled. Patients were evaluated for platelet indices including mean platelet volume (MPV), platelet distribution width (PDW), and platelet-lymphocyte-ratio (PLR), as well as for the simplified Pulmonary Embolism Severity Index (PESI) risk score. The primary endpoint was in-hospital all-cause mortality. Major adverse cardiopulmonary events (MACPE, composite of mortality, thrombolysis, mechanical ventilation and surgical embolectomy during index hospitalization) and all-cause death during follow-up were secondary endpoints. Results: MPV, PDW and PLR were 9.9±1.0 fl, 13.5±6.1%, and 14.7±14.5, respectively, in the total cohort. Whilst MPV was higher in those with adverse events (10.1±1.0 vs 9.9±1.0 fl; P = 0.019), PDW and PLR were not different between two groups. MPV with a cut-off point of 9.85 fl had a sensitivity of 81% and a specificity of 50% in predicting in-hospital mortality, but it had lower performance in predicting MACPE (Area under the curve: AUC 0.58; 95%CI 0.52-0.63) or long-term mortality (AUC 0.54; 95% CI 0.47-0.61). The AUC for all these three markers were lower than the AUC calculated for the simplified PESI score (0.80; 0.71-0.88). Conclusion: Platelet indices had only fair-to-good predictive performance in predicting in-hospital all-cause death. Established PTE risk scoring models such as simplified PESI outperform these indices in predicting adverse outcomes. Article info TUOMS P R E S SPlatelets indicies in acute pulmonary thromboembolism

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Thrombolysis is less effective and has more complications compared to surgery in treatment of obstructive PVT. Compromised hemodynamic status during presentation of these patients denotes higher in-hospital mortality.

Introduction: Investigating the clinical impact of serum uric acid (UA) and its lowering agents on the complications and mortality of acute ST-elevation myocardial infarction (STEMI) can open a new era in STEMI treatment. The aim of this study was to evaluate the effect of on admission serum UA level on the mortality and morbidity of patients admitted with STEMI. Methods: A number of 608 patients with STEMI were enrolled in this study from December 21, 2012 until February 19, 2014. Patients were followed for 20 months. Male to female ratio was 2.53, and the mean age of patients was 62.6±13.4. The relationship between the level of UA and patients’ mortality and morbidity, left ventricular ejection fraction (LVEF), atrial and ventricular arrhythmia was analyzed. Results: Patients with high serum UA level had higher Killip class after STEMI (P=0.001). Mean LVEF was measured to be 39.5±9.6 in normal UA group and 34.6±11.6 in high UA group (P=0.001). In comparison with normal UA group, high UA group had significantly higher cTnI (2.68±0.09 vs 4.09±0.42, respectively, P=0.001), increased blood pressure (P=0.009), and higher atrial fibrillation (AF) occurrence (P=0.03), but no association was seen between ventricular tachycardia and serum UA level. Short term and midterm mortality were not different in two groups (P=0.44 and 0.31, respectively). Conclusion: In the current study, high serum UA level in patients with acute myocardial infarction (MI) was not associated with higher in-hospital or midterm mortality, but it was associated with lower LVEF, higher Killip class, elevated cTnI, creatinine, triglyceride, and higher AF.