Neurophysiology

Contains reports on three research projects.National Institutes of Health (Training Grant 5 TO1 EY00090)Bell Laboratories (Grant

Aortic Arch Thrombus and Pulmonary Embolism in a COVID-19 Patient

© 2020 Elsevier Inc. Background: Coronavirus disease 2019 (COVID-19) is associated with endothelial inflammation and a hypercoagulable state resulting in both venous and arterial thromboembolic complications. We present a case of COVID-19-associated aortic thrombus in an otherwise healthy patient. Case Report: A 53-year-old woman with no past medical history presented with a 10-day history of dyspnea, fever, and cough. Her pulse oximetry on room air was 84%. She tested positive for severe acute respiratory syndrome coronavirus 2 infection, and chest radiography revealed moderate patchy bilateral airspace opacities. Serology markers for cytokine storm were significantly elevated, with a serum D-dimer level of 8180 ng/mL (normal \u3c 230 ng/mL). Computed tomography of the chest with i.v. contrast was positive for bilateral ground-glass opacities, scattered filling defects within the bilateral segmental and subsegmental pulmonary arteries, and a large thrombus was present at the aortic arch. The patient was admitted to the intensive care unit and successfully treated with unfractionated heparin, alteplase 50 mg, and argatroban 2 μg/kg/min. Why Should an Emergency Physician Be Aware of This?: Mural aortic thrombus is a rare but serious cause of distal embolism and is typically discovered during an evaluation of cryptogenic arterial embolization to the viscera or extremities. Patients with suspected hypercoagulable states, such as that encountered with COVID-19, should be screened for thromboembolism, and when identified, aggressively anticoagulated

Neurophysiology

Contains reports on five research projects.National Institutes of Health (Training Grant 5 TO1 EY00090)Bell Laboratories (Grant

Usefulness of Elevated Troponin to Predict Death in Patients with COVID-19 and Myocardial Injury.

Elevations in troponin levels have been shown to predict mortality in patients with coronavirus disease 2019 (COVID-19). The role of inflammation in myocardial injury remains unclear. We sought to determine the association of elevated troponin with mortality in a large, ethnically diverse population of patients hospitalized with COVID-19, and to determine the association of elevated inflammatory markers with increased troponin levels. We reviewed all patients admitted at our health system with COVID-19 from March 1 to April 27, 2020, who had a troponin assessment within 48 hours of admission. We used logistic regression to calculate odds ratios (ORs) for mortality during hospitalization, controlling for demographics, comorbidities, and markers of inflammation. Of 11159 patients hospitalized with COVID-19, 6247 had a troponin assessment within 48 hours. Of these, 4426 (71%) patients had normal, 919 (15%) had mildly elevated, and 902 (14%) had severely elevated troponin. Acute phase and inflammatory markers were significantly elevated in patients with mildly and severely elevated troponin compared to normal troponin. Patients with elevated troponin had significantly increased odds of death for mildly elevated compared to normal troponin (adjusted OR, 2.06; 95% CI, 1.68-2.53; P \u3c .001) and for severely elevated compared to normal troponin (OR, 4.51; 95% CI, 3.66-5.54; P \u3c .001) independently of elevation in inflammatory markers. In conclusion, patients hospitalized with COVID-19 and elevated troponin had markedly increased mortality compared to patients with normal troponin levels. This risk was independent of cardiovascular comorbidities and elevated markers of inflammation

Neurophysiology

Contains reports on seven research projects.National Institutes of Health (Grant 5 RO1 EY01149-02)Bell Telephone Laboratories, Inc. (Grant)National Institutes of Health (Grant 1 TO1 EY00090-01

Intravenous erythropoietin in patients with ST-segment elevation myocardial infarction - REVEAL: A randomized controlled trial

Context: Acute ST-segment elevation myocardial infarction (STEMI) is a leading cause of morbidity and mortality. In experimental models of MI, erythropoietin reduces infarct size and improves left ventricular (LV) function. Objective: To evaluate the safety and efficacy of a single intravenous bolus of epoetin alfa in patients with STEMI. Design, Setting, and Patients: A prospective, randomized, double-blind, placebo-controlled trial with a dose-escalation safety phase and a single dose (60 000 U of epoetin alfa) efficacy phase; the Reduction of Infarct Expansion and Ventricular Remodeling With Erythropoietin After Large Myocardial Infarction (REVEAL) trial was conducted at 28 US sites between October 2006 and February 2010, and included 222 patients with STEMI who underwent successful percutaneous coronary intervention (PCI) as a primary or rescue reperfusion strategy. Intervention: Participants were randomly assigned to treatment with intravenous epoetin alfa or matching saline placebo administered within 4 hours of reperfusion. Main Outcome Measure: Infarct size, expressed as percentage of LV mass, assessed by cardiac magnetic resonance (CMR) imaging performed 2 to 6 days after study medication administration (first CMR) and again 12±2 weeks later (second CMR). Results: In the efficacy cohort, the infarct size did not differ between groups on either the first CMR scan (n=136; 15.8% LV mass [95% confidence interval {CI}, 13.3-18.2% LV mass] for the epoetin alfa group vs 15.0% LV mass [95% CI, 12.6-17.3% LV mass] for the placebo group; P=.67) or on the second CMR scan (n=124; 10.6% LV mass [95% CI, 8.4-12.8% LV mass] vs 10.4% LV mass [95% CI, 8.5-12.3% LV mass], respectively; P=.89). In a prespecified analysis of patients aged 70 years or older (n=21), the mean infarct size within the first week (first CMR) was larger in the epoetin alfa group (19.9% LV mass; 95% CI, 14.0-25.7% LV mass) than in the placebo group (11.7% LV mass; 95% CI, 7.2-16.1% LV mass) (P=.03). In the safety cohort, of the 125 patients who received epoetin alfa, the composite outcome of death, MI, stroke, or stent thrombosis occurred in 5 (4.0%; 95% CI, 1.31%-9.09%) but in none of the 97 who received placebo (P=.04). Conclusions: In patients with STEMI who had successful reperfusion with primary or rescue PCI, a single intravenous bolus of epoetin alfa within 4 hours of PCI did not reduce infarct size and was associated with higher rates of adverse cardiovascular events. Subgroup analyses raised concerns about an increase in infarct size among older patients. Trial Registration: clinicaltrials.gov Identifier: NCT00378352. ©2011 American Medical Association. All rights reserved

Neurophysiology

Contains research objectives and summary of research on ten research projects.National Institutes of Health (Grant 5 R01 EY01149-02)National Institutes of Health (Grant 1 T01 EY00090-01)Bell Telephone Laboratories, Inc. (Grant)National Institutes of Health (Grant 5 TO1 GM00778-19)National Institutes of Health (Grant 5 TO1 GM01555-08