• Farrah Shahrzad Nasrollahi, Dino J Gutierrez, Judith Nocek, Jennifer Folami, Sahrish Ekram, Wesley Eilbert, and Joseph S Colla.
• University of Illinois, Department of Emergency Medicine, Chicago, IL, USA.
• Am J Emerg Med. 2024 Sep 1; 83: 126128126-128.

BackgroundSickle cell disease (SCD) is characterized by microvascular occlusion which leads to multiorgan damage, including left ventricular diastolic dysfunction. Left ventricular diastolic dysfunction has been shown to be an independent risk factor for death in SCD patients. Left atrial dilation (LAD) has been used as a surrogate marker for identification of left ventricular diastolic dysfunction.ObjectiveInvestigate the association of LAD, as determined by echocardiography, with increased disease burden in SCD as reflected by increased emergency department (ED) utilization, increased hemolysis markers, and worsening anemia.MethodsA retrospective cohort study of patients from a single university hospital were selected from a national registry. Age, sickle cell phenotype, echocardiogram findings, ED utilization, baseline hemoglobin, and lab values needed for calculation of hemolytic index were recorded for each patient. Patients were then stratified into two distinct groups based on the presence or absence of LAD to compare ED utilization, baseline hemoglobin and hemolytic index between the two groups.Results129 patients met the criteria for inclusion with 88 having normal left atrial volume and 41 with LAD. There was a higher percentage of high ED utilizers in the LAD group compared to the normal left atrial volume group [34% vs. 17%, p = 0.03]. Average hemoglobin was lower in the LAD group compared with the normal left atrial volume group [mean 8.57 g/dL vs. 9.47 g/dL, p = 0.011]. The mean hemolytic index was higher in the LAD group when compared with the normal left atrial volume group [0.44 vs. -0.21, p < 0.001].ConclusionsLAD was associated with higher ED utilization, lower hemoglobin level, and more hemolysis in patients with SCD.Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

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