Abstract #1641

Cerebral perfusion and oxygen extraction are similar in sickle cell disease patients with hemoglobin SS and hemoglobin S-thalassemia phenotypes

Spencer L. Waddle¹, Ifeanyi Ikwuanusi¹, Lori C. Jordan^1,2,3, Chelsea A. Lee^1,2, Niral J. Patel^1,2, Sumit Pruthi¹, L. Taylor Davis¹, Allison Griffin¹, Michael R. Debaun^4,5, Adetola A. Kassim⁵, and Manus J. Donahue^1,3,6

¹Department of Radiology, Vanderbilt University Medical Center, Nashville, TN, United States, ²Department of Pediatrics, Division of Pediatric Neurology, Vanderbilt University Medical Center, Nashville, TN, United States, ³Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, United States, ⁴Department of Pediatrics, Vanderbilt-Meharry Center for Excellence in Sickle Cell Disease, Vanderbilt University Medical Center, Nashville, TN, United States, ⁵Department of Internal Medicine, Division of Hematology/Oncology, Vanderbilt University Medical Center, Nashville, TN, United States, ⁶Department of Psychiatry, Vanderbilt University Medical Center, Nashville, TN, United States

Sickle cell disease (SCD) comprises multiple sickle phenotypes, yet it is assumed that most phenotypes have similar cerebral hemo-metabolic impact, despite differing hematological characteristics. Here, patients (n=120) with the two most common phenotypes, hemoglobin (Hb)-SS and HbSβ⁰-thalassemia, were evaluated using anatomical, cerebral blood flow (CBF)-weighted, and oxygen extraction fraction (OEF)-weighted 3T MRI. Results suggest that while CBF depends closely on hematocrit, SCD phenotype does not discriminate either CBF or OEF and anatomical findings of prior infarct and vasculopathy were not significantly different between groups. These findings are consistent with HbSβ⁰ and HbSS phenotypes having similar impact on cerebral hemo-metabolic dysfunction.

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