Infective endocarditis involving the aortic valve carries a high risk of rapid valvular destruction and hemodynamic compromise, particularly when complicated by sepsis. Patients with sickle cell disease are uniquely susceptible to severe infection due to functional asplenia, chronic hemolysis, endothelial dysfunction, and frequent exposure to intravascular devices, yet native valve endocarditis in this population remains rarely described. We report the case of a 51-year-old man with sickle cell disease who presented with sepsis and was found to have native aortic valve endocarditis caused by Staphylococcus capitis. Initial transthoracic echocardiography on hospital day three demonstrated a small aortic valve vegetation with mild-to-moderate aortic regurgitation. Despite initiation of appropriate antimicrobial therapy, transesophageal echocardiography performed thereafter on hospital day six revealed rapid progression to moderate-to-severe aortic regurgitation with associated atrial dilation, indicating accelerated valvular deterioration. The patient subsequently developed worsening volume overload and hemodynamic instability, prompting cardiothoracic surgical intervention. He underwent successful aortic valve replacement with perioperative transfusion support tailored to the hematologic and hypoxic risks associated with sickle cell disease and demonstrated clinical improvement postoperatively. This case highlights how sepsis-related inflammatory activation, superimposed on baseline vascular and hematologic abnormalities in sickle cell disease, may accelerate valvular destruction, even in infections caused by organisms traditionally considered low-virulence, underscoring the importance of serial echocardiographic assessment and timely multidisciplinary management.
Patel et al. (Sun,) studied this question.