Arterial Stiffness and Pulse Wave Reflection in Young Adult Heterozygous Sickle Cell Carriers

Objective: Pulse wave velocity (PWV) and aortic augmentation index (AI) are indicators of arterial stiffness. Pulse wave reflection and arterial stiffness are related to cardiovascular events and sickle cell disease. However, the effect of these parameters on the heterozygous sickle cell trait (HbAS) is unknown. The aim of this study is to evaluate the arterial stiffness and wave reflection in young adult heterozygous sickle cell carriers. Materials and Methods: We enrolled 40 volunteers (20 HbAS cases, 20 hemoglobin AA [HbAA] cases) aged between 18 and 40 years. AI and PWV values were measured by arteriography. Results: Aortic blood pressure, aortic AI, and brachial AT values were significantly higher in HbAS cases compared to the control group (HbAA) (p=0.033, 0.011, and 0.011, respectively). A statistically significant positive correlation was found between aortic pulse wave velocity and mean arterial pressure, age, aortic AI, brachial AI, weight, and low-density lipoprotein levels (p=0.000, 0.017, 0.000, 0.000, 0.034, and 0.05, respectively) in the whole study population. Aortic AT and age were also significantly correlated (p=0.026). In addition, a positive correlation between aortic PWV and systolic blood pressure and a positive correlation between aortic AT and mean arterial pressure (p=0.027 and 0.009, respectively) were found in HbAS individuals. Our study reveals that mean arterial pressure and heart rate are independent determinants for the aortic AI. Mean arterial pressure and age are independent determinants for aortic PWV. Conclusion: Arterial stiffness measurement is an easy, cheap, and reliable method in the early diagnosis of cardiovascular disease in heterozygous sickle cell carriers. These results may depend on the amount of hemoglobin S in red blood cells. Further studies are required to investigate the blood pressure changes and its effects on arterial stiffness in order to explain the vascular aging mechanism in the HbAS trait population.