Postnatal cerebral hemodynamics in infants with severe congenital heart disease: a scoping review

Abstract

Abstract Patients with severe congenital heart disease (CHD) are at risk for impaired neurodevelopment. Cerebral blood supply may be diminished by congenital anomalies of cardiovascular anatomy and myocardial function. The aim of this scoping review was to summarize the current knowledge on cerebral hemodynamics in infants with severe CHD. A scoping review was performed. Five databases were searched for articles published from 01/1990 to 02/2022 containing information on cerebral hemodynamics assessed by neuroimaging methods in patients with severe CHD within their first year of life. A total of 1488 publications were identified, of which 26 were included. Half of the studies used Doppler ultrasound, and half used magnetic resonance imaging techniques. Studies focused on preoperative findings of cerebral hemodynamics, effects of surgical and conservative interventions, as well as on associations between cerebral hemodynamics and brain morphology or neurodevelopment. Cerebral perfusion was most severely affected in patients with single ventricle and other cyanotic disease. Neuroimaging methods provide a large variety of information on cerebral hemodynamics. Nevertheless, small and heterogeneous cohorts complicate this field of research. Further studies are needed to improve our understanding of the link between CHD and altered cerebral hemodynamics to optimize neuroprotection strategies. Impact Postnatal cerebral hemodynamics are altered in infants with congenital heart disease (CHD) as compared to healthy controls, especially in most severe types such as single ventricle or other cyanotic CHD. Associations of these alterations with brain volume and maturation reveal their clinical relevance. Research in this area is limited due to the rarity and heterogeneity of diagnoses. Furthermore, longitudinal studies have rarely been conducted. Further effort is needed to better understand the deviation from physiological cerebral perfusion and its consequences in patients with CHD to optimize neuroprotection strategies.