Alterations in cerebral blood flow in children with congestive heart failure due to ventricular septal defect

Abstract

We aimed to investigate the effect of ventricular septal defect (VSD) and heart failure on cerebral blood flow (CBF) in children, whether heart failure treatment improves CBF, and if there is any relationship between CBF and serum N-terminal pro-brain natriuretic peptide (NT-proBNP) level. Forty children with VSD (13 with heart failure) aged between 1 and 36months were studied. The control group comprised 25 healthy children in the same age group. Maximum, minimum, and mean blood flow velocities and pulsatility indices of the right and left middle cerebral arteries were assessed using transcranial Doppler ultrasonography. Measurements of CBF and serum NT-proBNP levels were repeated in patients with heart failure a month post-heart failure treatment initiation. The groups were also compared in terms of defect diameters, cardiac structural changes, left ventricular systolic function, and findings related to pulmonary hypertension determined by echocardiography. Correlations between echocardiographic measurements and CBF parameters were analyzed. Although no significant difference was found between patient and control groups for CBF, right and left maximum CBF velocities significantly increased posttreatment in patients with heart failure (P=.04 and P=.01, respectively). Serum NT-proBNP levels in children with VSD associated with heart failure were significantly higher than those in children with VSD alone (P=.04) or in healthy children (P<.001). NT-proBNP levels were negatively correlated with right and left maximum CBF velocities (r=-0.39, P=.013 and r=-0.32, P=.043, respectively). Although no significant difference was found in CBF velocity among the study groups, increase in the CBF velocity post heart failure treatment and negative correlations between CBF velocity and both the VSD diameter and NT-proBNP levels indicate that the hemodynamic status due to VSD associated with heart failure has an effect on CBF.