The introduction of Doppler sonography in perinatology has enabled the non-invasive assessment of cardiovascular hemodynamics in human fetuses. Over the last 15 years, data on healthy as well as on compromised human fetuses have been collected, and Doppler has proved to be more sensitive than other methods in predicting adverse perinatal outcome. Furthermore, longitudinal Doppler examinations at the cardiac and extracardiac levels performed in compromised fetuses have provided us with information on Doppler signs of impending deterioration or fetal death. Thus, the new method has been readily adopted into the clinical management of high-risk pregnancies, especially those involving intrauterine growth retardation (IUGR). Animal studies demonstrated that growth-retarded fetuses with severely impaired uteroplacental perfusion showed a redistribution of ventricular output which increased blood flow to the brain, heart and adrenal glands'. Using Doppler ultrasonography in human fetuses, this redistribution was demonstrated at the level of the cerebral arteries(2), and the assessment of the 'brain-sparing effect' now forms part of the standard Doppler examination of a fetus with impaired peripheral perfusion. In this issue of the Journal, Gembruch and Baschat(3) report the first observation of increased coronary blood flow as a further manifestation of redistribution of ventricular output in fetuses with severe IUGR. Recognition of this phenomenon, which can be called the 'heart-sparing effect('4), depended on understanding the role of the coronary arteries in fetal asphyxia and on the use of high-resolution color Doppler imaging by experienced examiners in the field(5). We are now in the position to ask the following questions: What are the mechanisms behind the regulation of coronary artery perfusion; what role does it play in the cascade of the adaptation or decompensation in impaired fetal well-being; and how can it be assessed?