Retrograde aortic isthmus net blood flow and human fetal cardiac function in placental insufficiency.
OBJECTIVE
Retrograde aortic isthmus (AoI) net blood flow has been associated with diminished oxygen delivery to cerebral circulation. This study was designed to characterize the cardiac function in human fetuses with retrograde AoI net blood flow in pregnancies complicated by placental insufficiency.


METHODS
The control group comprised 43 fetuses in uncomplicated pregnancies. Study groups consisted of fetuses with placental insufficiency, and either antegrade (Group 1; n = 18) or retrograde (Group 2; n = 11) AoI net blood flow. Volume blood flows (Q) of left (LVCO) and right (RVCO) ventricles, ductus arteriosus (Q(DA)), pulmonary arterial bed (Q(P)) and foramen ovale (Q(FO)) were calculated and their proportions (%) of combined cardiac output (CCO) were determined. Ventricular ejection forces were calculated. Blood velocity waveforms of the mitral (MV) and tricuspid (TV) valves were obtained. The proportion of left ventricular isovolumetric relaxation time (IRT%) of the cardiac cycle, and index of myocardial performance (IMP) were calculated.


RESULTS
In Group 1, Q(DA)% was increased (P < 0.05) and Q(P)% decreased (P < 0.05) compared with the control group, and Q(FO)% was greater (P < 0.01) compared with the control group and Group 2. In Group 2, the distribution of CCO did not differ from that of the control group. Ventricular ejection forces were similar among the groups. In Group 2, the MV early filling/atrial contraction time-velocity integral ratio was greater (P < 0.05) compared with those of the control group and Group 1. In Groups 1 and 2, IRT% and IMP were increased (P < 0.001) compared with the control group.


CONCLUSIONS
In placental insufficiency, fetuses with antegrade AoI net blood flow show a shift in RVCO from the pulmonary to the systemic circulation, and Q(FO) makes up the majority of LVCO. Fetuses with retrograde AoI net blood flow fail to demonstrate these changes, suggesting a relative drop in the oxygen content of the blood entering the left ventricle.
Mäkikallio
K
K
Department of Obstetrics and Gynecology, University of Oulu, Oulu, Finland.
Jouppila
P
P
Räsänen
J
J
D001013:Aorta, Thoracic / Q000196:embryology / Q000503:physiopathology*; D001783:Blood Flow Velocity / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D003430:Cross-Sectional Studies; D003971:Diastole; D018618:Echocardiography, Doppler, Color; D005260:Female; D005318:Fetal Heart / Q000503:physiopathology*; D006801:Humans; D015588:Observer Variation; D010927:Placental Insufficiency / Q000503:physiopathology*; D011247:Pregnancy; D013599:Systole; D014469:Umbilical Arteries / Q000502:physiology