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(Circulation. 2002;105:2058.)
© 2002 American Heart Association, Inc.

Clinical Investigation and Reports

Ultrasonographic and Biochemical Markers of Human Fetal Cardiac Dysfunction in Placental Insufficiency

From the Departments of Obstetrics and Gynecology (K.M., P.J., J.R.) and Physiology, Biocenter Oulu (O.V.), University of Oulu, Oulu, Finland.

Correspondence to Juha Räsänen, MD, Department of Obstetrics and Gynecology, University of Oulu, Kajaanintie 50, 90220 Oulu, Finland. E-mail juharasa{at}cc.oulu.fi

Background— Placental insufficiency may lead to fetal cardiovascular compromise. We sought to determine whether ultrasonographic parameters of fetal cardiovascular function correlate with umbilical arterial levels of biochemical markers of myocardial dysfunction and damage in placental insufficiency.

Methods and Results— In 48 fetuses with placental insufficiency, umbilical artery blood was obtained at delivery for assessment of N-terminal peptide of proatrial natriuretic peptide (NT-proANP) and cardiac troponin-T (cTnT). Group 1 fetuses (n=12) had normal NT-proANP and cTnT serum concentrations. Group 2 fetuses (n=25) showed increased NT-proANP (>1145 pmol/L) and normal cTnT values. Group 3 fetuses (n=11) had increased NT-proANP and cTnT (>0.10 ng/mL) levels. The ultrasonographic parameters of fetal cardiovascular function were compared between the groups. Pulsatility indices for veins of the ductus venosus, left hepatic vein, and inferior vena cava correlated significantly with NT-proANP levels. In group 3, ductus venosus, left hepatic vein, and inferior vena cava pulsatility indices for veins were higher (P<0.01) than in groups 1 and 2. The proportion of left ventricular cardiac output of combined cardiac output was greater (P<0.05) and that of right ventricle was smaller (P<0.05) in group 3 than in group 2. In group 3, tricuspid regurgitation was noted most often (P<0.05), and right ventricular fractional shortening was less (P<0.01) than in group 2.

Conclusions— Pulsatility in human fetal systemic veins correlated significantly with the cardiac secretion of ANP. Fetuses with myocardial damage demonstrate increased systemic venous pressure, a change in the distribution of cardiac output toward the left ventricle, and a rise in right ventricular afterload.

Key Words: echocardiography • troponin • natriuretic peptides • fetal growth retardation • physiology

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