atrial-natriuretic-factor and Placental-Insufficiency

atrial-natriuretic-factor has been researched along with Placental-Insufficiency* in 2 studies

Other Studies

2 other study(ies) available for atrial-natriuretic-factor and Placental-Insufficiency

ArticleYear
Ultrasonographic and biochemical markers of human fetal cardiac dysfunction in placental insufficiency.
    Circulation, 2002, Apr-30, Volume: 105, Issue:17

    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.. 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.. 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.

    Topics: Adult; Atrial Natriuretic Factor; Biomarkers; Coronary Circulation; Cross-Sectional Studies; Echocardiography, Doppler; Female; Fetal Heart; Hemodynamics; Humans; Myocardial Contraction; Placental Insufficiency; Pregnancy; Protein Precursors; Troponin T; Umbilical Arteries

2002
Umbilical artery N-terminal peptide of proatrial natriuretic peptide in hypertensive pregnancies and fetal acidemia during labor.
    Obstetrics and gynecology, 2001, Volume: 97, Issue:1

    To assess the activity of the human fetal atrial natriuretic peptide system in hypertensive pregnancies with and without signs of increased fetal systemic venous pressure and in pregnancies complicated by fetal acidemia during labor.. Umbilical artery plasma N-terminal peptide of proatrial natriuretic peptide concentrations were measured in neonates by radioimmunoassay. The control group consisted of 50 neonates with uncomplicated gestation and labor. In group 1, there were 22 newborns of hypertensive pregnancies. Doppler ultrasonography showed abnormal umbilical artery blood velocity waveform in five cases and normal nonpulsatile umbilical vein blood velocity profile in every case. Group 2 consisted of five newborns of pregnancies complicated by maternal hypertensive disorder. Atrial pulsations in the umbilical vein and retrograde diastolic blood velocity pattern in the umbilical artery were detected in every case. Group 3 was composed of 27 newborns of uncomplicated pregnancies with fetal acidemia (pH 7.10 or less) during labor.. In groups 1-3, N-terminal peptide of proatrial natriuretic peptide concentrations were higher (P <.001) than in the control group. In group 1, neonates with abnormal umbilical artery blood velocity pattern had higher N-terminal peptide of proatrial natriuretic peptide concentrations than neonates with normal umbilical artery Doppler findings (P <.006). N-terminal peptide of proatrial natriuretic peptide concentrations were higher in group 2 (P <.002) than in groups 1 and 3. CONCLUSIONS Maternal hypertensive disorder and fetal acidemia during labor stimulate fetal atrial natriuretic peptide production, which was greatest in fetuses with severe placental insufficiency and signs of congestive heart failure.

    Topics: Adult; Atrial Natriuretic Factor; Blood Flow Velocity; Female; Fetal Diseases; Humans; Hypertension; Infant, Newborn; Placental Insufficiency; Pregnancy; Pregnancy Complications, Cardiovascular; Protein Precursors; Umbilical Arteries

2001