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Biomedical subjects

S R Weil

Publications and source records attributed to S R Weil.

6 recordsLinked to original sources

Human fetal right ventricular ejection force under abnormal loading conditions during the second half of pregnancy.

Our objective was to determine whether abnormal loading conditions can modify human fetal right ventricular ejection force during the second half of pregnancy. By Doppler echocardiography, we studied 73 normal fetuses between 19 and 41 weeks of gestation, 27 fetuses with hypoplastic left heart syndrome (chronic volume overload) between 18 and 38 weeks of gestation, 14 fetuses with mild to moderate constriction of the ductus arteriosus (pulsatility index (PI) between 1.0 and 1.9) and seven fetuses with severe constriction (PI < 1.0) or occlusion of the ductus arteriosus (relatively acute pressure overload) between 28 and 34 weeks of gestation. In the normal and ductal constriction/occlusion groups, blood velocity waveforms were recorded at the level of the aortic and pulmonary valves, and in the group with hypoplastic left heart syndrome at the level of the pulmonary valve. The ventricular ejection forces were calculated. In the normal group, right (RVEF; r = 0.91, p < 0.0001) and left (LVEF; r = 0.86, p < 0.0001) ventricular ejection forces increased and were equal during the second half of gestation. In the group with hypoplastic left heart syndrome the RVEF increased (r = 0.76, p < 0.0001) with advancing gestation. The RVEF (p < 0.0005) and its average weekly increase (p < 0.0001) were greater in the hypoplastic left heart syndrome group than in the normal group. In the group with mild to moderate ductal constriction, both ventricular ejection forces were similar to those of the normal group. The RVEF (p < 0.003) and its average weekly increase (p < 0.03) were lower in the group with severe ductal constriction or occlusion than in the normal group. The LVEF did not differ from that of the normal group We conclude that chronic volume overload increases and relatively acute pressure overload decreases human fetal RVEF. The right ventricular performance is modified by abnormal loading conditions.

Blood Flow Velocity↗

Fetal echocardiography during indomethacin treatment.

Fetal echocardiograms were evaluated in 315 studies performed in 107 fetuses exposed to indomethacin. In the majority of cases, the results of the fetal echocardiography study were within normal limits (74%). The most common abnormal phenomena were tricuspid valve regurgitation (10%), ductal constriction (6%), tricuspid valve regurgitation and ductal constriction (5%), an increased ductal velocity (2%), and other (3%). The difference between the prevalence of ductal constriction in the whole series of studies (11%) compared to the prevalence of ductal constriction per fetus (25%) (p < 0.001) suggests that this phenomenon was only temporary and disappeared when medication was discontinued. The mean gestational age for detection of tricuspid valve regurgitation was 27.7 +/- 2.8 weeks and for ductal constriction, 30.9 +/- 2.1 weeks (t-test, p < 0.01). Trivial tricuspid valve regurgitation was detected at a mean of 26.7 +/- 2.2 weeks and significant tricuspid valve regurgitation at 29.6 +/- 2.3 weeks (t-test, p < 0.01). We conclude that indomethacin treatment is relatively safe for the fetal heart. The most common side-effects are tricuspid valve regurgitation and ductal constriction. Tricuspid valve regurgitation may be detected before ductal constriction, but by itself it is not a contraindication for the continued use of indomethacin.

Arterial Occlusive Diseases↗

Extracardiac anomalies, aneuploidy and growth retardation in 100 consecutive fetal congenital heart defects.

The importance of extracardiac anomalies in 100 consecutive fetuses with congenital heart disease was evaluated. The most common cardiac diagnoses were hypoplastic left heart syndrome in 35% and atrioventricular canal defect in 15%. Extracardiac anomalies were present in 42%, abnormal karyotype in 19% and intrauterine growth retardation in 20%. There were 45 survivors (35 required neonatal surgery, ten did not require early surgery) and 80% (36/45) of the survivors had isolated congenital heart disease. Extracardiac anomalies and abnormal karyotype were more frequently present in non-survivors (p < 0.001). Also, intrauterine growth retardation was more frequent in non-survivors (p < 0.05).

Journal Article↗

The prevalence and clinical significance of fetal tricuspid valve regurgitation with normal heart anatomy.

OBJECTIVE: Our purpose was to assess the prevalence, cause, and clinical significance of fetal tricuspid valve regurgitation in structurally normal hearts during indicated fetal echocardiographic examination. STUDY DESIGN: The prevalence of fetal tricuspid regurgitation was retrospectively evaluated in a group of 733 singleton fetuses referred for routine fetal echocardiography. RESULTS: The prevalence of this abnormality was 6.8%. Tricuspid valve regurgitation was most frequent in the group referred for fetal echocardiography to evaluate indomethacin exposure, followed by maternal diabetes. Factors associated with tricuspid valve regurgitation included ductal constriction, abnormal heart rhythm, atrial septal aneurysm, congestive heart failure, pericardial effusion, myocardial hypertrophy, and extracardiac malformations. Fetal tricuspid valve regurgitation was trivial in 80% (nonholosystolic, maximum velocity < 2 m/sec) and was significant in 20% (holosystolic, maximum velocity > 2 m/sec). Neonatal follow-up of tricuspid valve regurgitation was unremarkable. CONCLUSIONS: Fetal tricuspid valve regurgitation with normal heart anatomy was a frequent finding during indicated fetal echocardiographic examination and may indicate abnormal physiologic characteristics (increased preload or afterload, myocardial impairment, or arrhythmia). In the majority of cases (92%) the possible cause may be established. In other cases (8%) there may be "idiopathic" tricuspid valve regurgitation.

Echocardiography↗

Pressure-volume relationship of the fetal lamb heart.

In contrast to the adult heart, the fetal heart reportedly has little functional reserve. With increased clinical emphasis on fetal cardiac diagnosis, neonatal surgery, and the potential for future fetal cardiac intervention, it is essential that we better understand fetal cardiac function. Therefore, to demonstrate the extent of fetal cardiac preload reserve, we studied 10 fetal lambs using an isolated, isovolumic, blood-perfused heart preparation. We maintained constant afterload, inotropic state, coronary blood flow, heart rate, and perfusate blood gas values. As left ventricular (LV) volume (preload) was incrementally increased, LV end-diastolic pressure and LV peak systolic pressure were recorded. Linear regression analysis demonstrated that increases in LV developed pressures were predicted by the LV volume, demonstrating the presence of the Frank-Starling mechanism in each case. The plateau of the Starling pressure-volume curve occurred at an LV end-diastolic pressure of 12.5 +/- 4.79 mm Hg (95% confidence interval, 9.07 to 15.9 mm Hg), lower than the plateau expected in the adult heart. This implies that, in the management of fetal and immature neonatal hearts, preload reserve plays an important but limited role in cardiac reserve.

Animals↗

Sonographic differential diagnosis of fetal cardiac abnormalities.

Ultrasonographic evaluation of the fetal heart for structural and functional abnormalities is vital for prenatal diagnosis and perinatal management. Even more important than up-to-date diagnostic equipment is keen observation and an understanding of fetal cardiac abnormalities. One diagnostic approach begins with the four-chamber view with particular attention to the normal symmetric sizes of all four cardiac chambers. Ventricular disproportion, inequality in ventricular size, is often an easily detectable sign of a cardiovascular abnormality. Segmental diagnosis of cardiac and visceral situs, ventricular outflow tracts for conotruncal abnormalities and the aortic and ductal arches is also vital for diagnosing affected fetuses.

Diagnosis, Differential↗