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This study was designed to examine the contribution of plasma lipids to the pathophysiology of cyclic mastopathy, before and after consideration of diet and sex hormones.Thirty-four women with severe cyclic mastopathy (case patients) and 29 women without cyclic mastopathy (control subjects) recorded their breast symptoms daily during 1 menstrual cycle. During each menstrual phase (follicular, early luteal, late luteal, and menstrual) they prospectively completed 2 24-hour dietary diaries, provided blood for lipid and hormone assays, and underwent anthropometric measurements.Mean age was 34 years. Premenstrual breast swelling and tenderness were significantly more severe in case patients (P.0001). Cyclic change (late luteal vs follicular) of high-density lipoprotein cholesterol differed between case patients and control subjects, with case patients having a relative excess of high-density lipoprotein cholesterol in the premenstrual phase (P = .01). Dietary fat intake was greater throughout the cycle in case patients (37.5 vs 33.7% of calories, P = .02), and case patients reported increased appetite in the premenstrual phase (P = .01). In multivariate analyses the contributions of mean dietary fat intake and of cyclic change in high-density lipoprotein cholesterol were independently significant, with odds ratios for upper versus lower quintiles being slightly5.Women with cyclic mastopathy had a relative excess of high-density lipoprotein cholesterol during the symptomatic late luteal phase of the menstrual cycle and a higher fat intake throughout the cycle than did control subjects. These observations support the hypothesis that lipids (notably high-density lipoprotein cholesterol) and a high-fat diet play a role in the pathophysiologic characteristics of cyclic mastopathy.

Objectives: Our purpose was to determine the sequence of fetal cardiac electrical and mechanical events associated with acute hypoxic acidemia and to correlate those events with terminal fetal heart rate patterns preceding fetal death. Study Design: Eight acutely catheterized fetal sheep were rendered hypoxic by placental embolization with microspheres until fetal death occurred. The fetal electrocardiogram, Doppler cardiogram, left ventricular and aortic pressures, and fetal heart rate were continuously recorded. Results: All eight fetuses showed a terminal bradycardia consisting of two phases: an initial phase of falling ventricular pressures, culminating in mechanical asystole, and a subsequent phase after asystole during which the electrocardiographic signal persisted for an average duration of 15.2 ± 8.7 minutes (range 3.1 to 32.4) and triggered a Hewlett-Packard 8040A monitor to show a heart rate pattern. Conclusions: The phenomenon of cardiac electromechanical dissociation may be occurring during similar terminal bradycardias that are observed in human labor and explains the delivery of a fresh stillbirth in spite of the recording of an electrocardiographic signal from a scalp electrode.

OBJECTIVE Our purpose was to investigate the three-dimensional architecture of placental villi from normal and growth-restricted fetuses and relate findings to umbilical artery blood flow velocity waveforms. STUDY DESIGN Placentas from term (n = 15) and preterm (n = 5) appropriately grown and term (n = 9) and preterm (n = 7) growth-restricted fetuses (birth weight < 10th percentile) were examined to determine the number of arteries per stem villus and the three-dimensional configuration of the villous trees and their vessels. Umbilical blood flow before delivery was assessed by Doppler ultrasonography. The effects of age and growth restriction were determined by two-way analyses of variance. RESULTS Growth restriction was associated with reduced large vessel wall thickness (p < or = 0.05) but no reduction in the number of these vessels per stem villus. The volumes and surface areas of intermediate and terminal villi were reduced (p < or = 0.001), especially in preterm growth-restricted cases, where a marked reduction in diastolic blood flow velocity was observed in the umbilical artery. CONCLUSIONS Reduced villous development may contribute to abnormal umbilical artery blood flood flow, as assessed by Doppler ultrasonography, in some cases of intrauterine growth restriction.

Our purpose was to assess the recurrence risk, course, and outcome of subsequent pregnancies in women with absent umbilical end-diastolic velocity.Absent umbilical end-diastolic velocity was detected in 88 women. Sixteen of them were prospectively followed up in their 19 subsequent pregnancies. These pregnancies were compared with their index pregnancies.The index pregnancy was invariably complicated with a perinatal mortality of 56%, growth restriction in 94% (15/16), and prematurity in 100% (75%32 weeks' gestation). In contrast, the outcome of the subsequent pregnancies was much better, and 74% (14/19) were uncomplicated. No perinatal deaths occurred, and none were delivered before 32 weeks' gestation. Absent umbilical end-diastolic velocity recurred in only two pregnancies, both of which were complicated. Six women had autoantibodies; these accounted for 80% (4/5) of subsequent complicated pregnancies.After an index pregnancy with absent umbilical end-diastolic velocity, subsequent pregnancies had favorable outcomes. Recurrence of absent umbilical end-diastolic velocity was low. The absence of autoantibodies and normal Doppler studies were associated with improved outcome.

The effect of hypoxic acidemia, hyperviscosity, and maternal hypertension on the umbilical arterial velocity waveform was studied in 23 chronically catheterized fetal sheep. Fetal hypoxic acidemia induced by lowering the maternal inspired oxygen concentration (n = 7) caused no change in the ratio of systolic/diastolic blood velocity even when fetal arterial pH was as low as 6.8. Fetal blood hyperviscosity (n = 7) induced by exchange transfusion with packed maternal blood cells increased placental vascular resistance by greater than or equal to 50% but had no significant effect on the systolic/diastolic ratio. Similarly, maternal hypertension induced by intravenous infusion of angiotensin II to the ewe (n = 9) did not affect the systolic/diastolic ratio despite a 50% increase in maternal arterial blood pressure. We conclude that umbilical arterial velocity waveform abnormalities observed in growth-restricted human fetuses are probably not a direct result of fetal hypoxemia or hyperviscosity or maternal hypertension.

Absent diastolic velocity and reversed diastolic velocity have been observed in the umbilical artery of growth-retarded human fetuses by means of Doppler ultrasonography. Because the physiologic mechanism is unknown, the purpose of this study was to determine whether such waveform changes could be induced in sheep fetuses by embolization of the resistance vessels of the placenta. Seven chronically catheterized sheep fetuses were instrumented with Doppler crystals mounted on one umbilical artery. The placenta was progressively embolized from the fetal side with plastic microspheres. In all cases the umbilical arterial waveform showed a progression from normal to zero diastolic velocity with embolization. In six of seven animals diastolic velocity eventually reversed in direction before fetal death. We conclude that occlusion of placental arteries and arterioles in fetal sheep recreates the waveform changes observed in severely growth-retarded human fetuses.

For clinical interpretation of Doppler waveforms, it is important to establish the extent to which fetal heart rate changes affect the umbilical artery velocity waveform. Umbilical artery waveforms were measured with continuous wave ultrasonography during spontaneous accelerations of the fetal heart rate in 20 uncomplicated, near-term pregnancies. On average, an acceleration of 20 beats/min of fetal heart rate within an individual was associated with a reduction in the systolic/diastolic velocity ratio of 0.25. There was, however, considerable variability in the response, and in six patients the systolic /diastolic ratio actually increased with heart rate. We conclude that fetal heart accelerations within the normal range cause only small and variable changes in the systolic/diastolic ratio.

It is common for women to undertake vigorous exercise in the late phase of pregnancy. This may have detrimental effects on the blood flow to the uterus and placenta or from the fetus to the placenta. Fifteen pregnant women with no obstetric or medical complications were subjected to a 5-minute exercise period. The maternal heart rate and blood pressure were elevated after exercise. The uteroplacental and umbilical circulations were assessed with Doppler ultrasonography. The ratio of the systolic/diastolic velocity in the uterine artery was elevated, which suggests that uteroplacental vascular resistance increased. The fetal heart rate was elevated after exercise, whereas the systolic/diastolic velocity ratio in the umbilical artery was unaltered. We conclude that moderate maternal exercise causes increased resistance to blood flow in the uterine circulation, whereas the umbilical circulation remains unaltered.