Altered fetal circulation in type‐1 diabetic pregnancies
Objective Type‐I diabetic pregnancies are associated with congenital cardiac malformations, fetal cardiomyopathy, venous thrombosis and altered placental vascularization, even with tight maternal glucose control. The aim of this study was to investigate if, with good glucose control achieved with co...
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Veröffentlicht in: | Ultrasound in obstetrics & gynecology 2003-04, Vol.21 (4), p.365-369 |
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Sprache: | eng |
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Zusammenfassung: | Objective
Type‐I diabetic pregnancies are associated with congenital cardiac malformations, fetal cardiomyopathy, venous thrombosis and altered placental vascularization, even with tight maternal glucose control. The aim of this study was to investigate if, with good glucose control achieved with continuous subcutaneous insulin infusion, normal blood flow within the fetal heart can be achieved.
Methods
Seventeen fetuses of women with well‐controlled type‐I diabetes were studied longitudinally to evaluate effects on the fetal circulation. Doppler frequency shift tracings, valve diameters and intercept angles were measured at right and left atrioventricular valve orifices at 4‐week intervals starting at 15 weeks' gestation. Atrioventricular valve flow was calculated and compared to normal fetal data obtained in previous studies.
Results
Maximum and mean temporal velocities across the atrioventricular valves increased in both groups during gestation but significantly more in fetuses of type‐I diabetic pregnancies. Combined ventricular output, both absolute and per kg estimated fetal weight, were also greater in these fetuses. In the normal group the ratio of the left/right ventricular output decreased significantly during gestation (from 1.34 ± 0.28 to 1.08 ± 0.28 standard deviations), but in type‐I diabetic pregnancies this decrease did not occur (1.2 ± 0.26 to 1.25 ± 0.29 standard deviations).
Conclusions
These data indicate that there are significant differences in the fetal circulation between normal pregnancy and well‐controlled type‐I diabetic pregnancy, suggesting the existence of a compensatory mechanism which increases fetal cardiac output and causes cardiac hypertrophy. Copyright © 2003 ISUOG. Published by John Wiley & Sons, Ltd. |
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ISSN: | 0960-7692 1469-0705 |
DOI: | 10.1002/uog.88 |