There is a delay in left ventricular filling which may reflect changes in myocardial relaxation and possible reduction in passive ventricular filling as a result of chronic hypoxemia in the SGA fetus and altered in utero metabolic environment in the IDDM fetus.

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Left ventricular isovolumic relaxation time was studied in 22 appropriate-for-gestational-age fetuses (AGA, 26-40 wk) and 12 small-for-gestational-age fetuses (SGA, 29-37 wk). Left ventricular isovolumic relaxation time was determined from the interval between aortic valve closure and maximal left atrial dimension by M-mode, and from the interval between aortic valve closure artefact and onset of transmitral flow by pulsed Doppler. Mean left ventricular isovolumic relaxation time by M-mode (36 +/- 6 ms) and by pulsed Doppler (49 +/- 10 ms) were significantly different (p < 0.05) in AGA while this was not so in SGA (56 +/- 10 ms vs. 60 +/- 8 ms). A significant difference (p < 0.05) in mean left ventricular isovolumic relaxation time by M-mode existed between AGA (36 +/- 6 ms) and SGA (56 +/- 10 ms), whereas this was not so for pulsed Doppler (48 +/- 10 ms vs. 60 +/- 8 ms). Mean left ventricular isovolumic relaxation time by Doppler was significantly larger (mean difference 14 +/- 8 ms; p < 0.05) than by M-mode in AGA. However, there was no difference in mean left ventricular isovolumic relaxation time between the two ultrasound modalities in SGA. These data suggest synchronization of mitral cusp separation and transmitral blood flow in the SGA fetus. We speculate that, in the SGA fetus, delayed left ventricular isovolumic relaxation time may reflect cardiac diastolic dysfunction.

Objective

No abstract