Background
Intraventricular pressure difference (IVPD), the diastolic suction during early diastole, is known as a useful marker of myocardial diastolic function in adults with different heart diseases, but there are no studies of fetal IVPD. The aim of this study was to determine whether IVPD exists and changes prenatally and whether IVPD correlates with preexisting parameters to evaluate fetal cardiac diastolic function and ventricular dominance.
Methods
Cross-sectional study data (stroke volume, fetal cardiac output, E/A ratio, and myocardial performance index) from 117 healthy fetuses at 17 to 36 weeks of gestation were retrospectively evaluated. The total IVPD was calculated using Euler’s equation with color M-mode data. Segmental IVPD was evaluated as apical, mid, and basal IVPDs.
Results
The total IVPD in the right ventricle and left ventricle significantly increased in late gestation compared with that in different fetuses studied at midgestation (right and left ventricles, ρ = 0.813 and ρ = 0.895, respectively; P < .001). In both ventricles, the apical IVPD percentage, but not basal or mid IVPD, significantly increased at late gestation compared with that in different fetuses studied at midgestation. Both stroke volumes were correlated with IVPD (right and left ventricles, ρ = 0.796 and ρ = 0.784, respectively; P < .001). Although myocardial performance index in the left ventricle did not show a significant correlation with IVPD, the E/A ratio had a very weak correlation with IVPD (right ventricle, ρ = 0.576, P < .001; left ventricle, ρ = 0.338, P < .01).
Conclusions
IVPD has been proved to exist in both ventricles during the fetal stage. The total IVPD increased in late gestation, and the ventricular length increased because of increased apical IVPD in both ventricles. Furthermore, the increase of IVPD in both ventricles was correlated with stroke volume and, accordingly, cardiac output. Left ventricular dominance in IVPD from the fetal stage may offer interesting insight into fetal cardiac development.
Highlights
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IVPD, which is ventricular suction, exists beginning in the fetal stage.
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The total IVPD increases during late gestation, along with an increase in apical IVPD.
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In the fetal stage, left ventricular IVPD was dominant compared to right ventricular IVPD.
The evaluation of fetal cardiac function is one of the important factors in predicting neonatal mortality in fetuses with congenital heart disease or fetal hydrops. Methods of quantifying cardiac function in fetuses are limited, including pulse Doppler assessment such as myocardial performance index (MPI), cardiac output (CO), venous Doppler patterns, tissue Doppler imaging, and speckle-tracking imaging. Parameters can evaluate only one aspect of fetal cardiac function, which is not enough. In addition, the right ventricle (RV) is slightly dominant because of the presence of the ductus arteriosus, which supplies much of the systemic output with high pulmonary vascular resistance in the fetal circulation, whereas the left ventricle (LV) primarily supplies the fetal brain with the flow from the placenta through the foramen ovale. Little is known about fetal cardiac function, especially diastolic function.
Because diastolic dysfunction may precede systolic dysfunction, detection of ventricular dysfunction earlier in the clinical course may be possible. The intraventricular pressure difference (IVPD) during early diastole creates a suction force, which draws blood from the left atrium into the LV. IVPD has been understood to play a fundamental and important role in diastolic function during early diastole. Although IVPD was well correlated with the τ index, which is the gold standard of diastolic function, IVPD could be measured only with invasive cardiac catheterization. IVPD in apical segments is the most important contributor to overall left ventricular suction force. The advent of noninvasive IVPD measurement with color M-mode also led to accurate IVPD measurement in both ventricles. Furthermore, it has been reported that IVPD can be measured in small species such as rat and mice, whose heart size is similar to that of a human fetus. However, there are no reports on fetal IVPD in either human or animals.
We first hypothesized that IVPD exists from the fetal stage and that this sucking force would develop with advancing gestation. Another hypothesis was that IVPD in the RV would be dominant compared with that in the LV during the fetal stage because of the fetal circulation. Therefore, the aims of this study were to determine the presence of IVPD during the fetal stage and to evaluate the change in IVPD with gestation. Furthermore, another aim was to determine whether IVPD correlated with preexisting parameters to evaluate ventricular diastolic function and ventricular dominance.
Methods
Cross-sectional studies from 117 healthy pregnant women at 17 to 36 weeks of gestation were retrospectively reviewed after approval was obtained from the ethics committee of Juntendo University Hospital. In this study, we defined midgestation as <28 weeks of gestation and late gestation as >28 weeks of gestation. None of the fetuses enrolled in this study had structural abnormalities, and all had normal cardiac function and rhythm. Their fetal growth was appropriate for their gestational age. Exclusion criteria were multiple pregnancy, fetal growth restriction, and maternal complications such as gestational diabetes, collagen disease, and maternal hypertension. Echocardiography was performed using the Acuson S2000 ultrasound system (Siemens Medical Solutions USA, Mountain View, CA) equipped with a CH6-2 (2–6 MHz) or 7CF2 transducer (2–7 MHz). In this study, we used color M-mode to achieve a high sampling rate (180–215 samples/sec).
Analysis of Two-Dimensional Imaging Modalities
Offline analysis was performed using Syngo workstation (Syngo US Workplace; Siemens Healthcare, Erlangen, Germany). The velocity-time integral (centimeters) and valve diameters were obtained from both ventricular outflow tracts to calculate CO. Right ventricular CO (milliliters per minute) was derived from the product of stroke volume (SV) and fetal heart rate (beats per minute). SV in the right ventricle was derived from the pulmonary arterial velocity-time integral and the diameter of the cross-sectional pulmonary artery. CO in the LV (milliliters per minute) was derived from aortic SV and fetal heart rate. Mitral and tricuspid valve blood flow velocities during rapid ventricular filling (E wave, centimeters per second) and atrial contraction (A wave, centimeters per second) were analyzed as the E/A ratio. On mitral inflow and aortic outflow Doppler imaging, MPI was calculated using the following equation :
MPI = Isovolumic contraction time + Isovolumic relaxation time Ejection time
IVPD Measurement
Color M-mode was recorded with the cursor parallel to the mitral and tricuspid inflow in the apical four-chamber view and analyzed using in-house code written in MATLAB (The MathWorks, Natick, MA). The dealiased Doppler images were reconstructed on the basis of a one-dimensional Euler equation (equation 2 ), where P is pressure, ρ is constant blood density (1,060 kg/m 3 ), v is velocity, s is position toward the depth, and t is time, which was used to calculate the relative pressures within the region of interest from the reconstructed velocity field. The pressure difference at each point along a scan line was measured relative to the position of the mitral/tricuspid annulus just before mitral/tricuspid valve opening by calculating the line integral between them. The first term on the right side of equation 2 is the inertial component, and the second term is the convective component.
d P d s = ρ ( d v d t + v d v d x )
IVPD = ∫ LV length ρ ( d v d t + v d v d x ) d s
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