There are limited data regarding the functional properties of the human fetal myocardium. However, the possibility to analyze the myocardial velocity profile provides new possibilities to gain further knowledge in this area. Examining of the myocardial wall motions using TVI allows for direct evaluation of myocardial motion as well as offline analysis using post-processing software. In the present study, using this technique, we show a longitudinal shortening of the fetal myocardium with gestational age, as shown in Figure 4c, which is most likely due to a gestational age-dependent physiological change in the myocardial contractile function.
As the myocardial growth of the left ventricle is uniform, the decreasing HR cannot be due to a change in cardiac movement pattern throughout gestation. Nor can this decrease due to a developed myocardial stiffness, since the E’/A’ ratio increases with gestational age. These findings, together with the conclusion that the displacement of the AV plane is not only dependent on the fetal LV length but also on gestational age, imply a molecular background to the change in cardiac muscle contractility during pregnancy.
Myocardial deformation results from a complex interaction between intrinsic contractile forces, extrinsic loading conditions and elastic properties. Animal studies have indicated that the degree of myocardial deformity reflects local contractile function, preload and afterload of the heart . Since preload is rather stable and afterload declines with advancing gestational age, it is unlikely that changes in load will be the major explanation for the relative decline in myocardial deformation. Rather a change in elastic properties and contractility are plausible explanations for this phenomenon. Most likely, as illustrated in the sheep fetus, contractility is correlated with the process of cardiomyocyte binucleation , a transition from mono- to binucleated cardiomyocytes that, as in the human fetus, occur before birth.
The present study demonstrates a linear relationship between LV length and gestational age. Stroke volumes of the ventricles have a curvilinear relationship with gestational age  and it seems that the relative high stroke volume of the most immature fetus is explained by increased myocardial deformation. These observations are in agreement with other studies demonstrating declining ejection fractions with advancing gestational age [7, 8]. Hypothetically, one could argue that if the immature fetus did not have a myocardium with these favourable elastic properties, the size of the left ventricle and the heart would need to be relatively larger than at term to ensure a constant cardiac output per 100 g of fetal tissue. Thus, since the ratio between the heart and thorax is stable over time and the fetal heart area is approximately one third that of the thorax from approximately 18th week gestation to term, we speculate that the increased contraction with declining gestational age is a prerequisite to ensure these relationships.
It is interesting to speculate how the human fetus can mount an increasing intracardiac pressure with a decreasing deformation of the heart with advancing gestational age. Johnson et al.  performed intracardiac punctures in human fetuses, and were able to demonstrate an increase in ventricular systolic and end diastolic pressure with advancing gestational age. Animal studies indicate that the cardiac output does not change in relation to body weight throughout gestation, and the demand of increased circulation to various organs and placenta is met by redistribution rather than an increase in cardiac output [10, 11]. Nevertheless, changes to cope with the transition towards LV dominance at birth are not answered for.
The fetal heart allows sustained development under low-oxygen conditions. A decrease in deformation and heart movement might also be an adaptive change to cope with a decline in oxygen supply with advancing gestational age . The birth process will be the ultimate challenge for the fetal heart in regard to oxygen supply and myocardial performance. Fetal cardiac muscle contractility needs to be studied by these means in risk pregnancies. There are some intriguing data indicating adaptive cardiovascular changes in the intrauterine growth restricted (IUGR) or preterm fetus that show increased aortic intima media thickness [13, 14], with changes in the modified myocardial performance index (Mod-MPI)  and increased coronary blood flow (CF) ; all of which correspond to changes of the mechanical pumping function of the fetal heart. We are presently evaluating this method in high risk pregnancies. It is tempting to speculate that myocardial maturation is critical in preparing the fetal heart to cope with the intrauterine environment and the increased demand at birth and to successfully adapt to extra uterine life [1, 17].