Fetal growth restriction and maternal cardiac function

Cardiac output rises in pregnancy, and most of this increase occurs in the first trimester. Both heart rate and stroke volume contribute to this increase, which, coupled with a decrease in mean arterial pressure, determines a reduction of maternal total vascular resistance (TVR) in physiological pregnancy. The absence of a 'correct' maternal cardiovascular compensatory response (absence of increase in cardiac output, heart rate, stroke volume, left ventricular mass and decrease in maternal TVR), in addition to abnormal trophoblastic invasion, might be one of the factors that could determine a reduced placental perfusion and, eventually, the development of fetal intrauterine growth restriction (IUGR). In fact, pregnancies complicated by IUGR appear to lack the stimulus to induce the hemodynamic changes typically present in physiological pregnancy such as the increase in preload, maternal heart rate, stroke volume, the enlargement of the left atrium and, above all, the reduction of TVR. It is difficult to establish whether these hemodynamic alterations found in IUGR patients develop from the early stages of pregnancy, but if future studies are able to support this hypothesis, this will open the opportunity to identify patients in a preclinical state and eventually treat them with new pharmacological protocols