condition, alcohol intake, drug abuse, or family history of preeclampsia made significant independent contribution in predicting cardiac output in the multiple regression model. The mean log MoM cardiac output was 0.000 [95% confidence interval (CI): À 0.0025 to 0.0025] in the unaffected group, 0.0261 (95% CI: 0.0065-0.0457) in the preeclampsia group, 0.0257 (95% CI: 0.0079-0.0435) in the PIH group, and -0.0085 (95% CI: À 0.0157 to À 0.0013) in the SGA group. In the patients with preeclampsia, log MoM cardiac output increased significantly with birth weight percentile (r = 0.346, P<0.001), with mean values of 0.0382 (95% CI: 0.0108-0.0656) in the preeclampsia group without SGA and 0.0111 (95% CI: À 0.0174 to 0.0396) in the preeclampsia group with SGA, respectively. Compared with the unaffected population, the mean log MoM cardiac output was higher in the preeclampsia group (P = 0.01), preeclampsia without SGA group (P = 0.008), and in the PIH group (P = 0.003). The statistic was lower in the SGA group (P = 0.03), and not significantly different in preeclampsia with SGA (P = 0.44). Significant prediction for SGA was provided by lower log MoM cardiac output [odds ratio (OR): 0.29; 95% CI: 0.09-0.92], smoking (OR: 3.1; 95% CI: 2.4-4.1), b-mimetic medication (OR: 2.9; 95% CI: 1.7-5.4), crown-rump length (OR: 0.97; 95% CI: 0.96-0.99), and ethic origin. Areas under receiver operating characteristics curves were 0.813, 0.830, 0.630, and 0.629 for all preeclampsia, preeclampsia without SGA, PIH, and SGA. For a 10% false-positive rate, the respective true positive rates were 43.4%, 52.2%, 23.3%, and 23.9%.Compared with values in women who go on to have uncomplicated pregnancies, maternal cardiac output, as measured by echocardiography at 11 to 13 weeks' gestation, is increased in pregnancies that go on to be complicated by preeclampsia. Cardiac output at 11 to 13 weeks is decreased in women who subsequently deliver SGA infants. These changes predate the clinical onset of both disorders.