Screening for pre-eclampsia by maternal serum glycosylated fibronectin at 11-13 weeks' gestation.

OBJECTIVE: To examine the performance of screening for preterm and term pre-eclampsia (PE) at 11-13 weeks' gestation by maternal factors and combinations of maternal serum glycosylated fibronectin (GlyFn), mean arterial pressure (MAP), uterine artery pulsatility index (UtA-PI) and serum placental growth factor (PlGF). METHODS: This was a case-control study in which maternal serum GlyFn was measured using a point-of-care device in stored samples from a non-intervention screening study of singleton pregnancies at 11 + 0 to 13 + 6 weeks' gestation. In the same samples, PlGF was measured by time-resolved fluorometry. We used samples from women who delivered with PE at < 37 weeks' gestation (n = 100), PE at ≥ 37 weeks (n = 100), gestational hypertension (GH) at < 37 weeks (n = 100), GH at ≥ 37 weeks (n = 100) and 1000 normotensive controls with no pregnancy complications. In all cases, MAP and UtA-PI had been measured during the routine 11-13-week visit. Levels of GlyFn were transformed to multiples of the expected median (MoM) values after adjusting for maternal demographic characteristics and elements of medical history. Similarly, the measured values of MAP, UtA-PI and PlGF were converted to MoMs. The competing-risks model was used to combine the prior distribution of gestational age at delivery with PE, obtained from maternal characteristics, with various combinations of biomarker MoM values to derive the patient-specific risks of delivery with PE or GH at < 37 and ≥ 37 weeks' gestation. Screening performance was estimated by examining the area under the receiver-operating-characteristics curve (AUC) and detection rate (DR) at 10% fixed false-positive rate (FPR). RESULTS: The maternal characteristics and elements of medical history with a significant effect on the measurement of GlyFn were maternal age, weight, height, race, smoking status and history of PE. In pregnancies that developed PE, GlyFn MoM was increased and the deviation from normal decreased with increasing gestational age at delivery. The DR and AUC of screening for delivery with PE at < 37 weeks' gestation by maternal factors alone were 50% and 0.834, respectively, and these increased to 80% and 0.949, respectively, when maternal risk factors were combined with MAP, UtA-PI and PlGF (triple test). The performance of the triple test was similar to that of screening by a combination of maternal factors, MAP, UtA-PI and GlyFn (DR, 79%; AUC, 0.946) and that of screening by a combination of maternal factors, MAP, PlGF and GlyFn (DR, 81%; AUC, 0.932). The performance of screening for delivery with PE at ≥ 37 weeks' gestation was poor; the DR for screening by maternal factors alone was 35% and increased to only 39% with use of the triple test. Similar results were obtained when GlyFn replaced PlGF or UtA-PI in the triple test. The DR of screening for GH with delivery at < 37 and ≥ 37 weeks' gestation by maternal factors alone was 34% and 25%, respectively, and increased to 54% and 31%, respectively, with use of the triple test. Similar results were obtained when GlyFn replaced PlGF or UtA-PI in the triple test. CONCLUSIONS: GlyFn is a potentially useful biomarker in first-trimester screening for preterm PE, but the findings of this case-control study need to be validated by prospective screening studies. The performance of screening for term PE or GH at 11 + 0 to 13 + 6 weeks' gestation by any combination of biomarkers is poor. © 2023 International Society of Ultrasound in Obstetrics and Gynecology.

Left atrial size and left ventricular function in coronary artery disease: an echocardiographic-angiographic correlative study.

M-mode echocardiography was used to determine left atrial size in 100 patients with coronary artery disease undergoing cardiac catheterization. Patients were divided in two groups on the basis of left atrial diameter (greater than or equal to 40 mm in 40 patients and less than 40 mm in 60). Patients with larger left atria had a higher frequency of electrocardiographic evidence of left atrial abnormality (p less than 0.01) and myocardial infarction (p less than 0.001). Pulmonary capillary wedge and left ventricular end-diastolic pressures were higher (p less than 0.005) in patients with larger left atria. An abnormal end-diastolic volume (greater than 100 ml/M2) was observed in 13 patients with enlarged left atria compared to none with normal left atrial size (p less than 0.001). Triple vessel disease was more frequent (63% vs 32%) and single vessel disease less frequent (10% vs 37%) in patients with larger left atria (p less than 0.005). Abnormal left ventricular contractile patterns were noted in 45% of patients with normal left atrial diameters compared to 80% in those with an enlarged left atrium (p less than 0.001). An abnormally low ejection fraction (less than 0.5) was observed in 25% and 80%, respectively, in patients with normal and enlarged left atria (p less than 0.001). Of 58 patients with normal ejection fractions, only 17% had left atrial diameters greater than or equal to 40 mm compared to 71% of 42 patients with abnormally low ejection fractions (p less than 0.001). Of 18 patients with left atrial diameters greater than 42 mm, only two had normal ejection fractions. The mean ejection fraction for patients with left atrial diameters less than 40 mm was 0.63 +/- 0.13 compared to 0.41 +/- 0.18 for those with diameters greater than or equal to 40 mm (p less than 0.001). The sensitivity, specificity, and predictive value for an enlarged left atrium in identifying an abnormal ejection fraction were, respectively, 71, 83, and 75%. These findings indicate that M-mode echocardiographic left atrial enlargement is a useful marker of advanced hemodynamic and angiographic abnormality in patients with coronary artery disease.