METHODS: This was a prospective cross-sectional study of pregnant and postnatal women aged between 18-35 years with no coexisting diseases. Serum samples were analysed for hs-TnI.
RESULTS: A total of 880 women (mean age = 29.1 years [standard deviation = 5.1 years]) were recruited with 129 (14%), 207 (24%), and 416 (47%) patients in the first, second, and third trimesters, respectively. Ninety (10%) participants were recruited in the postnatal period. During pregnancy 28 (3%) patients were classified as having pregnancy-induced hypertension and 10 (1%) as preeclampsia. High-sensitivity cardiac troponin I was measurable in 546 (62%) participants with a median of 1 ng/L (range 0 to 783 ng/L). Troponin concentrations were above the 99th percentile in 19 (2%) individuals. Patients with pregnancy-induced hypertension and preeclampsia had higher concentrations of hs-TnI (median 11 ng/L [interquartile range (IQR) 6 to 22 ng/L] vs 12ng/L [IQR 3 to 98 ng/L] vs 1 ng/L [IQR 0 to 1 ng/L]). In logistic regression modeling hs-cTnI concentration remained an independent predictor of pregnancy-induced hypertension or preeclampsia in both unadjusted and adjusted models (odds ratio 9.3 [95% confidence interval 5.8 to 16.3] and 11.5 [95% confidence interval 6.3 to 24.1], respectively, per doubling of hs-TnI concentrations).
CONCLUSIONS: Cardiac troponin measured using a high-sensitivity assay is quantifiable in the majority of young pregnant women with 2% of individuals having concentration above the 99th percentile sex-specific threshold. Patients with pregnancy-induced hypertension or preeclampsia had higher cardiac troponin concentrations. Cardiac troponin was a strong independent predictor of pregnancy-induced hypertension or preeclampsia in pregnant and postnatal women.
METHODS: This was a cross-sectional study consisted of 21 pregnant women with hypertension and 23 without hypertension. The gestational age ranged from 28 to 39 weeks (hypertensive) and 32 to 40 weeks (normotensive). The paraffin embedded formalin fixed placenta tissue blocks were retrieved from the pathology archives. Endocan immunohistochemistry was performed on tissue sections of full thickness and maternal surface of the placenta. The endocan expression was determined in fetal endothelial cells, maternal endothelial cells, cytotrophoblasts, syncytiotrophoblasts and decidual cells. The differences in endocan expression in placenta between hypertensive and normotensive subjects were evaluated by Pearson chi-square test and t-test were used in the statistical analysis.
RESULTS: The endocan expression was significantly higher in fetal endothelial cells (P pre-eclampsia (P = 0.03). Also, a positive endocan expression was associated with low birthweight (P = 0.001) and prematurity (P = 0.005) in the fetal outcomes.
CONCLUSION: This study showed endocan is highly expressed in fetal endothelial cells, maternal endothelial cells and decidual cells in placenta of hypertensive women. In addition, its expression was associated with poorer maternal and fetal outcomes. These findings suggest endocan may play an important role in the progression of hypertension in pregnancy.