Prediction model for hypertension in first decade after pre-eclampsia in initially normotensive women.

OBJECTIVE: To develop a prediction model for the development of hypertension in the decade following pre-eclampsia in women who were normotensive shortly after pregnancy. METHODS: This was a longitudinal cohort study of formerly pre-eclamptic women attending a university hospital in The Netherlands between 1996 and 2019. We developed a prediction model for incident hypertension using multivariable logistic regression analysis. The model was validated internally using bootstrapping techniques. RESULTS: Of 259 women, 185 (71%) were normotensive at the first cardiovascular assessment, at a median of 10 (interquartile range (IQR), 6-24) months after a pre-eclamptic pregnancy, of whom 49 (26%) had developed hypertension by the second visit, at a median of 11 (IQR, 6-14) years postpartum. The prediction model, based on birth-weight centile, mean arterial pressure, total cholesterol, left ventricular mass index and left ventricular ejection fraction, had good-to-excellent discriminative ability, with an area under the receiver-operating-characteristics curve (AUC) of 0.82 (95% CI, 0.75-0.89) and an optimism-corrected AUC of 0.80. The sensitivity and specificity of our model to predict hypertension were 98% and 34%, respectively, and positive and negative predictive values were 35% and 98%, respectively. CONCLUSIONS: Based on five variables, we developed a good-to-excellent predictive tool to identify incident hypertension following pre-eclampsia in women who were normotensive shortly after pregnancy. After external validation, this model could have considerable clinical utility in tackling the cardiovascular legacy of pre-eclampsia. © 2023 The Authors. Ultrasound in Obstetrics & Gynecology published by John Wiley & Sons Ltd on behalf of International Society of Ultrasound in Obstetrics and Gynecology.

Cardiac output and peripheral vascular resistance during normotensive and hypertensive pregnancy - a systematic review and meta-analysis.

BACKGROUND: In-depth insight into haemodynamic changes during normotensive pregnancy may help identify women at risk for gestational hypertensive complications. OBJECTIVES: To determine the magnitude of changes in cardiac output and its determinants stroke volume and heart rate, and total peripheral vascular resistance during singleton normotensive and hypertensive pregnancies. SEARCH STRATEGY: PubMed (NCBI) and Embase (Ovid) databases were searched from their inception up to November 2019. SELECTION CRITERIA: Studies reporting original measurements of haemodynamic parameters during pregnancy together with a non-pregnant reference measurement. Studies including women using antihypertensive medication were excluded. DATA COLLECTION AND ANALYSIS: Pooled mean differences between pregnant and non-pregnant women, and absolute values of haemodynamic parameters were calculated for predefined gestational intervals using a random-effects model in normotensive and hypertensive pregnancy. Meta-regression analysis was used to analyse group differences in adjustments and absolute values during pregnancy. MAIN RESULTS: In normotensive pregnancies, cardiac output increased from the first weeks on, reaching its highest level early in the third trimester (mean difference, 1.41 l·min1 ; 95% CI 1.18-1.63 l·min). In parallel, vascular resistance decreased progressively until its nadir in the early third trimester (mean difference, -331 dyn·sec-1 ·cm-5 ; 95% CI -384 to -277 dyn·sec-1 ·cm-5 ) and then increased slightly at term. In hypertensive pregnancies, the initial cardiac output increase was higher and vascular resistance did not change throughout gestation compared with reference values. CONCLUSIONS: Hemodynamic changes in women who eventually develop hypertensive complications are substantially different. Serial monitoring and plotting against developed normograms can identify women at risk and may allow timely intervention. TWEETABLE ABSTRACT: Monitoring haemodynamic changes in pregnancy helps identify women at risk for hypertensive complications.

Effect of pregnancy prolongation in early-onset pre-eclampsia on postpartum maternal cardiovascular, renal and metabolic function in primiparous women: an observational study.

OBJECTIVE: To evaluate the association between deferred delivery in early-onset pre-eclampsia and offspring outcome and maternal cardiovascular, renal and metabolic function in the postpartum period. DESIGN: Observational study. SETTING: Tertiary referral hospital. POPULATION: Nulliparous women diagnosed with pre-eclampsia before 34 weeks' gestation who participated in a routine postpartum cardiovascular risk assessment programme. Women with hypertension, diabetes mellitus or renal disease prior to pregnancy were excluded. METHODS: Regression analyses were performed to assess the association between pregnancy prolongation and outcome measures. MAIN OUTCOME MEASURES: Offspring outcome and prevalence of deviant maternal cardiovascular, renal and metabolic function. RESULTS: The study population included 564 women with a median pregnancy prolongation of 10 days (interquartile range [IQR] 4-18) who were assessed at on average 8 months (IQR 6-12) postpartum. Pregnancy prolongation after diagnosis resulted in a decrease in infant mortality (adjusted odd ratio [aOR] 0.907, 95% CI 0.852-0.965 per day prolongation). This improvement in offspring outcome was associated with an elevated risk of moderately increased albuminuria (aOR 1.025, 95% CI 1.006-1.045 per day prolongation), but not with aberrant cardiac geometry, cardiac systolic or diastolic dysfunction, persistent hypertension or metabolic syndrome. CONCLUSION: Pregnancy prolongation in early-onset pre-eclampsia is associated with improved offspring outcome and survival. These effects do not appear to be deleterious to short-term maternal cardiovascular and metabolic function but are associated with a modest increase in risk of residual albuminuria. TWEETABLE ABSTRACT: Pregnancy prolongation in pre-eclampsia has only a limited effect on postpartum maternal cardiovascular function.

Invalidity of the acetylene reduction assay in alkane-utilizing, nitrogen-fixing bacteria.

The cause of the failure of the C2H2-C2H4 assay for nitrogen-fixing bacteria growing on lower alkanes was studied. Acetylene was a strong competitive inhibitor of methane oxidation for methane-utilizing bacteria, as well as for the oxidation of lower alkanes by other bacteria, so that energy and reducing power were no longer available for the reduction of acetylene by nitrogenase. Nitrogen-fixing bacteria grown on alkanes may reduce acetylene when intermediates of alkane-breakdown or other substrates oxidizable in the presence of acetylene are supplied. Ethylene co-oxidation is not responsible for the failure of the test, because acetylene also inhibits this co-oxidation along with methane oxidation.