Association of Persistent Pulmonary Hypertension in Infants With the Timing and Type of Antidepressants In Utero.
Ontology highlight
ABSTRACT:
SUBMITTER: Munk-Olsen T
PROVIDER: S-EPMC8637253 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:ObjectiveTo examine the risk for persistent pulmonary hypertension of the newborn associated with antenatal exposure to antidepressants.DesignSystematic review and meta-analysis.Data sourcesEmbase, Medline, PsycINFO, and CINAHL from inception to 30 December 2012.EligibilityEnglish language studies reporting persistent pulmonary hypertension of the newborn associated with exposure to antidepressants. Two independent reviewers extracted data and assessed the quality of each article.ResultsOf the 3077 abstracts reviewed, 738 papers were retrieved and seven included. All seven studies were above our quality threshold. Quantitative analysis was only possible for selective serotonin reuptake inhibitors (SSRIs). Although exposure to SSRIs in early pregnancy was not associated with persistent pulmonary hypertension of the newborn (odds ratio 1.23, 95% confidence interval 0.58 to 2.60; P=0.58), exposure in late pregnancy was (2.50, 1.32 to 4.73; P=0.005). Effects were not significant for any of the moderator variables examined, including study design, congenital malformations, and meconium aspiration. It was not possible to assess for the effect of caesarean section, body mass index, or preterm delivery. The absolute risk difference for development of persistent pulmonary hypertension of the newborn after exposure to SSRIs in late pregnancy was 2.9 to 3.5 per 1000 infants; therefore an estimated 286 to 351 women would need to be treated with an SSRI in late pregnancy to result in an average of one additional case of persistent pulmonary hypertension of the newborn.ConclusionsThe risk of persistent pulmonary hypertension of the newborn seems to be increased for infants exposed to SSRIs in late pregnancy, independent of the potential moderator variables examined. A significant relation for exposure to SSRIs in early pregnancy was not evident. Although the statistical association was significant, clinically the absolute risk of persistent pulmonary hypertension of the newborn remained low even in the context of late exposure to SSRIs.
| S-EPMC3898424 | biostudies-literature
Project description:In persistent pulmonary hypertension of the newborn (PPHN), the ratio of pulmonary vascular resistance to systemic vascular resistance is increased. Extrapulmonary shunts (patent ductus arteriosus and patent foramen value) allow for right-to-left shunting and hypoxaemia. Systemic hypotension can occur in newborns with PPHN due to variety of reasons, such as enhanced peripheral vasodilation, impaired left ventricular function and decreased preload. Systemic hypotension can lead to end organ injury from poor perfusion and hypoxaemia in the newborn with PPHN. Thus, it must be managed swiftly. However, not all newborns with PPHN and systemic hypotension can be managed the same way. Individualised approach based on physiology and echocardiographic findings are necessary to improve perfusion to essential organs. Here we present a review of the physiology and mechanisms of systemic hypotension in PPHN, which can then guide treatment.
| S-EPMC8217132 | biostudies-literature
Project description:A review of the physiology of persistent pulmonary hypertension of the newborn is provided, followed by a critical review of many of the agents that have been employed to treat this condition. In addition, the authors speculate on what type of pharmacologic therapy may prove useful in the future.
| S-EPMC8885147 | biostudies-literature
Project description:ObjectiveThis study aims to determine the immediate outcome of persistent pulmonary hypertension of the newborn (PPHN) and risk factors for mortality in the era of inhaled nitric oxide (iNO).Study designThis observational cross-sectional study includes 195 confirmed PPHN with a gestational age of ≥34 weeks without congenital heart disease. Multivariable logistic regression was used to identify risk factors for mortality.ResultsThe mortality rate was 16.4%, with the highest mortality with pulmonary hypoplasia. Of 195, 65% received iNO; 18% were iNO non-responders with the majority having pulmonary hypoplasia. Independent risk factors for mortality were the presence of reversal of flow at the descending aorta, pulmonary hypoplasia, APGAR scores ≤ 5 at 5 min, and idiopathic PPHN with an adjusted odds ratio of 15.9, 7.5, 6.7, and 6.4, respectively.ConclusionsDespite the usage of iNO, mortality due to PPHN remains high and is related to etiology and cardiac function.
| S-EPMC7883964 | biostudies-literature
Project description:BACKGROUND:Persistent pulmonary hypertension of the newborn (PPHN) is a clinical syndrome characterized by suboptimal oxygenation as a result of sustained elevation in pulmonary vascular resistance after birth. Currently, the therapeutic mainstay for PPHN is optimal lung inflation and selective vasodilatation with inhaled nitric oxide (iNO). However, iNO is not available in all countries and not all infants will respond to iNO. Milrinone is a phosphodiesterase III inhibitor which induces pulmonary vasodilatation by its actions through a cyclic adenylate monophosphate mediated signaling pathway. OBJECTIVES:To assess efficacy and safety in infants with PPHN either treated with: milrinone compared with placebo or no treatment; milrinone compared with iNO; milrinone as an adjunct to iNO compared with iNO alone; milrinone compared with potential treatments for PPHN other than iNO. SEARCH STRATEGY:We searched the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 2, 2010), MEDLINE and EMBASE databases from their inception until January 2010. We searched the reference lists of potentially relevant studies without any language restriction. SELECTION CRITERIA:Fully published randomized controlled trials (RCTs) and quasi-RCTs comparing milrinone with placebo, iNO or potential treatments other than iNO in neonates with PPHN were included if trials reported any clinical outcome. DATA COLLECTION AND ANALYSIS:We found no studies meeting the criteria for inclusion in this review. MAIN RESULTS:We found no studies meeting the criteria for inclusion in this review. AUTHORS' CONCLUSIONS:The efficacy and safety of milrinone in the treatment of PPHN are not known and its use should be restricted within the context of RCTs. Such studies should address a comparison of milrinone with placebo (in clinical situations where iNO is not available) or, in well resourced countries, should compare milrinone with iNO or as an adjunct to iNO compared with iNO alone.
| S-EPMC6823268 | biostudies-literature
Project description:Background: There is an emerging evidence that pulmonary hypertension is associated with amino acid, carnitine, and thyroid hormone aberrations. We aimed to characterize metabolic profiles measured by the newborn screen (NBS) in infants with persistent pulmonary hypertension of the newborn (PPHN) METHODS: Nested case-control study from population-based database. Cases were infants with ICD-9 code for PPHN receiving mechanical ventilation. Controls receiving mechanical ventilation were matched 2:1 for gestational age, sex, birth weight, parenteral nutrition administration, and age at NBS collection. Infants were divided into derivation and validation datasets. A multivariable logistic regression model was derived from candidate metabolites, and the area under the receiver operator characteristic curve (AUROC) was generated from the validation dataset.Results: We identified 1076 cases and 2152 controls. Four metabolites remained in the final model. Ornithine (OR 0.32, CI 0.26-0.41), tyrosine (OR 0.48, CI 0.40-0.58), and TSH 0.50 (0.45-0.55) were associated with decreased odds of PPHN; phenylalanine was associated with increased odds of PPHN (OR 4.74, CI 3.25-6.90). The AUROC was 0.772 (CI 0.737-0.807).Conclusions: In a large, population-based dataset, infants with PPHN have distinct, early metabolic profiles. These data provide insight into the pathophysiology of PPHN, identifying potential therapeutic targets and novel biomarkers to assess the response.
| S-EPMC7691760 | biostudies-literature
Project description:ObjectiveTo determine the association of persistent pulmonary hypertension of the newborn (PPHN) with death or disability among infants with moderate or severe hypoxic ischemic encephalopathy (HIE) treated with therapeutic hypothermia.MethodsWe compared infants with and without PPHN enrolled in the hypothermia arm from three randomized controlled trials (RCTs): Induced Hypothermia trial, "usual care" arm of Optimizing Cooling trial, and Late Hypothermia trial. Primary outcome was death or disability at 18-22 months adjusted for severity of HIE, center, and RCT.ResultsAmong 280 infants, 67 (24%) were diagnosed with PPHN. Among infants with and without PPHN, death or disability was 47% vs. 29% (adjusted OR: 1.65, 0.86-3.14) and death was 26% vs. 12% (adjusted OR: 2.04, 0.92-4.53), respectively.ConclusionsPPHN in infants with moderate or severe HIE was not associated with a statistically significant increase in primary outcome. These results should be interpreted with caution given the limited sample size.
| S-EPMC7954876 | biostudies-literature
Project description:RationaleObesity is associated with pulmonary arterial hypertension (PAH), but its impact on outcomes such as health-related quality of life (HRQoL), hospitalizations and survival is not well understood.ObjectivesTo assess the effect of obesity on health-related quality of life (HRQoL), hospitalizations and survival in patients with PAH.MethodsWe performed a cohort study of adults with PAH from the Pulmonary Hypertension Association Registry, a prospective multicenter registry. Multivariate linear mixed effects regression was used to examine the relationship between weight categories and HRQoL using the Short Form-12 (SF-12) and emPHasis-10 (e10). We used multivariable negative binomial regression to estimate hospitalization incidence rate ratios (IRRs) and Cox regression to estimate hazard ratios (HRs) for transplant-free survival by weight status.Results767 subjects were included: mean age of 57 years, 74% female, 33% overweight and 40% obese, with median follow-up duration of 527 days. Overweight and obese patients had higher baseline e10 scores (worse HRQoL), which persisted over time (p<0.001). The overweight and obese have a trend towards increased incidence of hospitalizations compared to normal weight (IRR 1.34, 95% confidence interval (95%CI) 0.94-1.92 and 1.33, 95%CI 0.93-1.89, respectively). Overweight and obese patients had lower risk of transplant or death as compared to normal weight patients (HR 0.45, 95%CI 0.25-0.80 and 0.39, 95%CI 0.22-0.70, respectively).ConclusionsIn a large multicenter, prospective cohort of PAH, overweight and obese patients had worse disease-specific HRQoL despite better transplant-free survival compared to normal weight patients. Future interventions should address the specific needs of these patients.
| S-EPMC7869778 | biostudies-literature
Project description:OBJECTIVES:To determine the prevalence and factors associated with persistent pulmonary hypertension (PH) following transcatheter aortic valve replacement (TAVR) and its relationship with long-term mortality. METHODS:Consecutive patients who underwent TAVR from July 2011 through January 2016 were studied. The prevalence of baseline PH (mean pulmonary artery pressure ?25?mm Hg on right heart catheterisation) and the prevalence and the predictors of persistent?moderate?PH (pulmonary artery systolic pressure (PASP)>45?mm Hg on 1?month post-TAVR transthoracic Doppler echocardiography) were collected. Cox models quantified the effect of persistent PH on subsequent mortality while adjusting for confounders. RESULTS:Of the 407 TAVR patients, 273 (67%) had PH at baseline. Of these, 102 (25%) had persistent?moderate?PH. Mortality at 2 years in patients with no baseline PH versus those with PH improvement (follow-up PASP?45?mm Hg) versus those with persistent?moderate?PH was 15.4%, 16.6% and 31.3%, respectively (p=0.049). After adjusting for Society of Thoracic Surgeons Predicted Risk of Mortality and baseline right ventricular function (using tricuspid annular plane systolic excursion), persistent?moderate?PH remained associated with all-cause mortality (HR=1.82, 95%?CI 1.06 to 3.12, p=0.03). Baseline characteristics associated with increased likelihood of persistent?moderate?PH were ?moderate?tricuspid regurgitation, ?moderate?mitral regurgitation, atrial fibrillation/flutter, early (E) to late (A) ventricular filling velocities (E/A ratio) and left atrial volume index. CONCLUSIONS:Persistency of even moderate or greater PH at 1?month post-TAVR is common and associated with higher all-cause mortality.
| S-EPMC5876149 | biostudies-literature
Project description:Recent studies have suggested associations between certain genetic variants and susceptibility to persistent pulmonary hypertension of the newborn (PPHN). The aim of the study was to evaluate the association of EDN1, NOS3, ACE and VEGFA genes with PPHN. Neonates with respiratory distress were enrolled in the study, whose gestational age ?34 weeks, age ?3 days. They were divided into PPHN and non-PPHN group. The EDN1, NOS3, ACE and VEGFA genes were detected by next-generation sequencing, and the results were validated by Sanger sequencing. Serum endothelin-1 (ET-1) levels were quantified by ELISA. A total of 112 neonates were enrolled (n?=?55 in PPHN group; n?=?57 in non-PPHN group). There is a significantly difference in the genotype distribution of EDN1 rs2070699 between the PPHN and non-PPHN group (P?=?0). A higher frequency of the rs2070699 T allele was observed in the PPHN group (54.5% vs 27.2%; OR?=?3.89; 95%CI 1.96-7.72). The rs2070699 T allele was associated with higher ET-1 levels (3.333?±?2.517 pg/mL vs 1.223?±?0.856 pg/mL; P?=?0.002) and a longer ventilation period (5.8?±?2.6 days vs 3.6?±?3.3 days; P?=?0). The results suggest there is an association between EDN1 and PPHN. The presence of the rs2070699 T allele increased the risk of PPHN in neonates with respiratory distress.
| S-EPMC4947908 | biostudies-literature