Association of Persistent Pulmonary Hypertension in Infants With the Timing and Type of Antidepressants In Utero.
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ABSTRACT:
SUBMITTER: Munk-Olsen T
PROVIDER: S-EPMC8637253 | biostudies-literature | 2021 Dec
REPOSITORIES: biostudies-literature
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Association of Persistent Pulmonary Hypertension in Infants With the Timing and Type of Antidepressants In Utero.
Munk-Olsen Trine T Bergink Veerle V Rommel Anna-Sophie AS Momen Natalie N Liu Xiaoqin X
JAMA network open 20211201 12
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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:BackgroundPersistent 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.ObjectivesTo 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 strategyWe 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 criteriaFully 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 analysisWe found no studies meeting the criteria for inclusion in this review.Main resultsWe found no studies meeting the criteria for inclusion in this review.Authors' conclusionsThe 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:To evaluate pulmonary hemodynamics in patients who had been followed up for bronchopulmonary dysplasia (BPD)-associated pulmonary hypertension (PH) in the mid-term by right heart catheterization (RHC). A retrospective study was conducted among 56 patients who were born at a gestational age < 28 weeks during 2018-2020, and the consecutive patients complicated by BPD and ultrasound-defined PH (n = 10, 18%), of whom 7 patients were treated with sildenafil, were examined by RHC in the mid-term follow-up (median age: 25 months [IQR: 19-32]). Ultrasound study at RHC showed improvement in PH as represented by left ventricular end-systolic eccentricity index (median [IQR], 1.05 [IQR: 1.03-1.06] vs. 1.18 [IQR: 1.15-1.33]), pulmonary artery acceleration time (PAAT) (mean ± SD, 97.3 ± 18.2 vs. 55.2 ± 10.1) and a ratio of PAAT to right ventricular ejection time (0.35 ± 0.05 vs. 0.25 ± 0.04) compared with those at 40 weeks of postmenstrual age (PMA) (p < 0.05, respectively). RHC (mean pulmonary artery [PA] pressure: 21 [19-22] mmHg; pulmonary vascular resistance index [PVRi]: 2.63 [1.95-2.94] Wood Units·m2) revealed that 5 infants (50%) had mild PH (21-24 mmHg) and reduced peripheral PAs by pulmonary wedge angiography. The presence of emphysema on chest CT at 40 weeks of PMA and moderate/marked reduction of contrast filling in peripheral PAs on angiography were correlated with increased PVRi (p < 0.05, respectively).ConclusionWe observed that even after apparent resolution of ultrasound-defined PH, half of patients had catheterization-defined PH and vasculopathy at 2 years of age. These findings warrant long-term follow-up studies of BPD-associated PH.What is known• Pulmonary hypertension (PH) is associated with increased mortality in infants with bronchopulmonary dysplasia (BPD). Mortality in patients with BPD-associated PH predominantly occurs within the first 6 months of life and most patients who survive beyond 6 months show resolution of PH on echocardiography by 2 to 3 years of age.What is new• Even after the resolution of echocardiography-derived PH in infants with BPD-associated PH in the mid-term, the majority of such patients have abnormal pulmonary vasculature with PH or mildly elevated pulmonary artery pressure on right heart catheterization (RHC), indicating that echocardiography is insufficient and RHC may be necessary to follow up this population of patients.
| S-EPMC11573848 | biostudies-literature
Project description:Pulmonary hypertension (PH) in newborns and adults is a disease that can lead to right heart failure and result in a shorter lifespan. PH was induced by maintaining pregnant rats in a hypoxic chamber for 4 h twice a day, from days 7‑21 of pregnancy. Hypoxia was confirmed by a decrease in the partial pressure of oxygen (PaO2) and the oxygen saturation (SaO2) of arterial blood in the aorta. The body weight of newborns from hypoxic rats was ~20% decreased compared with the control newborns of normoxic rats. The vascular wall thickness/vascular diameter values of hypoxia treated pubs were increased compared with that of control newborns 7 days after birth; however, it decreased to similar levels than in the control group after 3 months, and then further decreased to significantly lower levels than in the control group at 6 months after birth. At birth, the lung tissues of newborns from hypoxic rats exhibited an increase in the levels of mRNA and proteins associated with PH such as HIF‑1α, HIF‑2α, V2R, TGF‑β, TNF‑α, Ang‑2 and α‑SMA. At 3 and 6 months after birth, the levels of both V2R mRNA and protein in offspring from hypoxic rats were at least 2‑fold higher, whereas the expression of all other factors decreased compared with the control offspring. By contrast, HIF‑2α and Ang‑2 expression levels were significantly increased in the 6‑month‑old control offspring from normoxic rats. V2R overexpression in pups induced by hypoxia in maternal rats was sustained until their adulthood. V2R may be a marker for detecting PH.
| S-EPMC7533485 | 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