Effect of patent ductus arteriosus on the heart in preterm infants

Philip, Ranjit; Towbin, Jeffrey A.; Sathanandam, Shyam; Goldberg, Jason F.; Yohannan, Thomas; Swaminathan, N.; Johnson, Jason N.

doi:10.1111/chd.12701

Cited by 18 publications

(16 citation statements)

References 15 publications

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“… Faster development of pulmonary overcirculation: The intrinsic tone in their pulmonary arteries is relatively lesser due to a smaller amount of muscle in the media. This precludes appropriate pulmonary constriction and leads to pulmonary overcirculation and cardiac volume overload earlier (2–3 weeks of age) than in term infants (3–6 weeks) [ 3 ]. Delayed pulmonary vascular maturation: Similar to respiratory distress syndrome, preterm infants have differential perfusion, i.e, poorly aerated lung segments have decreased PBF and well-aerated segments have good PBF.…”

Section: Pathophysiologymentioning

confidence: 99%

“…The mean airway pressures rise to provide adequate oxygenation to non-compliant lungs. This can cause lung damage and possibly lead to BPD [ 3 ].…”

Section: Pathophysiologymentioning

confidence: 99%

“…The presence of severe PAH with bronchopulmonary dysplasia (BPD) in a preterm infant bestows a 40% mortality by 2 years of age [ 2 ]. It is difficult to predict the risk of developing PAH in preterm infants as it is multifactorial, with conditions such as BPD, necrotizing enterocolitis (NEC), and sepsis being risk factors [ 3 ]. In addition to these factors, there is an enhanced risk of developing PAH early in premature infants with post-tricuspid shunts [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

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Pulmonary Hypertension with Prolonged Patency of the Ductus Arteriosus in Preterm Infants

et al. 2020

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There continues to be a reluctance to close the patent ductus arteriosus (PDA) in premature infants. The debate on whether the short-term outcomes translate to a difference in long-term benefits remains. This article intends to review the pulmonary vasculature changes that can occur with a chronic hemodynamically significant PDA in a preterm infant. It also explains the rationale and decision-making involved in a diagnostic cardiac catheterization and transcatheter PDA closure in these preterm infants.

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Section: Pathophysiologymentioning

confidence: 99%

“…The mean airway pressures rise to provide adequate oxygenation to non-compliant lungs. This can cause lung damage and possibly lead to BPD [ 3 ].…”

Section: Pathophysiologymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pulmonary Hypertension with Prolonged Patency of the Ductus Arteriosus in Preterm Infants

et al. 2020

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“…While a very tiny ductus may be safely left untreated, a large ductus can cause pulmonary over-circulation and cardiac failure. A moderate ductus can lead to pulmonary hypertension [10,11] in the long-term. Even a small ductus is at risk for developing endocarditis [12].…”

Section: Consequences Of Pda In Elbw Infantsmentioning

confidence: 99%

“…With evidence mounting against the use of COX inhibitors and surgical ligation, the trend towards permissive conservative observation of this lesion has developed, reserving surgery for only the most severe cases [13][14][15][16][17]32]. Unfortunately, recent data suggests that this approach is associated with an increased risk for the development of chronic lung disease and death, especially in infants born ≤26 weeks' gestation [8][9][10][11][12][13][14][15][16][17]. More recently in the United States, survival of infants born as early as 22 weeks' gestation is now possible [33], making the need for effective PDA therapy in this high risk, ELBW population more important than ever.…”

Section: Controversy and Practice Variationmentioning

confidence: 99%

PDA Closure in ELBW Infants: If, When, and How to Do It

Whiting¹,

Sathanandam²

2020

Update on Critical Issues on Infant and Neonatal Care

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Patent ductus arteriosus (PDA) is the most common cardiovascular condition afflicting premature neonates especially those born extremely low birth weight (ELBW). Despite five decades of scientific inquiry which has produced thousands of publications including over 65 randomized controlled trials, cardiologists, neonatologists, and surgeons still cannot answer simple questions such as if, when and how to close to the PDA in ELBW infants. This chapter will examine current evidence in order to answer these fundamental questions. The chapter will specifically focus on transcatheter PDA closure (TCPC), which albeit a new therapy, has displayed great potential to be the best therapeutic option in the future. It is about time that physicians from all sub-specialties come together and integrate the evidence to develop a management algorithm for ELBW infants with hemodynamically significant PDA.Update on Critical Issues on Infant and Neonatal Care 2 3. Normal closure of the ductus When a baby takes its first breath, the increased alveolar oxygen content leads to pulmonary vasodilation, resulting in a decreased ratio of pulmonary vascular resistance (R P ) to systemic vascular resistance (R S ). This drop in R P /R S can reverse the flow of blood across the ductus arteriosus from right-to-left to left-to-right (aorta to PA). At this point, the ductus is exposed to high systemic arterial pO 2 , which results in vasoconstriction of the ductus arteriosus through mechanisms not fully elucidated [3][4][5]. A sharp decline in circulating PGE and PGIE along with a rapid increase in pO 2 following birth contributes to constriction, and ultimately functional closure of the ductus. Nearly all healthy, term infants achieve functional closure with 24-72 h [2][3][4][5]. Eventually, hypoxia and fibrosis cause the inner layers of the ductus to permanently close, leaving only a fibrous remnant called the ligamentum arteriosum.

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Association of Preterm Birth With Long-term Risk of Heart Failure Into Adulthood

et al. 2021

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IMPORTANCE Preterm birth has been associated with increased risk of heart failure (HF) early in life, but its association with new-onset HF in adulthood appears to be unknown. OBJECTIVE To determine whether preterm birth is associated with increased risk of HF from childhood into mid-adulthood in a large population-based cohort. DESIGN, SETTING, AND PARTICIPANTS This national cohort study was conducted in Sweden with data from 1973 through 2015. All singleton live births in Sweden during 1973 through 2014 were included. EXPOSURES Gestational age at birth, identified from nationwide birth records. MAIN OUTCOMES AND MEASURES Heart failure, as identified from inpatient and outpatient diagnoses through 2015. Cox regression was used to determine hazard ratios (HRs) for HF associated with gestational age at birth while adjusting for other perinatal and maternal factors. Cosibling analyses assessed for potential confounding by unmeasured shared familial (genetic and/or environmental) factors. RESULTS A total of 4 193 069 individuals were included (maximum age, 43 years; median age, 22.5 years). In 85.0 million person-years of follow-up, 4158 persons (0.1%) were identified as having HF (median [interquartile range] age, 15.4 [28.0] years at diagnosis). Preterm birth (gestational age <37 weeks) was associated with increased risk of HF at ages younger than 1 year (adjusted HR [aHR], 4.49 [95% CI, 3.86-5.22]), 1 to 17 years (aHR, 3.42 [95% CI, 2.75-4.27]), and 18 to 43 years (aHR, 1.42 [95% CI, 1.19-1.71]) compared with full-term birth (gestational age, 39-41 weeks). At ages 18 through 43 years, the HRs further stratified by gestational age were 4.72 (95% CI,) for extremely preterm births (22-27 weeks), 1.93 (95% CI, 1.37-2.71) for moderately preterm births (28-33 weeks), 1.24 (95% CI, 1.00-1.54) for late preterm births (34-36 weeks), and 1.09 (95% CI, 0.97-1.24) for early term births (37-38 weeks). The corresponding HF incidence rates (per 100 000 person-years) at ages 18 through 43 years were 31.7, 13.8, 8.7, and 7.3, respectively, compared with 6.6 for full-term births. These associations persisted when excluding persons with structural congenital cardiac anomalies. The associations at ages 18 through 43 years (but not <18 years) appeared to be largely explained by shared determinants of preterm birth and HF within families. Preterm birth accounted for a similar number of HF cases among male and female individuals. CONCLUSIONS AND RELEVANCEIn this large national cohort, preterm birth was associated with increased risk of new-onset HF into adulthood. Survivors of preterm birth may need long-term clinical follow-up into adulthood for risk reduction and monitoring for HF.

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Effect of patent ductus arteriosus on the heart in preterm infants

Cited by 18 publications

References 15 publications

Pulmonary Hypertension with Prolonged Patency of the Ductus Arteriosus in Preterm Infants

Pulmonary Hypertension with Prolonged Patency of the Ductus Arteriosus in Preterm Infants

PDA Closure in ELBW Infants: If, When, and How to Do It

Association of Preterm Birth With Long-term Risk of Heart Failure Into Adulthood

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