Defining the Risk and Associated Morbidity and Mortality of Severe Respiratory Syncytial Virus Infection Among Infants with Congenital Heart Disease

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Abstract

Introduction

The REGAL (RSV Evidence—a Geographical Archive of the Literature) series provide a comprehensive review of the published evidence in the field of respiratory syncytial virus (RSV) in Western countries over the last 20 years. This fourth publication covers the risk and burden of RSV infection in infants with congenital heart disease (CHD).

Methods

A systematic review was undertaken for articles published between January 1, 1995 and December 31, 2015 across PubMed, Embase, The Cochrane Library, and Clinicaltrials.gov. Studies reporting data for hospital visits/admissions for RSV infection among children with CHD as well as studies reporting RSV-associated morbidity, mortality, and healthcare costs were included. The focus was on children not receiving RSV prophylaxis. Study quality and strength of evidence (SOE) were graded using recognized criteria.

Results

A total of 1325 studies were identified of which 38 were included. CHD, in particular hemodynamically significant CHD, is an independent predictor for RSV hospitalization (RSVH) (high SOE). RSVH rates were generally high in young children (<4 years) with CHD (various classifications), varying between 14 and 357/1000 (high SOE). Children (<6 years) with RSV infection spent 4.4–14 days in hospital, with up to 53% requiring intensive care (high SOE). Infants (<2 years) with CHD had a more severe course of RSVH than those without CHD (high SOE). Case fatality rates of up to 3% were associated with RSV infection in children with CHD (high SOE). RSV infection in the perioperative period of corrective surgery and nosocomial RSV infection in intensive care units also represent important causes of morbidity (moderate SOE).

Conclusion

CHD poses a significant risk for RSVH and subsequent morbidity and mortality. RSV infection often complicates corrective heart surgery. To reduce the burden and improve outcomes, further research and specific studies are needed to determine the longer-term effects of severe RSV infection in young children with CHD.

Electronic supplementary material

The online version of this article (doi:10.1007/s40121-016-0142-x) contains supplementary material, which is available to authorized users.

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Most cited references 45

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Palivizumab prophylaxis reduces hospitalization due to respiratory syncytial virus in young children with hemodynamically significant congenital heart disease

Timothy F Feltes, Allison Cabalka, H.Cody Meissner … (2003)

To evaluate the safety, tolerance, and efficacy of palivizumab in children with hemodynamically significant congenital heart disease (CHD). A randomized, double-blind, placebo-controlled trial included 1287 children with CHD randomly assigned 1:1 to receive 5 monthly intramuscular injections of 15 mg/kg palivizumab or placebo. Children were followed for 150 days. The primary efficacy end point was antigen-confirmed respiratory syncytial virus (RSV) hospitalization. Palivizumab recipients had a 45% relative reduction in RSV hospitalizations (P=.003), a 56% reduction in total days of RSV hospitalization per 100 children (P=.003), and a 73% reduction in total RSV hospital days with increased supplemental oxygen per 100 children (P=.014). Adverse events were similar in the treatment groups; no child had drug discontinued for a related adverse event. Serious adverse events occurred in 55.4% of palivizumab recipients and 63.1% of placebo recipients (P<.005); none were related to palivizumab. Twenty-one children (3.3%) in the palivizumab group and 27 (4.2%) in the placebo group died; no deaths were attributed to palivizumab. The rates of cardiac surgeries performed earlier than planned were similar in the treatment groups. Monthly palivizumab (15 mg/kg IM) was safe, well-tolerated, and effective for prophylaxis of serious RSV disease in young children with hemodynamically significant CHD.

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Rates of hospitalization for respiratory syncytial virus infection among children in medicaid.

T Boyce, B Mellen, E F Mitchel … (2000)

To determine rates of hospitalization associated with respiratory syncytial virus (RSV) infection among children with and without specific medical conditions. Retrospective cohort study of all children <3 years old enrolled in the Tennessee Medicaid program from July 1989 through June 1993 (248,652 child-years). During the first year of life, the estimated number of RSV hospitalizations per 1000 children was 388 for those with bronchopulmonary dysplasia, 92 for those with congenital heart disease, 70 for children born at < or = 28 weeks' gestation, 66 for those born at 29 to <33 weeks, 57 for those born at 33 to <36 weeks, and 30 for children born at term with no underlying medical condition. In the second year of life, children with bronchopulmonary dysplasia had an estimated 73 RSV hospitalizations per 1000 children, whereas those with congenital heart disease had 18 and those with prematurity 16 per 1000. Overall, 53% of RSV hospitalizations occurred in healthy children born at term. Children with bronchopulmonary dysplasia have high rates of RSV hospitalization until 24 months of age. In contrast, after the first year of life, children with congenital heart disease or prematurity have rates no higher than that of children at low risk who are <12 months old.

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Genetics of congenital heart disease: the glass half empty.

Akl Fahed, Bruce Gelb, J G Seidman … (2013)

Congenital heart disease (CHD) is the most common congenital anomaly in newborn babies. Cardiac malformations have been produced in multiple experimental animal models, by perturbing selected molecules that function in the developmental pathways involved in myocyte specification, differentiation, or cardiac morphogenesis. In contrast, the precise genetic, epigenetic, or environmental basis for these perturbations in humans remains poorly understood. Over the past few decades, researchers have tried to bridge this knowledge gap through conventional genome-wide analyses of rare Mendelian CHD families, and by sequencing candidate genes in CHD cohorts. Although yielding few, usually highly penetrant, disease gene mutations, these discoveries provided 3 notable insights. First, human CHD mutations impact a heterogeneous set of molecules that orchestrate cardiac development. Second, CHD mutations often alter gene/protein dosage. Third, identical pathogenic CHD mutations cause a variety of distinct malformations, implying that higher order interactions account for particular CHD phenotypes. The advent of contemporary genomic technologies including single nucleotide polymorphism arrays, next-generation sequencing, and copy number variant platforms are accelerating the discovery of genetic causes of CHD. Importantly, these approaches enable study of sporadic cases, the most common presentation of CHD. Emerging results from ongoing genomic efforts have validated earlier observations learned from the monogenic CHD families. In this review, we explore how continued use of these technologies and integration of systems biology is expected to expand our understanding of the genetic architecture of CHD.

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Author and article information

Contributors

Xavier Carbonell-Estrany: carbonell@comb.cat

Journal

Journal ID (nlm-ta): Infect Dis Ther

Journal ID (iso-abbrev): Infect Dis Ther

Title: Infectious Diseases and Therapy

Publisher: Springer Healthcare (Cheshire )

ISSN (Print): 2193-8229

ISSN (Electronic): 2193-6382

Publication date (Electronic): 9 January 2017

Publication date PMC-release: 9 January 2017

Publication date (Print): March 2017

Volume: 6

Issue: 1

Pages: 37-56

Affiliations

[1 ]ISNI 0000 0001 2200 2638, GRID grid.416975.8, Baylor College of Medicine, , Texas Children’s Hospital Houston, ; Houston, TX USA

[2 ]ISNI 0000 0004 1936 8227, GRID grid.25073.33, Neonatal Division, Department of Paediatrics, , McMaster University, ; Hamilton, Canada

[3 ]ISNI 0000000090126352, GRID grid.7692.a, , University Medical Center Utrecht, ; Utrecht, The Netherlands

[4 ]ISNI 0000 0004 1789 4557, GRID grid.415236.7, , Sant’Anna Hospital, ; Turin, Italy

[5 ]ISNI 0000 0001 0703 675X, GRID grid.430503.1, , University of Colorado School of Medicine, ; Aurora, CO USA

[6 ]ISNI 0000 0004 0593 9113, GRID grid.412134.1, , Necker University Hospital and Paris 5 University, ; Paris, France

[7 ]ISNI 0000 0004 1937 0247, GRID grid.5841.8, Hospital Clínic, Catedràtic de Pediatria, , Universitat de Barcelona, ; Barcelona, Spain

[8 ]ISNI 0000 0000 9635 9413, GRID grid.410458.c, , Hospital Clinic, Institut d’Investigacions Biomediques August Pi Suñer (IDIBAPS), ; Barcelona, Spain

Article

Publisher ID: 142

DOI: 10.1007/s40121-016-0142-x

PMC ID: 5336417

PubMed ID: 28070870

SO-VID: f6f23283-1ab4-40e6-965f-2f5b2a8eeee8

History

Date received : 7 November 2016

Funding

Funded by: FundRef http://dx.doi.org/10.13039/100006483, AbbVie;

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Keywords: burden,congenital heart disease,hemodynamically significant,high risk,hospitalization,morbidity,mortality,non-hemodynamically significant,respiratory syncytial virus

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Keywords: burden, congenital heart disease, hemodynamically significant, high risk, hospitalization, morbidity, mortality, non-hemodynamically significant, respiratory syncytial virus

Defining the Risk and Associated Morbidity and Mortality of Severe Respiratory Syncytial Virus Infection Among Infants with Congenital Heart Disease

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Abstract

Introduction

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Results

Conclusion

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Decoding Infection and Transmission

Most cited references 45

Palivizumab prophylaxis reduces hospitalization due to respiratory syncytial virus in young children with hemodynamically significant congenital heart disease

Rates of hospitalization for respiratory syncytial virus infection among children in medicaid.

Genetics of congenital heart disease: the glass half empty.

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