scholarly journals Association between advanced paternal age and congenital heart defects: a systematic review and meta-analysis

2020 ◽  
Vol 35 (9) ◽  
pp. 2113-2113
Author(s):  
F Joinau-Zoulovits ◽  
N Bertille ◽  
J F Cohen ◽  
B Khoshnood

Abstract STUDY QUESTION Is there an association between advanced paternal age and congenital heart defects (CHD)? SUMMARY ANSWER Advanced paternal age is associated with a 16% increase in the overall odds of CHD. WHAT IS KNOWN ALREADY CHD are the most common congenital malformations. Several risk factors for CHD have been identified in the literature, but the association between advanced paternal age and CHD remains unclear. STUDY DESIGN, SIZE, DURATION We conducted a systematic literature search on MEDLINE and EMBASE (1960–2019) to identify studies assessing the association between advanced paternal age (≥35 years) and the risk of CHD, unrestrictive of language or sample size. We used a combination of Medical Subject Headings (MeSH) terms and free text words such as ‘paternal age’, ‘paternal factors’, ‘father’s age’, ‘parental age’, ‘heart’, ‘cardiac’, ‘cardiovascular’, ‘abnormalities, congenital’, ‘birth defects’, ‘congenital malformations’ and ‘congenital abnormalities’. PARTICIPANTS/MATERIALS, SETTING, METHODS We included observational studies aiming at assessing the association between paternal age and CHD. The included population could be live births, fetal deaths and terminations of pregnancy for fetal anomaly. To be included, studies had to provide either odds ratios (OR) with their 95% confidence interval (CI) or sufficient information to recalculate ORs with 95% CIs per paternal age category. We excluded studies if they had no comparative group and if they were reviews or case reports. Two independent reviewers selected the studies, extracted the data and assessed risk of bias using a modified Newcastle–Ottawa Scale. We used random-effects meta-analysis to produce summary estimates of crude OR. Associations were also tested in subgroups. MAIN RESULTS AND THE ROLE OF CHANCE Of 191 studies identified, we included nine studies in the meta-analysis (9 917 011 participants, including 34 447 CHD), including four population-based studies. Five studies were judged at low risk of bias. Only one population-based study specifically investigated isolated CHD. The risk of CHD was higher with advanced paternal age (summary OR 1.16, 95% CI, 1.07–1.25). Effect sizes were stable in population-based studies and in those with low risk of bias. LIMITATIONS AND REASONS FOR CAUTION The available evidence did not allow to assess (i) the risk of isolated CHD in population-based studies, (ii) the association between paternal age and the risk for specific CHD and (iii) the association between paternal age and CHD after adjustment for other risk factors, such as maternal age. WIDER IMPLICATIONS OF THE FINDINGS Our findings suggest that advanced paternal age may be a risk factor for CHD. However, because the association is modest in magnitude, its usefulness as a criterion for targeted screening for CHD seems limited. STUDY FUNDING/COMPETING INTEREST(S) None. PROSPERO REGISTRATION NUMBER CRD42019135061.

2017 ◽  
Vol 41 (1) ◽  
pp. 40-52
Author(s):  
Mohammad Abdullah Al Mamun ◽  
Manzoor Hussain ◽  
Mohammad Nurul Akhtar Hasan ◽  
Rezoana Rima

Prognosis of children with congenital heart defects (CHDs) continues to improve with advancement in technology and training in pediatric cardiology and cardiac surgery; however, lack of information about risk factors for malformations in cardiovascular development impeded the prevention of CHDs. Etiology of CHDs are complex and possibly lies within the interaction of environmental exposures and inherited factors. Studies found multiple maternal environmental exposures, including living in newly renovated rooms, residential proximity to main traffic, smoking and maternal occupation as manual worker significantly associated with CHDs. Advanced maternal age, low socioeconomic status, maternal perinatal diseases including maternal fever, diabetes, influenza, maternal certain medication use and alcohol intake were also significantly associated with CHDs. Isolated CHDs and multiple defects have different profiles of risk factors, while subtype of CHDs share common risk factors. Because of differences in methods, these studies are only suggestive. Relatively less information has been reported on noninherited factors that may have an adverse effect on the cardiovascular development, which has made it difficult to create population-based strategies to reduce the burden of illness from CHDs and for couples to choose lifestyles to reduce the risk of delivering a child with CHDs.Bangladesh J Child Health 2017; VOL 41 (1) :40-52


2021 ◽  
Vol 11 (6) ◽  
pp. 562
Author(s):  
Olga María Diz ◽  
Rocio Toro ◽  
Sergi Cesar ◽  
Olga Gomez ◽  
Georgia Sarquella-Brugada ◽  
...  

Congenital heart disease is a group of pathologies characterized by structural malformations of the heart or great vessels. These alterations occur during the embryonic period and are the most frequently observed severe congenital malformations, the main cause of neonatal mortality due to malformation, and the second most frequent congenital malformations overall after malformations of the central nervous system. The severity of different types of congenital heart disease varies depending on the combination of associated anatomical defects. The causes of these malformations are usually considered multifactorial, but genetic variants play a key role. Currently, use of high-throughput genetic technologies allows identification of pathogenic aneuploidies, deletions/duplications of large segments, as well as rare single nucleotide variants. The high incidence of congenital heart disease as well as the associated complications makes it necessary to establish a diagnosis as early as possible to adopt the most appropriate measures in a personalized approach. In this review, we provide an exhaustive update of the genetic bases of the most frequent congenital heart diseases as well as other syndromes associated with congenital heart defects, and how genetic data can be translated to clinical practice in a personalized approach.


Author(s):  
Ali Ghanchi ◽  
Neil Derridj ◽  
Damien Bonnet ◽  
Nathalie Bertille ◽  
Laurent J. Salomon ◽  
...  

Newborns with congenital heart defects tend to have a higher risk of growth restriction, which can be an independent risk factor for adverse outcomes. To date, a systematic review of the relation between congenital heart defects (CHD) and growth restriction at birth, most commonly estimated by its imperfect proxy small for gestational age (SGA), has not been conducted. Objective: To conduct a systematic review and meta-analysis to estimate the proportion of children born with CHD that are small for gestational age (SGA). Methods: The search was carried out from inception until 31 March 2019 on Pubmed and Embase databases. Studies were screened and selected by two independent reviewers who used a predetermined data extraction form to obtain data from studies. Bias was assessed using the Critical Appraisal Skills Programme (CASP) checklist. The database search identified 1783 potentially relevant publications, of which 38 studies were found to be relevant to the study question. A total of 18 studies contained sufficient data for a meta-analysis, which was done using a random effects model. Results: The pooled proportion of SGA in all CHD was 20% (95% CI 16%–24%) and 14% (95% CI 13%–16%) for isolated CHD. Proportion of SGA varied across different CHD ranging from 30% (95% CI 24%–37%) for Tetralogy of Fallot to 12% (95% CI 7%–18%) for isolated atrial septal defect. The majority of studies included in the meta-analysis were population-based studies published after 2010. Conclusion: The overall proportion of SGA in all CHD was 2-fold higher whereas for isolated CHD, 1.4-fold higher than the expected proportion in the general population. Although few studies have looked at SGA for different subtypes of CHD, the observed variability of SGA by subtypes suggests that growth restriction at birth in CHD may be due to different pathophysiological mechanisms.


2018 ◽  
Vol 32 (21) ◽  
pp. 3606-3611 ◽  
Author(s):  
Jan Pavlicek ◽  
Eva Klaskova ◽  
Martin Prochazka ◽  
Erika Dolezalkova ◽  
David Matura ◽  
...  

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