Background Despite remarkable success in the surgical and medical management of congenital heart disease ( CHD ), some survivors still experience cardiovascular complications over the long term. The goal of this study was to evaluate the association between CHD and risk of cardiovascular disease ( CVD ) by conducting a meta‐analysis of cohort studies. Methods and Results A systematic literature search of several databases was conducted through April 2018 to identify studies reporting the risk of CVD , stroke, heart failure, and coronary artery heart disease in CHD survivors. The quality of individual studies was assessed using the Newcastle‐Ottawa scale. The overall risk estimates were pooled using fixed‐effects meta‐analysis. Subgroup analyses were performed to explore possible sources of heterogeneity. Nine cohort studies comprising 684 200 participants were included. The overall combined relative risks for people with CHD compared with the controls were 3.12 (95% CI, 3.01–3.24) for CVD , 2.46 (95% CI, 2.30–2.63) for stroke, 5.89 (95% CI, 5.58–6.21) for heart failure, and 1.50 (95% CI, 1.40–1.61) for coronary artery heart disease. Significant heterogeneity was detected across studies regarding these risk estimates. Heterogeneity in the risk estimate of CVD was explained by geographic region, type of study design, sample source, age composition, and controlled confounders. Conclusions This meta‐analysis of cohort studies of CHD found an association of increased risk of CVD in later life, although we cannot determine whether this association is confounded by a risk factor profile of CVD among CHD survivors or whether CHD is an independent risk factor.

Objective The aim of this study was to provide updated evidence to assess the association between parental alcohol consumption and the risk of total congenital heart diseases (CHDs) and specific CHD phenotypes in offspring, and explore the possible dose–response pattern. Methods PubMed, Embase and Chinese databases were searched with an end-date parameter of July 24, 2019 to identify studies meeting pre-stated inclusion criteria. A random-effects model was used to calculate the overall combined risk estimates. A meta-analysis of the dose–response relationship was performed. Subgroup analysis, sensitivity analysis, and Galbraith plot were conducted to explore potential heterogeneity moderators. Results A total of 55 studies involving 41,747 CHD cases and 297,587 controls were identified. Overall, both maternal (odds ratio (OR) = 1.16; 95% confidence interval (CI): 1.05–1.27) and paternal (OR = 1.44; 95% CI: 1.19–1.74) alcohol exposures were significantly associated with risk of total CHDs in offspring. Additionally, a nonlinear dose–response relationship between parental alcohol exposure and risk of total CHDs was observed. With an increase in parental alcohol consumption, the risk of total CHDs in offspring also gradually increases. For specific CHD phenotypes, a statistically significant association was found between maternal alcohol consumption and risk of tetralogy of fallot (OR = 1.20; 95% CI: 1.08–1.33). Relevant heterogeneity moderators have been identified by subgroup analysis, and sensitivity analysis yielded consistent results. Conclusions Although the role of potential bias and evidence of heterogeneity should be carefully evaluated, our review indicates that parental alcohol exposures are significantly associated with the risk of CHDs in offspring, which highlights the necessity of improving health awareness to prevent alcohol exposure during preconception and conception periods.

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Background At present, the association between maternal viral infection and risk of congenital heart diseases ( CHD ) in offspring is uncertain; additionally, a complete overview is missing. A meta‐analysis of observational studies was performed to address the question of whether women who had a history of viral infection in early pregnancy were at an increased risk of CHD in offspring, compared with mothers without viral infection. Methods and Results Unrestricted searches were conducted, with an end date parameter of July 15, 2018, of PubMed, Embase, Google Scholar, Cochrane Libraries, and Chinese databases, to identify studies that met prestated inclusion criteria. Seventeen case‐control studies involving 67 233 women were included for analysis. Both fixed‐effects models (odds ratio [OR], 1.83; 95% CI , 1.58–2.12; P <0.0001) and random‐effects models ( OR , 2.28; 95% CI , 1.54–3.36; P <0.0001) suggested that mothers who had a history of viral infection in early pregnancy experienced a significantly increased risk of developing CHD in offspring. For specific viral infections, the risk of developing CHD in offspring was significantly increased among mothers with rubella virus (OR, 3.49, 95% CI, 2.39–5.11 in fixed‐effects models; and OR, 3.54; 95% CI, 1.75–7.15 in random‐effects models) and cytomegalovirus (OR, 3.95; 95% CI, 1.87–8.36 in fixed‐effects models) in early pregnancy; however, other maternal viral infections in early pregnancy were not significantly associated with risk of CHD in offspring. Sensitivity analysis yielded consistent results. No evidence of publication bias was observed. Conclusions Although the role of potential bias and evidence of heterogeneity should be carefully evaluated, the present study suggests that maternal viral infection is significantly associated with risk of CHD in offspring.

Objective Although previous reviews confirmed maternal active smoking was significantly associated with risk of fetal congenital heart defects (CHDs), association between maternal passive smoking and paternal smoking and risk of CHDs is inconclusive nowadays; furthermore, a complete overview is lacking. A meta-analysis of observational studies was conducted to assess the risk of CHDs associated with maternal active and passive smoking and paternal smoking. Methods Seven electronic databases were searched for qualified research up to June 2018. We summarized study characteristics and the summary risk estimates were calculated using either the random-effect model or fixed-effect model. Sensitivity and subgroup analysis were carried out to identify the potential heterogeneity moderators. Results One hundred and twenty-five studies involving 137,574 CHDs cases in 8,770,837 study participants were included. Overall, maternal active (risk ratio (RR) = 1.25; 95% confidence interval (CI): 1.16–1.34; p < 0.01) and passive (RR = 2.24, 95% CI: 1.81–2.77; p < 0.01) smoking as well as paternal active smoking (RR = 1.74, 95% CI: 1.48–2.06; p < 0.01) were significantly associated with CHDs risk. For specific CHD subtypes, our study showed that maternal active smoking was significantly associated with risk of atrial septal defect (RR = 1.27, 95% CI: 1.02–1.59; p = 0.03) and right ventricular outflow tract obstruction (RR = 1.43, 95% CI: 1.04–1.97; p = 0.03). Relevant heterogeneity moderators have been identified by subgroup analysis. Sensitivity analysis yielded consistent results. Conclusion Maternal active smoking, maternal passive smoking as well as paternal smoking all increased the risk of CHDs in offspring. Preventing parental smoking during peri-pregnancy is a priority for CHDs prevention.