Congenital heart disease (CHD) is the most common congenital abnormality worldwide, affecting 8 to 12 infants per 1000 births globally and causing >40% of prenatal deaths. However, its causes remain mainly unknown, with only up to 15% of CHD cases having a determined genetic cause. Exploring the complex relationship between genetics and environmental exposures is key in understanding the multifactorial nature of the development of CHD. Multiple population-level association studies have been conducted on maternal environmental exposures and their association with CHD, including evaluating the effect of maternal disease, medication exposure, environmental pollution, and tobacco and alcohol use on the incidence of CHD. However, these studies have been done in a siloed manner, with few examining the interplay between multiple environmental exposures. Here, we broadly and qualitatively review the current literature on maternal and paternal prenatal exposures and their association with CHD. We propose using the framework of the emerging field of the exposome, the environmental complement to the genome, to review all internal and external prenatal environmental exposures and identify potentiating or alleviating synergy between exposures. Finally, we propose mechanistic pathways through which susceptibility to development of CHD may be induced via the totality of prenatal environmental exposures, including the interplay between placental and cardiac development and the internal vasculature and placental morphology in early stages of pregnancy.

Purpose: Poorer short-term outcomes have been described for females after cardiovascular surgery. We examined the influence of sex on the outcomes after aortic root replacement (ARR). Methods: Medical records of 848 patients (females, n = 159/848, 19%) who underwent ARR at our center from 2005 to 2018 were retrospectively reviewed. Sex differences of the following outcomes were analyzed: the primary end point (inhospital mortality or stro111ke), secondary end point (new requirement for permanent pacemaker), and long-term survival (median follow-up 21.4 months [interquartile range,1.3-60.0]).Results: Females were significantly older (61.3 vs 58.7 [male]) with higher rates of pre-existing cerebrovascular disease (14% [22/159] vs 7% [52/689]) and previous valve intervention (20% [32/159] vs 13% [89/689]) but less myocardial infarction [1%(1/159) vs 7%(48/689)]. The surgical indication was different (aneurysm 75% [120/159] vs 87% [602/689], dissection 13% [21/159] vs 6% [41/689]; P < .01]). Females had larger average aneurysm size after controlling for body size (P ≤ .001). There was no sex difference in in-hospital mortality (3% [5/159] vs 2% [16/689]) or stroke (4% [7/159] vs 4% [29/689]). Multivariable logistic regression indicated that female sex was not an independent predictor of combined in-hospital stroke or death (odds ratio [OR], 0.59; 95% confidence interval [CI], 0.28-1.25), confirmed by propensity score analysis. There was no difference in long-term survival (5-year survival, 90.96% vs 93.03%; P = .44). Females had higher incidence of permanent pacemaker requirement [11% (18/159) vs 6% (39/689), P = .03] and female sex was an independent predictor of permanent pacemaker requirement (OR, 2.01; 95% CI, 1.085-3.724; P = .03).

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