Heart failure is a worldwide health problem with important consequences for the overall wellbeing of affected individuals as well as for the healthcare system. Over recent decades, numerous pieces of evidence have demonstrated that the associated gut microbiota represent an important component of human physiology and metabolic homeostasis, and can affect one’s state of health or disease directly, or through their derived metabolites. The recent advances in human microbiome studies shed light on the relationship between the gut microbiota and the cardiovascular system, revealing its contribution to the development of heart failure-associated dysbiosis. HF has been linked to gut dysbiosis, low bacterial diversity, intestinal overgrowth of potentially pathogenic bacteria and a decrease in short chain fatty acids-producing bacteria. An increased intestinal permeability allowing microbial translocation and the passage of bacterial-derived metabolites into the bloodstream is associated with HF progression. A more insightful understanding of the interactions between the human gut microbiome, HF and the associated risk factors is mandatory for optimizing therapeutic strategies based on microbiota modulation and offering individualized treatment. The purpose of this review is to summarize the available data regarding the influence of gut bacterial communities and their derived metabolites on HF, in order to obtain a better understanding of this multi-layered complex relationship.

The gastrointestinal (GI) tract is one of the most studied compartments of the human body as it hosts the largest microbial community including trillions of germs. The relationship between the human and its associated flora is complex, as the microbiome plays an important role in nutrition, metabolism and immune function. With a dynamic composition, influenced by many intrinsic and extrinsic factors, there is an equilibrium maintained in the composition of GI microbiota, translated as “eubiosis”. Any disruption of the microbiota leads to the development of different local and systemic diseases. This article reviews the human GI microbiome’s composition and function in healthy individuals as well as its involvement in the pathogenesis of different digestive disorders. It also highlights the possibility to consider flora manipulation a therapeutic option when treating GI diseases.

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Overweight and obesity in childhood are associated with early cardiovascular dysfunction and promote heightened risk of cardiovascular morbidity and mortality in adulthood. Waist circumference (WC) correlates with visceral obesity, which is why obese children with elevated WC need to be carefully monitored to prevent long-term cardio-metabolic complications. The purpose of our study was to establish if WC could be a predictor of cardiovascular complications in children. The authors conducted a retrospective study that included 160 overweight and obese children and adolescents, aged 6 to 18 years. Patients were evaluated completely anthropometrically, biologically, and imagistic. The anthropometric data tracked were height, weight, WC, and body mass index. Echocardiography evaluated the following parameters: the interventricular septum, left ventricular mass, the relative thickness of the ventricular wall, the pathological epicardial fat. Our results confirm that the presence of visceral obesity was significantly associated (χ 2 = 11.72, P = .0006) with pathological epicardial fat. In children, visceral obesity is not a risk factor for vascular or cardiac impairment, but in adolescents, the results showed that visceral obesity is an important predictive factor for the occurrence of vascular (AUC = 0.669, P = .021) and cardiac (AUC = 0.697, P = .037) impairment. Concentric left ventricular (LV) hypertrophy is significantly influenced by the presence of visceral obesity (AUC = 0.664, P = .013 children; AUC = 0.716, P = .026 adolescents). WC above the 90th percentile is a predictive factor for increased LVM index and concentric hypertrophy in both children and adolescents.

The corpus callosum is the largest white matter structure connecting the two cerebral hemispheres. Agenesis of the corpus callosum (ACC), complete or partial, is one of the most common cerebral malformations in humans with a reported incidence ranging between 1.8 per 10,000 livebirths to 230–600 per 10,000 in children and its presence is associated with neurodevelopmental disability. ACC may occur as an isolated anomaly or as a component of a complex disorder, caused by genetic changes, teratogenic exposures or vascular factors. Genetic causes are complex and include complete or partial chromosomal anomalies, autosomal dominant, autosomal recessive or X-linked monogenic disorders, which can be either de novo or inherited. The extreme genetic heterogeneity, illustrated by the large number of syndromes associated with ACC, highlight the underlying complexity of corpus callosum development. ACC is associated with a wide spectrum of clinical manifestations ranging from asymptomatic to neonatal death. The most common features are epilepsy, motor impairment and intellectual disability. The understanding of the genetic heterogeneity of ACC may be essential for the diagnosis, developing early intervention strategies, and informed family planning. This review summarizes our current understanding of the genetic heterogeneity in ACC and discusses latest discoveries.