This review, which is intended for both radiologists and clinical cardiologists, highlights the use of cardiac MRI in pediatric and adult patients after completion of the Fontan procedure and provi... Cardiac MRI has become a widely accepted standard for anatomic and functional assessment of complex Fontan physiology, because it is noninvasive and suitable for comprehensive follow-up evaluation ...

Congenital heart diseases (CHDs) are among the most common congenital malformations. Despite significant advancements in understanding the embryonic development of the heart, the etiology of CHDs remains largely unknown. The complexity of the processes involved in heart formation limits our ability to identify all molecular mechanisms underlying CHDs. Recently, microRNAs (miRNAs) have provided new insights into the molecular mechanisms of CHDs. This narrative review evaluates the evidence linking expression to CHDs and discusses the potential of RNA expression regulation as a promising avenue for therapeutic biomarker development. A search of the literature, focusing on the role of miRNAs in CHDs, was carried out to identify pertinent studies published over the last decade. The literature search was performed utilizing the PubMed and Scopus databases. The selection criteria included peer-reviewed original studies, clinical research, meta-analyses, and review articles written in English. Multiple investigations have highlighted the essential role of miRNAs in cardiac development and function, showing that their distinct expression patterns can broadly and specifically influence cellular signaling pathways involved in heart abnormalities. The regulation of mRNA expression emerges as a key factor in the pathogenesis of CHD, paving the way for the identification of novel molecular biomarkers. Alterations in transcriptional profiles could offer innovative and highly specific tools for risk stratification and the clinical monitoring of patients. In conclusion, although further studies are needed to validate the efficacy and clinical applicability of these biomarkers, the mRNA-based approach stands out as a promising perspective for precision medicine in the CHD context.

Background/Objectives: Fetal growth restriction (FGR), historically termed intrauterine growth restriction (IUGR), is a multifactorial condition in which the fetus fails to reach its genetically determined growth potential, most often due to placental insufficiency. Beyond its link with increased perinatal morbidity and mortality, FGR has been associated with long-term cardiovascular risk through early-life programming. The developing fetal heart is vulnerable to chronic hypoxia and nutrient deprivation, potentially inducing structural and functional alterations with lifelong consequences. This narrative review summarizes and critically appraises experimental and clinical evidence on the impact of FGR on myocardial development and cardiovascular health from fetal life to adulthood. Methods: We conducted a narrative review using a structured literature search of studies published in the last 15 years in PubMed and Scopus, focusing on experimental, imaging, and epidemiological research evaluating cardiac structure, function, and long-term cardiovascular outcomes in FGR. Evidence from fetal and neonatal echocardiography, including Doppler and speckle-tracking techniques, as well as molecular and histological studies, was examined. No statistical meta-analysis was performed. Results: FGR has been associated with reduced cardiomyocyte number, altered myocardial architecture, increased interstitial fibrosis, and persistent ventricular remodeling. Functional studies suggest early impairments in systolic and diastolic performance, with alterations in cardiac energy metabolism and epigenetic regulation. Advanced imaging may enable detection of subclinical cardiac dysfunction in utero and early postnatally. Epidemiological data suggest an increased risk of hypertension, ischemic heart disease, heart failure, and metabolic disorders in adulthood among individuals born growth-restricted. Conclusions: FGR represents an early cardiovascular risk condition. Improved understanding of fetal cardiac programming may help refine risk stratification, surveillance, and preventive strategies to reduce long-term cardiovascular morbidity in individuals born growth-restricted.

The endocrine system plays a pivotal role in all stages of cardiac development and in maintaining the structural and functional integrity of the heart. Notably, the heart itself functions as an endocrine organ, producing hormones that regulate blood pressure, fluid balance, and myocardial remodeling. This narrative review explores the endocrine mechanisms underlying cardiac development and function, with a focus on fetal and pediatric life. Special attention is given to the heart’s intrinsic endocrine activity and how hormonal signals interact with the cardiovascular system during early development. Hormonal signaling is essential for maintaining physiological homeostasis and supporting proper heart development during growth. Disruptions in these signals may serve as silent precursors to structural or functional heart disease, potentially manifesting later in life. Understanding these interactions is clinically relevant, as endocrine imbalances can contribute to the onset, progression, and prognosis of pediatric cardiac disorders. Early identification of hormonal dysregulation can help prevent or mitigate adverse cardiovascular outcomes. Furthermore, recognizing age-specific patterns in hormone–heart interactions may enable the development of targeted diagnostic and therapeutic strategies.

Funding Acknowledgements: Type of funding sources: None. Background: Changes in the right ventricular outflow tract (RVOT) and pulmonary arteries (PAs) are often seen in paediatric patients with congenital heart disease (CHD), pulmonary hypertension or genetic disorders (e.g. Marfan syndrome, Loeys-Dietz syndrome, Williams syndrome, DiGeorge syndrome). Cardiovascular magnetic resonance (CMR) imaging is an excellent method to visualize the RVOT and PAs without the use of ionizing radiation and contrast media but for the interpretation of CMR data in the paediatric population the knowledge of normal values is crucial. However, normal values for pulmonary arteries from contrast-free cine CMR images are lacking. Purpose: The aim of this retrospective multicentre study was to establish reference ranges for the diameters of the mean PA (MPA), right PA (RPA) and left PA (LPA). Methods: 163 CMR scans of healthy children and adolescents (mean age 13.8 ± 2.9 years; range 5-18 years) from two centres in the UK and Germany were included. The diameter of the MPA was measured in sagittal-oblique RVOT cine images and transaxial cine stacks, whereas the diameter of the RPA and LPA were measured from transaxial stacks and specific pulmonary artery branch cine images. Results: Mean systolic and diastolic diameters for the MPA were 22.1 ± 2.8 mm (14.4 ± 2.2 mm/m²)/ 17.2 ± 2.3 mm (11.3 ± 1.9 mm/m²) measured in RVOT cine stacks. Mean systolic and diastolic diameters for the RPA and LPA were: 1) RPA, 12.4 ± 1.7 mm (7,9 ± 1,6 mm/m²)/ 9.8 ± 1.6 mm (5.9 ± 1.8 mm/m²) and 2) LPA, 13.3 ± 1.5 mm (8.3 ± 2.1 mm/m²)/ 10.8 ± 1.5 mm (6.8 ± 1.8 mm/m²). Separate centile charts for boys and girls for the MPA were created. Conclusions: We established CMR normal values for the MPA, RPA and LPA for children and adolescents. Our data might be useful for the detection of PA stenosis and dilatation and may serve as a reference in future studies.