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Human immunodeficiency virus infected children and adolescents are a pediatric group with increased risk of premature cardiovascular disease. The virus itself, the antiretroviral therapy and the lifestyle establish a complex interplay of factors that promotes an accelerated atherosclerosis. This process is probably mediated by dyslipidaemia, dysregulation of glucose metabolism, lipodystrophy, inflammation, endothelial dysfunction and a prothrombotic state. The clinical approach to this population in terms of cardiovascular prevention is mainly based on efficient treatment of the infection, reduction of the modifiable risk factors and promotion of lifestyle changes.

Introduction: Obesity-related comorbidities are present in young obese children, providing a platform for early adult cardiovascular disorders., Objectives: To compare and correlate markers of adiposity to metabolic disturbances, vascular and cardiac morphology in a European pediatric obese cohort., Methods: We carried out an observational and transversal analysis in a cohort consisting of 121 obese children of both sexes, between the ages of 6 and 17 years. The control group consisted of 40 children with normal body mass index within the same age range. Markers of adiposity, plasma lipids and lipoproteins, homeostasis model assessment-insulin resistance, common carotid artery intima-media thickness and left ventricular diameters were analyzed., Results: There were statistically significant differences between the control and obese groups for the variables analyzed, all higher in the obese group, except for age, high-density lipoprotein cholesterol and adiponectin, higher in the control group. In the obese group, body mass index was directly correlated to left ventricular mass (r=0.542; p=0.001), the homeostasis model assessment-insulin resistance (r=0.378; p=<0.001) and mean common carotid artery intima-media thickness (r=0.378; p=<0.001). In that same group, insulin resistance was present in 38.1%, 12.5% had a combined dyslipidemic pattern, and eccentric hypertrophy was the most common left ventricular geometric pattern., Conclusions: These results suggest that these markers may be used in clinical practice to stratify cardiovascular risk, as well as to assess the impact of weight control programs.

Introduction: Obesity is considered a global epidemic with important public health issues as it is an independent risk factor in the development of cardiovascular disorders., Material and Methods: Approximately 10% of the worldâÄôs paediatric population has excess weight or obesity and 40% of these will be obese adults. Obesity is characterized by a chronic, low grade, pro-inflammatory process that ultimately results in endothelial dysfunction, the trigger lesion leading to adult cardiovascular disease. This leads to an imbalance in the synthesis of mediators that normally regulate vascular homeostasis, particularly nitric oxide bioavailability, favoring a pro-atherosclerotic status, the hallmark of cardiovascular disorders., Results: These changes begin early in childhood and anatomopathological studies in children with excess weight or obesity have shown endothelial changes that represent the precursors of the atherosclerotic lesion., Discussion: Endothelial dysfunction is the earliest manifestation of the atherosclerotic lesion. It is evident in obese children and, as such, it potentially contributes towards cardiovascular disease in the adult., Conclusion: Although the clinical impact of these changes rarely manifest themselves in infancy, the presence of related biomarkers as well as vascular morphological changes can, at this early stage, be found and assessed.

Objectives: A growing number of reports in the literature have been correlating cardiovascular alterations with the presence of chronic liver disease, such as cirrhosis and cholestasis. The objective of this work was to compare mitochondrial bioenergetics and calcium loading capacity in the hearts of rats injected with alpha-naphthylisothiocyanate (ANIT), a compound used to induce cholestasis in animal models., Methods: Female Wistar rats (n = 12) were randomly divided into two groups. One of the groups was injected with six weekly doses of ANIT. Each group was evaluated in terms of mitochondrial bioenergetic capacity and susceptibility to the mitochondrial permeability transition (MPT), a deleterious phenomenon associated with oxidative stress and excessive mitochondrial calcium accumulation., Results: Our data showed unequivocally that cardiac mitochondria of rats chronically injected with ANIT lost their ability to accumulate calcium, in a cyclosporin A sensitive manner. This was reflected in a higher calcium-dependent swelling rate and amplitude (p < 0.01). The RCI value, an index of mitochondrial integrity, was also lower in the ANIT-treated group (p < 0.05)., Conclusions: This suggests that during cholestasis development, cardiac mitochondria lose their normal ability to control cytosolic calcium due to increased susceptibility to the MPT. Our results may suggest an explanation for the occurrence of cardiomyopathies associated with cholestatic disease, which may persist even in the absence of serum markers for liver disease.

Diabetes is one of the most common metabolic diseases of our times. Specific cardiovascular alterations are often associated with the progression of this disease. Considerable controversy exists in the literature concerning the greater or lesser susceptibility of the diabetic heart to ischemia and reperfusion. Cardiac mitochondria may be fundamental to the differential susceptibility of the cardiomyocyte to pathologic phenomena, particularly those due to the induction of the degenerative process known as the mitochondrial permeability transition (MPT), which is triggered by excessive mitochondrial calcium accumulation. The MPT has been associated with cellular dysfunction resulting from ischemia and reperfusion. The objective of this work was to examine the susceptibility of mitochondria isolated from diabetic rats to the MPT, in comparison to healthy control rats of the same age. Cardiac mitochondria from the diabetic rats had higher calcium loading capacity before the development of the MPT, with a decreased incidence of MPTP-associated features. This was associated with a greater capacity to sustain multiple pulses of externally added calcium, simultaneously with maintenance of the transmembrane electrical potential and reduced swelling amplitude. This could mean that cardiomyocytes from diabetic hearts may indeed be less prone to dysfunctions resulting from ischemia and reperfusion, at least in milder diabetic conditions, thus explaining many reports in the literature.