Physical activity plays a pivotal role in preventing obesity and cardiovascular risks. The six-minute walk test (6MWT) is a tool to assess functional capacity and predict cardiovascular events. The aim of this cross-sectional study was to compare the performance and haemodynamic parameters before and after a 6MWT between obese/overweight vs. normal-weight children (average age 8.7 ± 0.7 years) participating in a project involving four primary schools in South Verona (Italy). Validated questionnaires for physical activity and diet, as well as blood drops, were collected. Overweight or obese children (OW&OB; n = 100) covered a shorter 6MWT distance compared to normal-weight children (NW, n = 194). At the test’s conclusion, the OW&OB group exhibited a higher Rate Pulse Product (RPP = Systolic Blood Pressure × Heart Rate) as compared to the NW. Body Mass Index, waist-to-height ratio, fat mass by electrical impedance, and trans fatty acids showed direct correlations with pre and post-test haemodynamic parameters, such as RPP, and inverse correlations with oxygen saturation. OW&OB children demonstrated lower performance in this low-intensity exercise test, along with an elevated haemodynamic response. Excess fat in childhood can be considered a risk factor for haemodynamic stress, with potential deleterious consequences later in life. Efforts should be initiated early to break this cycle.

Childhood overweight and obesity represent a major global public health emergency, with a steadily increasing prevalence over recent decades in both developed and developing countries. Approximately one fifth of children and adolescents are overweight or obese, with marked differences across ethnic groups and geographical areas. Accurate estimation of this condition is complicated by the lack of a unique and universally accepted definition of childhood obesity, which is based on different anthropometric criteria. Although body mass index (BMI) remains the most widely used tool, growing evidence indicates that abdominal obesity, assessed by waist circumference and waist-to-height ratio, is a better predictor of cardiometabolic risk, even in children with a normal BMI. Childhood obesity is associated with several comorbidities, including arterial hypertension, non-alcoholic fatty liver disease (NAFLD) and obstructive sleep apnea syndrome (OSAS). Early diagnosis and an integrated therapeutic approach are essential to reduce the risk of long-term complications. Although lifestyle modifications remain the cornerstone of treatment, new pharmacological options for pediatric obesity have been approved in recent years. This narrative review explores the impact of childhood obesity on the early development of hypertension, NAFLD, and OSAS, emphasizing the implications that can already be observed during childhood and adolescence. It examines the association between pediatric obesity and these conditions by synthesizing current epidemiological evidence, describing the underlying pathophysiological mechanisms linking excess adiposity to disease onset, and reviewing pediatric-specific diagnostic criteria as well as preventive and therapeutic strategies.

Neurodegenerative synucleinopathies—including Parkinson’s disease, multiple system atrophy, pure autonomic failure, and dementia with Lewy bodies—often feature cardiovascular autonomic dysfunction. Neurogenic orthostatic hypotension (nOH) is common and symptomatic, while neurogenic supine hypertension (nSH) is less frequent but may carry long-term cardiovascular risks. Lifestyle measures are first-line for managing nSH, yet persistent hypertension unresponsive to nonpharmacological strategies presents a treatment dilemma. Limited trial data and unclear guidelines make it difficult to determine when antihypertensive therapy is appropriate. Evidence from studies on hypertension-mediated organ damage (HMOD)—assessed through markers such as carotid intima-media thickness, pulse wave velocity, left ventricular hypertrophy, estimated glomerular filtration rate, and white matter hyperintensities—suggests that nSH, rather than the underlying neurodegenerative disorder, drives vascular, cardiac, renal, and cerebral injury. Therefore, treatment decisions should be individualized. While antihypertensive therapy may help prevent subclinical organ damage, clinicians must balance this benefit against the risk of worsening nOH and further compromising overall prognosis.