Abstract-Childhood obesity is increasingly prevalent in the community and is related to adverse cardiovascular outcomes during adulthood. In this study of healthy children, we evaluated the influence of adiposity and physical activity on carotid-femoral pulse wave velocity (PWV), an index of arterial stiffness and a marker of cardiovascular risk in adults. In 573 community-based children (mean age: 10.1Ϯ0.3 years; 51% boys), we measured body mass index and waist circumference. Percentage body fat was quantitated by dual-energy x-ray absorptiometry. Cardiorespiratory fitness (CRF) and physical activity levels were assessed using a 20-m shuttle run and 7-day pedometer count, respectively. PWV was estimated by applanation tonometry. In univariate analysis, PWV was positively correlated with body mass index (rϭ0.34), waist circumference (rϭ0.32), and percentage body fat (rϭ0.32; PϽ0.001 for all) and negatively correlated with CRF (rϭϪ0.23; PϽ0.001) and pedometer count (rϭϪ0.08; Pϭ0.046). In separate multivariable linear regression models, body mass index, waist circumference, and percentage of body fat were independently and positively associated with PWV (PϽ0.01 for all) after adjusting for age, sex, systolic blood pressure, mean arterial pressure, heart rate, and CRF (PϽ0.01 for all). The influence of CRF on PWV was attenuated after adjusting for adiposity. In conclusion, increased body mass and adiposity and decreased CRF are associated with arterial stiffening in healthy prepubescent children.

Objective: To estimate the prevalence of heart failure (HF) and left ventricular (LV) systolic dysfunction in a population‐based sample of older Australians. Design, setting and participants: A cross‐sectional survey of 2000 randomly selected residents of Canberra, aged 60–86 years, conducted between February 2002 and June 2003. Participants were assessed by history, physical examination by a cardiologist, and echocardiography. Main outcome measures: Age‐ and sex‐specific prevalence rates of clinical HF and LV systolic dysfunction (defined as LV ejection fraction ≤ 50%). Results: Of 1846 people eligible for our study, 1388 (75%) agreed to participate and 1275 completed all investigations (mean age, 69.4 years; 50% men). In the study sample, 72 subjects (5.6%; 95% CI, 4.4%–7.1%) had clinical HF that had been previously diagnosed and was confirmed by our assessment. A further 0.6% (95% CI, 0.3%–1.2%) had undiagnosed clinical HF (ie, evidence of structural heart disease and symptoms/signs of cardiac insufficiency without a previous diagnosis of clinical HF). Thus, the overall prevalence of clinical HF in the sample was 6.3% (95% CI, 5.0%–7.7%). Clinical HF increased in prevalence with advancing age (a 4.4‐fold increase from the 60–64‐years age group to the 80–86‐years age group; P < 0.0001). Of the 75 subjects (5.9%; 95% CI, 4.7%–7.3%) with LV systolic dysfunction, 44 (59%) were in the preclinical stage of disease. Conclusion: Diagnosed HF cases represent the “tip of the iceberg” for the national burden of HF and LV systolic dysfunction. Clinically identifiable HF cases can remain undiagnosed, and the majority of people with LV systolic dysfunction are in a preclinical stage of the disease.

Background: Obesity has been associated with the development of atrial fibrillation (AF); however the mechanisms by which it results in a pro-arrhythmic substrate remain unknown.Methods: Thirty sheep were studied at baseline, four months and eight months, following an ad libitum calorie dense diet. Ten were sampled at each time point for cardiac MRI, invasive haemodynamic evaluation (left atrial and arterial pressure) and detailed electrophysiologic study. An additional six maintenance-fed control sheep were sampled at four and eight months to control for time/age-related effects. A custom made 128-electrode plaque applied to the right and left atria was used to quantify; bi-atrial effective refractory periods (ERP); conduction velocity (CV); conduction heterogeneity index (CHI) at four pacing cycle lengths (PCL) from four sites; and AF inducibility. Quantitative myocardial histology was performed for myocardial fibrosis, inflammation and lipidosis.Results: Weight increased from 58 ± 7 kg to 77 ± 5 kg to 105 ± 13 kg (P < 0.001). With increasing weight there was: progressive decrement in atrial CV (P = 0.01), increasing atrial volumes (P = 0.01), atrial fibrosis (P = 0.007) and lipidosis (P = 0.049). There was regional variation in conduction heterogeneity (P = 0.04) with increasing weight. Electrophysiologic disturbances persisted after adjusting for haemodynamic variables. No changes were observed in the control cohort (ERP; P = 0.5, CV; P = 0.8, CHI; P = 0.9). With increasing adiposity, AF event number (P = 0.001) and duration (P < 0.001) significantly increased. No significant change was observed in ERP with increasing adiposity (P = 0.198).Conclusion: Obesity induces early and progressive atrial structural and electrophysiological remodelling. These electrophysiological abnormalities were independent of adverse haemodynamic changes and occurred with a step-wise increase in AF burden.