Structural and functional ventriculo-arterial changes in obesity : mechanisms , implications and reversibility after weight loss

Obesity epidemiology Th e global prevalence of excessive weight has doubled in the last 30 years and is at a level of approximately 33% for obesity and 50% for overweight and obesity. In the world there are currently registered 200 million obese men, 300 million obese women and 1.4 billion overweight subjects, there are regions (from U.S.A.) where overweight and obese individuals account for over 65% of the population. Equally worrying is the current number of obese adults and high prevalence of obesity among children ‒ in 2010 more than 40 million of children younger than 5 years were overweight1,2. Abstract: Ob esity is a p ublic health problem, being the fi ft h cause of death worldwide. Adverse cardio vascular prognosis of obesity is linked to: endothelial dysfunction, abnormal left ventricular geometry, systolic and diastolic left ventricular dysfunction, heart failure, increased arterial stiff ness, coronary artery disease, dilated left atrium and atrial fi brillation. Pathophysiolog ic mechanisms of structural and functional cardiovascular changes of obesity are complex: cardiac metabolism disturbances, mitochondrial dysfunction, impaired insulin signalling, infl ammation, neuro-hormonal activation, impaired production of adipokines, fi brosis, changes in the extracellular matrix and cardiomyocytes apoptosis. Obesity is characterized by a mixed left ventricular overload, with predominance of one component (pressure or volume), depending on which a certain type of cardiac remodelling appears (eccentric or concentric hypertrophy, concentric remodelling), with specifi c prognostic implications. Th e main modalities of obesity treatment are diet, physical activity, behaviour modifi cation, pharmacological therapy and bariatric surgery. Favorable meta bolic and blood pressure changes were demonstrated aft er losing weight by any means, but reversibility of cardiac morphological changes (mainly regression of left ventricular hypertrophy) and of left ventricular diastolic and systolic dysfunction were demonstrated only aft er bariatric surgery. Described eff ects are probably due to a large and sustained weight loss.