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Heart remodelling and obesity: the complexities and variation of cardiac geometry
  1. Hutan Ashrafian1,
  2. Thanos Athanasiou1,
  3. Carel W le Roux2
  1. 1Department of Surgery and Cancer, Imperial College London, UK
  2. 2Section of Investigative Medicine, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, UK
  1. Correspondence to Dr Carel W le Roux, Section of Investigative Medicine, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, UK; c.leroux{at}

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Obesity and the heart

Obesity and heart failure are a global epidemic associated with increased cardiovascular risk and significant healthcare costs.1 2 Epidemiological evidence suggests that obese patients are 30% more likely to develop heart failure3 and each incremental body mass index (BMI) rise of 1 kg/m2 can increase the risk of heart failure by 5% for men and by 7% for women.4 Moreover, heart weight and body weight have a linear relationship,5 and long-term obesity is associated with left ventricular hypertrophy and dilatation, which may result in cardiac failure. It remains difficult to distinguish whether symptoms of poor exercise tolerance, dyspnoea and peripheral oedema are secondary to obesity alone or ‘obesity cardiomyopathy’. On echocardiography left ventricular dilatation is present in 8–40% of obese individuals, and increased left ventricular wall mass exists in up to 87% of obese patients.6

Traditional haemodynamic model and its limitations

Obesity results in increased numbers of adipocytes, leading to an expanded circulating volume thereby raising metabolic demands.7 The subsequent increase of left ventricular stroke volume induces a persistent rise in cardiac output, which in turn results in systemic hypertension. In obese individuals, it was therefore proposed that the left ventricular stroke workload is higher owing to an increased preload and stroke volume so …

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