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Obesity and sudden death: visceral response?
  1. Kyndaron Reinier,
  2. Sumeet S Chugh
  1. The Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA
  1. Correspondence to Professor Sumeet S Chugh, Cedars-Sinai Medical Center, Advanced Health Sciences Pavilion, Suite A3100, 127 S. Vicente Blvd., Los Angeles, CA 90048, USA; sumeet.chugh{at}cshs.org

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The public health burden of sudden cardiac death (SCD) is high, accounting for about 50% of cardiovascular deaths, and resulting in more years of potential life lost than any single cancer.1 There is an established association between obesity and SCD2 ,3 which has attained increased importance due to the burgeoning global rise in the proportion of overweight and obese individuals. In the USA, obesity has reached epidemic proportions. A third of the population is obese, with median body mass index (BMI) above 27 kg/m2 and age-adjusted obesity prevalence above 35% for both sexes.4

Obesity appears to drive overall cardiovascular morbidity and mortality largely by its link to cardiovascular risk factors including diabetes, total cholesterol, low density lipoprotein, and hypertension. Traditionally, BMI has been used in analyses of obesity and outcomes, but there is a growing literature suggesting that the distribution of body fat is important in determining cardiovascular disease (CVD) risk. In particular, abdominal adiposity appears to confer a higher risk for CVD than obesity in general.5

Obesity as a risk factor

From a mechanistic perspective, there are several reasons why a detailed examination of obesity as a risk factor for SCD is warranted. Obesity is associated with a variety of ECG abnormalities, including prolonged ventricular repolarisation (QT interval), which increases susceptibility to ventricular arrhythmias. Obesity also increases risk for heart failure, LV hypertrophy and dilatation, sleep apnoea, and altered sympathetic tone, all of which may increase risk of SCD beyond traditional CVD risk …

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Footnotes

  • Contributors KR drafted the initial manuscript; SSC made critical revisions; both authors made subsequent revisions and approved the final document.

  • Funding Funded in part, by US National Heart, Lung, and Blood Institute grants R01 HL105170 and R01 HL122492 to SSC. SSC is the Pauline and Harold Price Chair in Cardiac Electrophysiology at the Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA

  • Competing interests None.

  • Provenance and peer review Commissioned; internally peer reviewed.

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