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The global obesity epidemic is well established, with increases in obesity prevalence in most countries since the 1980s. Obesity directly contributes to incident cardiovascular risk factors, including dyslipidemia, type 2 diabetes, hypertension and sleep disorders. Obesity also leads to the development of cardiovascular disease and cardiovascular disease mortality independently of other cardiovascular risk factors.
The most recent data highlight abdominal obesity , determined by waist circumference, as a risk marker for cardiovascular disease that is independent of body mass index. There have also been significant advances in imaging modalities to characterize body composition, including visceral adiposity.
Studies quantifying fat depots, including ectopic fat , support excess visceral adiposity as an independent predictor of poor cardiovascular outcomes. Lifestyle modification and subsequent weight loss improve both metabolic syndrome and associated systemic inflammation and endothelial dysfunction.
However, clinical trials of medical weight loss have not shown a reduction in rates of coronary artery disease.
In contrast, prospective studies comparing patients undergoing bariatric surgery with nonsurgical patients with obesity have shown a reduced risk of coronary artery disease with surgery.
In this statement, we summarize the impact of obesity on the diagnosis, clinical management, and outcomes of atherosclerotic cardiovascular disease, heart failure, and arrhythmias, especially sudden cardiac death and atrial fibrillation. In particular, we examined the influence of obesity on non-invasive and invasive diagnostic procedures for coronary artery disease. Additionally, we review the impact of obesity on cardiac function and outcomes related to heart failure with reduced and preserved ejection fraction.
Finally, we describe the effects of lifestyle and weight loss surgical interventions on outcomes related to coronary artery disease, heart failure, and atrial fibrillation.
The following are key points to remember from this American Heart Association (AHA) scientific statement on obesity and cardiovascular disease (CVD):
Obesity is a multifactorial disease with a complex pathogenesis related to biological, psychosocial, socioeconomic and environmental factors, with heterogeneity in the pathways and mechanisms by which obesity is associated with adverse outcomes.
The World Health Organization defines overweight as a body mass index (BMI) between 25 and 29 kg/m2, and obesity as a BMI ≥30 kg/m2. Variation by sex, age, and race/ethnicity limits the relationship between BMI and body fat percentage. An estimated 603.7 million adults worldwide meet the criteria for obesity. The prevalence of obesity has doubled between 1980 and 2015 in 73 countries. As of 2015, an estimated 4 million deaths are related to obesity.
Despite the strong correlation between BMI and abdominal obesity, additional metrics such as waist circumference (WC), an indicator of abdominal obesity, are associated with cardiometabolic disease. WC is predictive of mortality. In fact, some societies recommend measuring WC in addition to BMI at clinical visits. Visceral adipose tissue (VAT) in the abdominal cavity is positively associated with CV risk. The relationship between WC and height has been used as a predictor of CVD. Waist-to-hip ratio (WHR) has also been shown to predict CV mortality.
Pericardial fat , or fat in the pericardial sac, is associated with higher BMI and traditional CV risk factors. However, pericardial fat is not significantly associated with CV events after adjustment for traditional risk factors.
Exercise can reduce VAT, and most data supports aerobic exercise . However, not all studies have demonstrated this association between exercise and VAT reduction. Data on epicardial fat reduction with exercise are inconclusive.
The impact of obesity on CV health begins in childhood . Obesity accelerates early atherosclerotic changes, including the development of fatty streaks. Obesity is associated with elevated blood pressure, dyslipidemia, and hyperglycemia in children and young adults.
Visceral adiposity promotes systemic and vascular inflammation, essential for the development of atherosclerosis. In a meta-analysis of more than 300,000 adults, at each BMI level, higher measures of central adiposity (WC and WHR) were associated with increased risk of coronary artery disease and CV mortality, including those with a normal BMI. Microvascular disease is independently associated with higher BMI, while weight loss (through bariatric surgery) has been associated with improvements in coronary microvascular function.
Cardiac testing in the context of obesity can be challenging. Left ventricular hypertrophy may be underdiagnosed by electrocardiography in the context of obesity. Imaging tests, including computed tomography and stress echocardiography, may have higher degrees of artifact and require different protocols for obese and nonobese patients. Stress cardiac MRI and positron emission tomography may be the diagnostic tests least affected by obesity.
For many CV events, a U-shaped association between BMI and adverse events has been observed. In a large cohort of patients undergoing percutaneous coronary intervention or coronary artery bypass grafting, a U-shaped association was observed for BMI and all-cause mortality, and major adverse cardiac events. BMI may be more strongly associated with heart failure (HF) with preserved ejection fraction compared to HF with reduced EF. A U-shaped curve also appears in the association of BMI with HF outcomes.
Obesity may account for 20% of atrial fibrillation (AF) cases . Postoperative AF also correlates with BMI. Epicardial adipose tissue has become an important proarrhythmic substrate. Weight loss is associated with reduced time in AF and better success of AF ablations.
