The links between obesity and cardiovascular disease are many, including direct cause and effect. Click through the 10-slide summary of a new AHA statement for a first look.
"... the trends in obesity prevalence in the United States and around the world highlight the significant impact that obesity will continue to have on CVD incidence and prevalence globally."
The American Heart Association's recent publication, "Obesity and cardiovascular disease: a scientific statement from the American Heart Association" reflects the already large and now rapidly growing body of evidence that ever-more precisely links obesity with cardiovascular (CV) risk factors as well as with CV disease (CVD) and mortality independently of other CV risk factors.
The new statement focuses on the impact of obesity on the pathophysiology, diagnosis, treatment, and clinical outcomes of ASCVD, heart failure (HF), and arrhythmias and begins with a review of recent data linking abdominal obesity and visceral adiposity to CVD risk.
As a preview, we summarized in a slide show the statement's 10 key points as highlighted by the American College of Cardiology.
1. 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 the disease is associated with adverse outcomes.
2. The obesity epidemic. Globally, ~603.7 million adults meet criteria for obesity. Obesity prevalence doubled between 1980 and 2015 in 73 countries. As of 2015, an estimated 4.0 million deaths were related to obesity, more than 2/3rds caused by CVD.
4. Pericardial and epicardial fat. Pericardial fat is associated with higher BMI, traditional CV risk factors, and more atherogenic lipoprotein particles but not significantly with CV events. Epicardial adipose tissue originates from embryonic brown adipose tissue & releases proinflammatory proteins into the vasculature and is associated with overall CV health score and arterial stiffness in patients with CVD and type 2 diabetes.
5. Exercise-adipose reduction link still unclear. Exercise may reduce VAT, even in absence of weight loss; but not all studies demonstrate exercise-VAT reduction association. Data on reductions in epicardial fat with exercise remain inconclusive. Caloric restriction has been demonstrated to reduce hepatic, epicardial, and pericardial fat
6. Dangers of obesity begin in childhood. Obesity accelerates early atherosclerotic changes via mechanisms such as insulin resistance, inflammation. In children and young adults, obesity is associated with: elevated blood pressure, dyslipidemia, hyperglycemia.
7. Impact of visceral adiposity on events, mortality. Visceral adiposity promotes systemic & vascular inflammation, fundamental to the development of atherosclerosis. Meta-analysis: >300 000 adults found at each level of BMI, higher measures of central adiposity were associated with an increased risk for CAD & CV mortality, including in those with a normal BMI.
8. Obesity may impede cardiac testing. LVH may be underdiagnosed by electrocardiography. Imaging testing including CT/stress echocardiography may have higher degrees of artifact & require different protocols for the obese vs the nonobese. Stress cardiac MRI and PET may be the diagnostic tests least affected by obesity.
BMI association with CV events. In a large cohort of patients undergoing PCI or CABG, u-shaped association for BMI and all-cause mortality, and MACE were observed. BMI may be more strongly associated with HFpEF vs HFrEF. A u-shaped curve also appears in the association of BMI with HF outcomes.
10. Obesity associated with atrial fibrillation. Obesity may account for 20% of atrial fibrillation (AF) cases. Postoperative AF is also correlated with BMI. Epicardial adipose has emerged as an important proarrhythmic substrate. Weight loss is associated with reduced time in AF and improved success of AF ablations.