Since the 1980s, the prevalence of obesity has increased in most countries around the world. According to the Global Burden of Disease Study, 600 million people worldwide are obese. Between 39% and 49% of the world’s population (2.8 to 3.5 billion people) is overweight or obese.Between 1980 and 2015, the prevalence of obesity doubled in 73 countries.
Obesity can lead to dyslipidemia, type 2 diabetes, and hypertension, increasing the risk of cardiovascular morbidity and mortality. in 2015, high body mass index led to 4 million deaths, with more than two-thirds caused by cardiovascular disease.
Recently, the American Heart Association (AHA) published a scientific statement on obesity and cardiovascular disease, pointing out that obesity is a complex chronic disease and is multifactorial, with biological, environmental, psychosocial and other multilevel factors contributing to obesity.
The statement points out that excess visceral fat is an independent indicator of poor cardiovascular prognosis. Obesity leading to cardiovascular complications is not only related to the amount of total body fat, but also depends to a large extent on fat distribution.
Imaging studies have shown that in patients with visceral obesity, the most common is hepatic fat accumulation, which manifests as nonalcoholic fatty liver.
Guidelines recognize abdominal obesity, as marked by waist circumference, as a risk marker for cardiovascular disease.
Waist circumference of more than half of height is associated with a higher risk of cardiovascular disease
For the assessment of obesity, although waist circumference is the primary indicator for assessing abdominal obesity, waist circumference/height as an indicator of obesity may be a better predictor of cardiovascular disease given body size.
The PURE-China research group found that if the body “grows horizontally” and the waist circumference is more than half of the height, metabolic problems such as dyslipidemia and hyperglycemia may exist, and the risk of cardiovascular disease is also higher.
In addition, waist-to-hip ratio (WHR) has been shown to predict cardiovascular mortality independently of BMI. Obesity as assessed by waist circumference, WHR has been shown to be a cardiovascular disease factor independent of BMI.
Exercise reduces visceral fat, even without weight change
Physical activity, or physical activity interventions combined with diet, have been shown to reduce visceral, pericardial and epicardial fat.
Randomized studies of men and women of different ages have found that exercise 3 to 5 times per week for 12 to 52 weeks reduces visceral fat compared with non-exercise controls.
Exercise also reduces visceral fat even in the absence of weight loss, with one Meta-analysis reporting a 6.1% reduction in visceral fat in the absence of weight loss.
The reduction in visceral fat in the absence of weight loss may be related to an increase in muscle etc.
Reducing calories, the statement noted, may also reduce abdominal fat. However, most studies have shown exercise to be more beneficial in reducing visceral fat compared to dietary interventions.
The most beneficial physical activity for reducing abdominal obesity is aerobic exercise; the effect of strength exercise is unclear.
Similarly, high-intensity exercise’s is not always superior to moderate-intensity exercise. Even 3 months of walking can significantly reduce visceral fat.
Although there are many medications that can reduce body fat, lifestyle interventions may be as effective or even more effective than medications.
An analysis of the study found that meeting the current recommendation of 150 minutes of physical activity per week may be sufficient to reduce abdominal fat.
Should antiplatelet drug doses be adjusted in obese individuals?
Studies have shown that obesity may promote platelet activation and that platelet inhibition is diminished by the application of antiplatelet drugs, but the lack of clinical findings that obese patients with acute coronary syndromes have a better prognosis instead is contradicted by platelet assay results, and the statement does not make any recommendations regarding antiplatelet drug dose adjustment in obese patients, as the sample sizes of the studies were too small to allow for decisive conclusions regarding the clinical outcomes. Recommendations.
The harms of obesity are not exclusively mediated by concurrent risk factors
Based on several prospective epidemiologic studies, obesity is associated with a high risk of developing coronary heart disease (CHD), primarily mediated by hypertension, dyslipidemia, diabetes mellitus, and other co-morbidities, and there is a significant residual risk of coronary heart disease associated with obesity, even after correction for these risk factors.
The statement noted that excessive obesity can impair cardiac function indirectly through obesity-related co-morbidities, as well as directly on the myocardium and vascular system.
In addition to the aforementioned effects of excessive obesity on the coronary vasculature, obesity is also associated with coronary microvascular abnormalities.
At present, however, no studies have shown that weight loss through lifestyle changes significantly reduces cardiovascular disease or mortality, although cardiovascular risk factors have improved.
Obesity is an independent risk factor for heart failure
Many studies have confirmed that obesity is a major cause of hypertension, cardiovascular disease and left ventricular hypertrophy
risk factors, and several studies have confirmed that obesity is a major risk factor for heart failure.
Obesity has potentially adverse effects on left ventricular systolic function, especially left ventricular diastolic function.
Other anthropometric parameters of excessive obesity, such as waist circumference, waist-to-hip ratio, and waist/height ratio, are also independently associated with heart failure risk.
Currently, there is little evidence that weight loss improves prognosis in patients with heart failure, but weight loss can reduce symptoms and improve quality of life and other concomitant conditions such as sleep apnea or diabetes. However, in patients with heart failure, there is an obesity paradox, with obese individuals having a relatively better prognosis.
Orlistat has limited efficacy and safety in the treatment of obesity with heart failure. The novel hypoglycemic agents sodium⁃glucose cotransporter protein 2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP⁃1A, e.g., liraglutide) have been shown to be effective in reducing weight and hospitalizations for heart failure and cardiovascular death. Trials of these drugs are currently underway and results will be published within the next 5 years.
In obese individuals, the risk of sudden cardiac death and atrial fibrillation is also increased
The statement also noted that there is now compelling evidence to support that excessive obesity is a significant risk factor in cardiac arrhythmias, particularly sudden cardiac death and atrial fibrillation.
For every 5-unit increase in body mass index, the risk of sudden cardiac death increases by 16%. Obesity is the most common non-ischemic cause of sudden cardiac death, and abdominal obesity plays an important role.
An estimated one-fifth of atrial fibrillation is associated with obesity. Elevated body mass index in midlife is strongly associated with the development of AF in later life.
The benefits of weight loss are also well documented. The statement noted that weight management should be included as part of the management of AF management.
As the population ages and the prevalence of obesity increases in the elderly population, there is a need to evaluate the potential mechanisms of obesity-related cardiac insufficiency and to improve the management of patients with obesity and cardiovascular disease through future research.
The statement emphasized that the dramatic increase in the proportion of young patients with severe obesity requires more upstream interventions for primary prevention and better treatment of obesity as a chronic disease.