Abstract
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Background: Issues with obesity often begin in childhood for congenital heart disease (CHD) patients.
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More than 25% of children with CHD are overweight [1–3].
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There are risk factors unique to CHD population that likely contribute to obesity:
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Children initially experience failure to thrive and malnutrition in infancy, and they are often prescribed interventions for weight gain prior to surgical interventions, which include high-calorie and high-fat supplements [1].
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Children are often also put on physical activity restrictions prior to surgical intervention [1].
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However, these habits often persist into adulthood despite resolution of need for diet supplementation and activity restriction after repair, which contributes to obesity. Activity restriction in children with CHD is the strongest predictor of obesity [4].
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Obesity in children with CHD is associated with traditional risk factors in childhood obesity as well, such as parental obesity and Hispanic ethnicity [3, 5].
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More boys with CHD have obesity than girls, which is disparate with general population trends where there are no gender differences [2].
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Poor self-esteem and perceived confidence in children with CHD may also limit a child’s initiative to participate in physical activity [6].
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Pediatric cardiologists may recommend activity limitation in excess of guideline recommendations, and parents may further impose unnecessary exercise restrictions [7]. Only slightly more than half of parents of children with CHD know the appropriate exercise restriction for their children [8].
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Rates of obesity in adults with congenital heart disease (ACHD):
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Various studies have indicated that rates of obesity in adults with CHD are similar to or slightly less than overall rates of adult obesity [2, 9, 10] Approximately 25% of the ACHD population in the USA is overweight or obese [10].
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The obesity rate in the overall population is obviously not an ideal standard. Furthermore, CHD patients are ideally in lifelong cardiac care and should benefit from optimal obesity prevention.
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Prevention:
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As more children with CHD are surviving into adulthood, awareness of the risk of obesity and optimizing lifestyle modification to prevent obesity is of utmost importance to their overall health.
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Providers must strive to include lifestyle counseling as part of all care visits with ACHD patients.
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Cardiopulmonary exercise testing may guide safe exercise prescription in most patients.
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In general, exercise recommendations are based on expert consensus rather than outcome-driven data. Exercise recommendations should be made on an individualized patient-by-patient basis with an emphasis on risk/benefit analysis and with a team-based approach involving providers with expertise in congenital disease and sports cardiology.
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Exercise recommendations per phenotype:
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Shunt patients (atrial and ventricular septal defects, patent ductus arteriosus) [11, 12]:
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Asymptomatic patients with repaired shunts or unrepaired small shunts can participate in activities without restriction.
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Symptomatic patients with shunts should limit competitive activities prior to repair if their pulmonary artery pressures are elevated.
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Unrepaired shunt patients with Eisenmenger’s physiology have a high risk of sudden cardiac death during intense activities, and competitive exercise and isometrics should be avoided. Individualized exercise programs should be created for patients who are asymptomatic, have an oxygen saturation greater than 80%, have no evidence of arrhythmia, and have no ventricular dysfunction.
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Patients with obstructive lesions(coarctation of the aorta, aortic stenosis, pulmonary valve stenosis) [11, 12]:
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Patients with obstructive lesions with moderate to severe pressure gradients should refrain from activity, especially static exercise, until repair.
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Asymptomatic patients with low gradients can participate without restriction.
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Cyanotic heart disease (tetralogy of Fallot, double-outlet right ventricle, transposition of the great arteries, univentricular circulation) [11, 12]:
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Repaired tetralogy of Fallot, double-outlet right ventricle, and transposition of the great arteries can have liberal exercise recommendations. This is the subgroup where unnecessary exercise limitations are most imposed.
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Asymptomatic repaired Fontan (univentricular circulation) patients have reduced exercise capacity due to single ventricular circulation but should be encouraged to do low-intensity exercise as they will benefit from it.
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Patients with Marfan syndrome can participate in low-moderate static and low-intensity dynamic exercise if they do not have aortic root dilation, moderate or severe mitral regurgitation, or a family history of dissection or sudden cardiac death [12].
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Patients with aortic root dilatation (Marfan, familiar aortic aneurysm) should participate in low-intensity activities. They should refrain from contact sports regardless of presence or absence of aortic root dilatation [11].
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Patients with hypertrophic cardiomyopathy should refrain from competitive sports except low-intensity activities, regardless of symptoms, LV outflow tract obstruction, or prior interventions [13].
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Patients withanomalous origins of the coronary arteries [12]:
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Patients with anomalous left coronary that arises from the right sinus of Valsalva are advised to avoid strenuous exercise, especially when the course of the artery passes between the aorta and pulmonary artery.
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Patients with anomalous right coronary that arises from the left sinus of Valsalva should receive a stress test prior to exercise. They should be advised to avoid strenuous exercise if they are symptomatic or have signs of ischemia or arrhythmia on the stress test.
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Repair may be offered to remove exercise restriction. If repair is successful, patients may be able to participate in all sports if asymptomatic with negative stress test 3Â months after repair.
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Flannery, L.D. (2018). Obesity and Exercise Recommendations in Adult Congenital Heart Disease. In: DeFaria Yeh, D., Bhatt, A. (eds) Adult Congenital Heart Disease in Clinical Practice. In Clinical Practice. Springer, Cham. https://doi.org/10.1007/978-3-319-67420-9_35
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