Obese children show early signs of heart disease

Obese children show early signs of heart disease


Oct. 16, 2007 -- Children who are obese or who are at risk for obesity show early signs of heart disease similar to obese adults with heart disease, a study by researchers at Washington University School of Medicine in St. Louis has found.


"Based on this study, these subtle markers can help us predict who could be at risk for heart disease and heart attacks," said Angela Sharkey, M.D., associate professor of pediatrics at Washington University School of Medicine and a pediatric cardiologist at St. Louis Children's Hospital.

The study was published in the Winter 2007 issue of the Journal of Cardiometabolic Syndrome

Childhood obesity in the United States is an epidemic — nationwide, 19 percent of children ages 6 to 11 and 17 percent of those 12 to 19 are overweight, according to the Centers for Disease Control and Prevention (CDC). Those who are overweight during childhood also have an increased risk of obesity in adulthood and are at greater risk for complications such as diabetes, high blood pressure and heart disease, because obesity increases total blood volume, which leads to extra stress on the heart.

Sharkey and Steven M. Lorch, M.D., a former fellow at the School of Medicine now at University of Texas Health Science Center at Houston, analyzed data from 168 children ages 10 to 18 who had been referred to them for cardiac ultrasound with symptoms including heart murmur, chest pain, acid reflux or high blood cholesterol. Based on CDC guidelines for body mass index for age (BMIA), 33 patients were found to have a BMIA as obese, or the 95th percentile or above for their age; 20 had a BMIA that classified them as at risk for obesity, or between the 85th and 94th percentile; and 115 were considered normal, or below the 85th percentile.

To analyze the hearts of the obese children and those at risk, Sharkey and Lorch used a new tissue Doppler imaging technique called vector velocity imaging which tracks the movement of the heart's muscular wall. Any changes in the rate of motion of heart muscle were averaged within each group and compared to the normal rate of motion.

"In the patients who are obese, the rate of motion of heart muscle changed," Sharkey said. "As a child's BMIA increases, we see alterations in both the relaxation and contraction phase of the heartbeat. Many of these changes that have been seen in adults were assumed to be from long-standing obesity, but it may be that these changes start much earlier in life than we thought."

As vector velocity imaging becomes more broadly available, Sharkey said, it could potentially help pediatric cardiologists follow these children more closely over time to see if changes in the heart progress.

"We may be able to determine whether we could intervene in the process, such as focusing the families on understanding the importance of regular exercise and dietary modifications for weight loss and prescribing statin drugs for high-blood cholesterol," she said.

Sharkey said the results of the study give more ammunition to physicians to use in counseling pediatric patients and their parents about the risks of obesity and the need to attain a healthy weight.

"Even in teenagers, obesity leads to decreased myocardial performance and abnormal diastolic function," she said.

Further study is needed to determine how soon the changes in the heart set in after a child becomes obese and whether those changes are reversible with weight loss.

Lorch SM, Sharkey A. Myocardial Velocity, Strain, and Strain Rate Abnormalities in Healthy Obese Children. Journal of Cardiometabolic Syndrome. 2007 Winter; 2(1):30-4.

Statin Treatment in Children With Familial Hypercholesterolemia

Statin Treatment in Children With Familial Hypercholesterolemia
The Younger, the Better


Published online before print July 30, 2007, doi:10.1161/CIRCULATIONAHA.106.671016


Jessica Rodenburg, MD, PhD; Maud N. Vissers, PhD; Albert Wiegman, MD, PhD; A. S. Paul van Trotsenburg, MD, PhD; Anouk van der Graaf, MD; Eric de Groot, MD, PhD; Frits A. Wijburg, MD, PhD; John J.P. Kastelein, MD, PhD; Barbara A. Hutten, PhD

From the Departments of Vascular Medicine (J.R., M.N.V., A.v.d.G., E.d.G., J.J.P.K.), Paediatrics (A.W., A.S.P.v.T., F.A.W.), and Clinical Epidemiology, Biostatistics and Bioinformatics (B.A.H.), Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.


Background— We previously demonstrated in a randomized placebo-controlled trial that 2-year pravastatin treatment induced a significant regression of carotid intima-media thickness (IMT) in 8- to 18-year-old children with familial hypercholesterolemia. Subsequently, we continued to follow up these children to explore the relation between the age of statin initiation and carotid IMT after follow-up on statin treatment. We also examined safety aspects of statin therapy during this long-term follow-up.

Methods and Results— All 214 children who initially participated in the previous placebo-controlled study were eligible for the follow-up study. After completion of the placebo-controlled study, all children continued treatment with pravastatin 20 or 40 mg, depending on their age. Blood samples were taken on a regular basis for lipids and safety parameters, and a carotid IMT measurement was performed after an average treatment period of 4.5 years. Follow-up data for 186 children were available for the statistical analyses. Multivariate analyses revealed that age at statin initiation was an independent predictor for carotid IMT after follow-up with adjustment for carotid IMT at initiation of statin treatment, sex, and duration of treatment. Early initiation of statin treatment was associated with a subsequently smaller IMT. Furthermore, no serious laboratory adverse events were reported during follow-up, and statin treatment had no untoward effects on sexual maturation.

Conclusions— These data indicate that early initiation of statin treatment delays the progression of carotid IMT in adolescents and young adults. The present study shows for the first time that early initiation of statin therapy in children with familial hypercholesterolemia might be beneficial in the prevention of atherosclerosis in adolescence.

Primary source:

Circulation: Journal of the American Heart AssociationSource reference: Rodenburg J, et al "Statin Treatment in Children With Familial Hypercholesterolemia: The Younger, the Better" Circulation 2007;116: 664-668.

Secondhand Smoke Causes Endothelial Dysfunction in Children

Secondhand Smoke Causes Endothelial Dysfunction in Children


from Heartwire — a professional news service of WebMD


June 6, 2007 — Children as young as 11 develop endothelial dysfunction in response to secondhand smoke, in a dose-dependent fashion, even when exposure is minimal, a new study suggests. The study adds to other evidence demonstrating the harmful effects of passive smoking in teenagers and adults. Dr Katariina Kallio (University of Turku, Turku, Finland) and colleagues report the results of their study in a Rapid Access issue of Circulation, June 4, 2007.

"Because endothelial dysfunction related to passive smoking may be only partially reversible after cessation of the exposure, the present data strongly emphasize the importance of implementing smoke-free environments for children at home and in public places," the authors write.

Study Highlites:


Families of 5-month-old infants were invited to participate in this prospective study from Finland. Subjects were randomized to receive education regarding cardiovascular risk factors in childhood or no intervention (control).

Serum cotinine levels were evaluated annually beginning at the age of 8 years, and flow-mediated vasodilatory responses were measured with ultrasonography of the brachial artery at the age of 11 years.

The main study outcome was the relationship between serum cotinine levels and endothelial function. To interpret this relationship, children were stratified into the following levels of cotinine: none, low (0.2 - 1.6 ng/mL), and top decile (1.7 ng/mL or greater). The main study result was adjusted for other cardiovascular risk factors, including serum lipid and high-sensitivity C-reactive protein levels.


402 (73% of the study cohort) children had ultrasound and cotinine data available for analysis. 57% of the children had undetectable levels of cotinine, whereas 33% and 10% of subjects fit into the low- and top-decile cotinine groups, respectively.

No child reported active smoking. 16% of mothers and 25% of fathers smoked.


There was no significant trend across cotinine groups in terms of body mass index, blood pressure, lipid levels, or C-reactive protein values.

Peak endothelium-dependent dilation fell as cotinine levels increased (9.10% in the no-cotinine group vs 8.57% and 7.73% in the low- and top-decile cotinine groups, respectively). This difference was significant after multivariate analysis. Serum cotinine level was also inversely associated with total dilation response.

Cotinine levels had no effect on brachial diameter at baseline, increase in blood flow after cuff release, or endothelium-independent dilation after administration of sublingual nitrate.

When the authors limited their analysis to only children with 4 cotinine values measured between the ages of 8 and 11 years, the relationship between higher cotinine concentrations and impaired endothelial function was even stronger.

Higher levels of low-density lipoprotein cholesterol also impaired flow-mediated dilation, but C-reactive protein levels did not significantly affect this outcome.

Pearls for Practice:

Both active and passive smoking can reduce levels of intra-arterial nitric oxide and impair endothelial function and as little as 30 minutes of passive smoke exposure can induce changes in coronary flow velocity reserve.

The current study demonstrates that exposure to environmental tobacco smoke impairs endothelium-dependent dilation in children.