Keila N. Lopez

Obesity: from the agricultural revolution to the contemporary pediatric epidemic.

Obesity is pandemic in Western society. Currently, approximately 100 million Americans are overweight (body mass index > 25 kg/m2) or obese (body mass index > 30 kg/m2). The pandemic is largely attributable to the relatively recent (from an evolutionary perspective) adoption of a sedentary lifestyle, coupled with the high availability of foods with high caloric content in Western cultures. These factors superimposed on dated genotypes have given rise to the global obesity epidemic. Over the past two decades, the discovery of leptin and other new molecules (e.g., adiponectin, resistin, ghrelin) has shed significant light on the pathophysiologic mechanisms of obesity-related morbidities, many of which became apparent through human epidemiologic studies during the last half of the 20th century. Of high concern for modern Western societies is the pediatric obesity epidemic, which stands to cripple Western cultures, both literally and financially in terms of health care costs and exhaustion of finite medical resources. The prevalence of childhood obesity has more than tripled since the 1960s, and 12.5 million (~17%) of children and teenagers are obese in the United States today. The rate of increasing prevalence of childhood obesity is staggering, and the collective efforts of the pediatric medical community and scientists are essential for battling the epidemic.

Web-based intervention for adolescent nonsmokers to help parents stop smoking: A pilot feasibility study

A novel approach to tobacco control is to engage adolescent nonsmokers in support roles to encourage and help their parents stop smoking. This pilot study examined the feasibility and potential efficacy of a web-based support skills training (SST) intervention for adolescents to help a parent stop smoking. Forty nonsmoking adolescents 13-19 years of age (70% female, 93% White) were enrolled and randomly assigned to a health education (HE) control group (n=20) or SST (n=20). Both consisted of written materials and five weekly, 30 min, web-based, counselor-facilitated group sessions. Parents were enrolled for assessments only. Adolescents and parents completed assessments at baseline, week 6 (post-treatment), week 12 and 6-months follow-up. Both interventions were feasible based on treatment acceptability ratings, study retention and treatment compliance. The biochemically confirmed 6-month smoking abstinence rate was higher for parents linked to teens in HE (35%, 7/20) than in SST (10%, 2/20), p=0.13. About half of parents in each group reported a quit attempt since study enrollment. Teens can be engaged to help parents stop smoking. Future research is warranted on determining effective intervention approaches.

Homozygous mutation in SCN5A associated with atrial quiescence, recalcitrant arrhythmias, and poor capture thresholds

Case report A 6-year-old Hispanic girl was referred to cardiology for irregular heartbeats. On electrocardiogram (ECG), she was noted to have sinus bradycardia with nonspecific intraventricular conduction delay, as well as frequent sinus pauses with junctional escape on Holter monitoring. Despite multiple attempts to contact her, she did not follow up, and at 11 years of age collapsed while running at school. She was unresponsive, and an automated external defibrillator determined her rhythm to be “shockable” ventricular tachycardia. After defibrillation, perfusion was re-established, and she was taken to a local emergency room, where a lidocaine infusion was initiated with temporary stabilization in her rhythm. While in the emergency room, she had recurrent episodes of unstable, sustained ventricular tachycardia, requiring 6 separate cardioversions and ongoing cardiopulmonary resuscitation. A chest radiograph showed moderate cardiomegaly. Electrocardiography revealed no discernible atrial activity, with a slow junctional escape and frequent premature ventricular contractions (Fig. 1). It also revealed low-voltage QRS complexes and a prolonged QT interval, although this was after cardiac arrest. Subsequent telemetry revealed frequent episodes of polymorphic ventricular tachycardia. An echocardiogram was performed, which revealed severely depressed biventricular function (ejection fraction 19%), with normal anatomy and coronary origins. Because of recurrent episodes of ventricular tachycardia/ventricular fibrillation, she was transitioned to an amiodarone infusion. She was transferred to our institution and was ultimately placed on extracorporeal membrane oxygenation for recalcitrant arrhythmias and progressive metabolic acidosis. In the operating room, it was noted that her atria were dilated and not contracting.

Pilot study of chronic maternal hyperoxygenation and effect on aortic and mitral valve annular dimensions in fetuses with left heart hypoplasia.

Acute maternal hyperoxygenation (AMH) results in increased fetal left heart blood flow. Our aim was to perform a pilot study to determine the safety, feasibility and direction and magnitude of effect of chronic maternal hyperoxygenation (CMH) on mitral and aortic valve annular dimensions in fetuses with left heart hypoplasia (LHH) after CMH.

Racial disparities in heterotaxy syndrome.

BACKGROUND Heterotaxy syndrome (HTX) is a constellation of defects including abnormal organ lateralization and often including congenital heart defects. HTX has widely divergent population-based estimates of prevalence, racial and ethnic predominance, and mortality in current literature. METHODS The objective of this study was to use a population-based registry to investigate potential racial and ethnic disparities in HTX. Using the Texas Birth Defects Registry, we described clinical features and mortality of HTX among infants delivered from 1999 to 2006. We calculated birth prevalence and crude prevalence (cPR) ratios for infant sex, maternal diabetes, and sociodemographic factors. RESULTS A total of 353 HTX cases were identified from 2,993,604 births (prevalence ratio = 1.18 per 10,000 live births. HTX prevalence was approximately 70% higher among infants of Hispanic and non-Hispanic black mothers and 28% higher among female infants (cPR = 1.28; 95% confidence interval,1.04-1.59). There was a twofold higher female preponderance for infants of mothers who were non-Hispanic white or black. Mothers with diabetes were three times more likely to have a child with HTX compared with nondiabetics (cPR = 3.13; 95% confidence interval, 2.12-4.45). Among nondiabetics, HTX cases were 86% more likely to have a Hispanic mother and 72% a non-Hispanic black mother. First-year mortality for live born children with HTX was 30.9%. CONCLUSION This study represents one of the largest population-based studies of HTX to date, with a novel finding of higher rates of HTX among Hispanic infants of mostly Mexican origin, as well as among female infants of only non-Hispanic white and black mothers. These findings warrant further investigation.

Comprehensive Neighborhood Portraits and Child Asthma Disparities

Objectives Previous research has established links between child, family, and neighborhood disadvantages and child asthma. We add to this literature by first characterizing neighborhoods in Houston, TX by demographic, economic, and air quality characteristics to establish differences in pediatric asthma diagnoses across neighborhoods. Second, we identify the relative risk of social, economic, and environmental risk factors for child asthma diagnoses. Methods We geocoded and linked electronic pediatric medical records to neighborhood-level social and economic indicators. Using latent profile modeling techniques, we identified Advantaged, Middle-class, and Disadvantaged neighborhoods. We then used a modified version of the Blinder-Oaxaca regression decomposition method to examine differences in asthma diagnoses across children in these different neighborhoods. Results Both compositional (the characteristics of the children and the ambient air quality in the neighborhood) and associational (the relationship between child and air quality characteristics and asthma) differences within the distinctive neighborhood contexts influence asthma outcomes. For example, unequal exposure to PM2.5 and O3 among children in Disadvantaged and Middle-class neighborhoods contribute to asthma diagnosis disparities within these contexts. For children in Disadvantaged and Advantaged neighborhoods, associational differences between racial/ethnic and socioeconomic characteristics and asthma diagnoses explain a significant proportion of the gap. Conclusions for Practice Our results provide evidence that differential exposure to pollution and protective factors associated with non-Hispanic White children and children from affluent families contribute to asthma disparities between neighborhoods. Future researchers should consider social and racial inequalities as more proximate drivers, not merely as associated, with asthma disparities in children.

Does neighborhood social and environmental context impact race/ethnic disparities in childhood asthma?

Abstract Utilizing over 140,000 geocoded medical records for a diverse sample of children ages 2–12 living in Houston, Texas, we examine whether a comprehensive set of neighborhood social and environmental characteristics explain racial and ethnic disparities in childhood asthma. Adjusting for all individual risk factors, as well as neighborhood concentrated disadvantage, particulate matter, ozone concentration, and race/ethnic composition, reduced but did not fully attenuate the higher odds of asthma diagnosis among black (OR=2.59, 95% CI=2.39, 2.80), Hispanic (OR=1.22, 95% CI=1.14, 1.32) and Asian (OR=1.18, 95% CI=1.04, 1.33) children relative to whites.

Public Health Research in Congenital Heart Disease

Public health research is an integral part of the study of congenital heart disease. While this type of research has become more popular, particularly over the past decade, it has a history that stretches back to almost the beginnings of pediatric cardiology as a field. This review aims to introduce the concepts and methodologies of public health and how they relate to congenital heart disease, describe some of the challenges of traditional research methods in congenital heart disease, describe the history of public health research, and demonstrate the relevance of public health research, particularly databases, to pediatric cardiology fellows.

Serum digoxin concentrations and clinical signs and symptoms of digoxin toxicity in the paediatric population

BACKGROUND Serum digoxin levels have limited utility for determining digoxin toxicity in adults. Paediatric data assessing the utility of monitoring serum digoxin concentration are scarce. We sought to determine whether serum digoxin concentrations are associated with signs and symptoms of digoxin toxicity in children. METHODS We carried out a retrospective review of patients 2 ng/ml). RESULTS There were 87 patients who met study criteria (male 46%, mean age 8.4 years). CHD was present in 67.8% and electrocardiograms were performed in 72.4% of the patients. The most common indication for digoxin toxicity was heart failure symptoms (61.5%). Toxic serum digoxin concentrations were present in 6.9% of patients (mean 2.6 ng/ml). Symptoms associated with digoxin toxicity occurred in 48.4%, with nausea/vomiting as the most common symptom (36.4%), followed by tachycardia (29.5%). Compared with those without toxic serum digoxin concentrations, significantly more patients with toxic serum digoxin concentrations were female (p=0.02). The presence of electrocardiogram abnormalities and/or signs and symptoms of digoxin toxicity was not significantly different between patients with and without serum digoxin concentrations (p>0.05). CONCLUSION Serum digoxin concentrations in children are not strongly associated with signs and symptoms of digoxin toxicity.

Increased Fracture Risk with Furosemide Use in Children with Congenital Heart Disease

Objectives To determine the association of furosemide therapy with the incidence of bone fractures in children with congenital heart disease. Study design We conducted a retrospective cohort study with data extracted from the 2008‐2014 Texas Medicaid databases. Pediatric patients aged <12 years diagnosed with congenital heart disease, cardiomyopathy, or heart failure were included. Patients taking furosemide were categorized into a furosemide‐adherent group (medication possession ratio of ≥70%), and a furosemide‐nonadherent group (medication possession ratio of <70%). A third group of patients was matched to the furosemide user groups by using propensity score matching. A multivariate logistic regression and Cox proportional hazard model with a Kaplan–Meier plot (time‐to‐fracture) were used to compare the 3 groups, controlling for baseline demographics and clinical characteristics. Results After matching, 3912 patients (furosemide adherent, n = 254; furosemide nonadherent, n = 724; no furosemide, n = 2934) were identified. The incidence of fractures was highest for the furosemide‐adherent group (9.1%; 23 of 254), followed by the furosemide‐nonadherent group (7.2%; 52 of 724), which were both higher than for patients who did not receive furosemide (5.0%; 148 of 2934) (P < .001). Using logistic regression, both furosemide groups were more likely to have fractures than the no furosemide group: furosemide‐adherent OR of 1.9 (95% CI, 1.17‐2.98; P = .009); furosemide nonadherent OR of 1.5 (95% CI, 1.10‐2.14; P = .01). In the Cox proportional hazard model, the risk of fractures for the furosemide‐adherent group was significantly higher compared with the no furosemide group (HR, 1.6; 95% CI, 1.00‐2.42; P = .04). Conclusions Furosemide therapy, even with nonconsistent dosing, was associated with an increased risk of bone fractures in children with congenital heart disease.