Environmental Exposures and Pediatric Cardiology: A Scientific Statement From the American Heart Association.

Environmental toxicants and pollutants are causes of adverse health consequences, including well-established associations between environmental exposures and cardiovascular diseases. Environmental degradation is widely prevalent and has a long latency period between exposure and health outcome, potentially placing a large number of individuals at risk of these health consequences. Emerging evidence suggests that environmental exposures in early life may be key risk factors for cardiovascular conditions across the life span. Children are a particularly sensitive population for the detrimental effects of environmental toxicants and pollutants given the long-term cumulative effects of early-life exposures on health outcomes, including congenital heart disease, acquired cardiac diseases, and accumulation of cardiovascular disease risk factors. This scientific statement highlights representative examples for each of these cardiovascular disease subtypes and their determinants, focusing specifically on the associations between climate change and congenital heart disease, airborne particulate matter and Kawasaki disease, blood lead levels and blood pressure, and endocrine-disrupting chemicals with cardiometabolic risk factors. Because children are particularly dependent on their caregivers to address their health concerns, this scientific statement highlights the need for clinicians, research scientists, and policymakers to focus more on the linkages of environmental exposures with cardiovascular conditions in children and adolescents.

Food Is Medicine: A Presidential Advisory From the American Heart Association.

Unhealthy diets are a major impediment to achieving a healthier population in the United States. Although there is a relatively clear sense of what constitutes a healthy diet, most of the US population does not eat healthy food at rates consistent with the recommended clinical guidelines. An abundance of barriers, including food and nutrition insecurity, how food is marketed and advertised, access to and affordability of healthy foods, and behavioral challenges such as a focus on immediate versus delayed gratification, stand in the way of healthier dietary patterns for many Americans. Food Is Medicine may be defined as the provision of healthy food resources to prevent, manage, or treat specific clinical conditions in coordination with the health care sector. Although the field has promise, relatively few studies have been conducted with designs that provide strong evidence of associations between Food Is Medicine interventions and health outcomes or health costs. Much work needs to be done to create a stronger body of evidence that convincingly demonstrates the effectiveness and cost-effectiveness of different types of Food Is Medicine interventions. An estimated 90% of the $4.3 trillion annual cost of health care in the United States is spent on medical care for chronic disease. For many of these diseases, diet is a major risk factor, so even modest improvements in diet could have a significant impact. This presidential advisory offers an overview of the state of the field of Food Is Medicine and a road map for a new research initiative that strategically approaches the outstanding questions in the field while prioritizing a human-centered design approach to achieve high rates of patient engagement and sustained behavior change. This will ideally happen in the context of broader efforts to use a health equity-centered approach to enhance the ways in which our food system and related policies support improvements in health.

Toward a Roadmap for Best Practices in Pediatric Preventive Cardiology: A Science Advisory From the American Heart Association.

Cardiovascular disease risk factors are highly prevalent among youth in the United States and Canada. Pediatric preventive cardiology programs have independently developed and proliferated to address cardiovascular risk factors in youth, but there is a general lack of clarity on best practices to optimize and sustain desired outcomes. We conducted surveys of pediatric cardiology division directors and pediatric preventive cardiology clinicians across the United States and Canada to describe the current landscape and perspectives on future directions for the field. We summarize the data and conclude with a call to action for various audiences who seek to improve cardiovascular health in youth, reduce the burden of premature cardiovascular disease, and increase healthy longevity. We call on heart centers, hospitals, payers, and policymakers to invest resources in the important work of pediatric preventive cardiology programs. We urge professional societies to advocate for pediatric preventive cardiology and provide opportunities for training and cross-pollination across programs. We encourage researchers to close evidence gaps. Last, we invite pediatric preventive cardiology clinicians to collaborate and innovate to advance the practice of pediatric preventive cardiology.

Arterial stiffness but not carotid intima-media thickness progression precedes premature structural and functional cardiac damage in youth: A 7-year temporal and mediation longitudinal study.

BACKGROUND AND AIMS: The longitudinal relations of cardiac indices with the aorta and carotid vessel and the time sequence for early cardiac disease development are uncharacterized in youth. We examined the temporal longitudinal associations of carotid-femoral pulse wave velocity (cfPWV) and carotid intima-media thickness (cIMT) with left ventricular hypertrophy (LVH) and diastolic dysfunction (LVDD). METHODS: From the Avon Longitudinal Study of Parents and Children, UK birth cohort, 1856 adolescents (1011 females) at a mean (SD) age 17.7 (0.3) years were followed up for 7 years. Vicorder-measured cfPWV and ultrasound-measured cIMT were grouped in tertiles as low (reference), moderate, and high. Echocardiography measured cardiac abnormalities are left ventricular mass indexed for height2.7 (LVMI2.7) ≥51 g/m2.7 as LVH; relative wall thickness ≥44 as hiRWT; LVD function E/A <1.5 as LVD dysfunction (LVDD); and LV filling pressure E/e' ≥8 as hiLVFP. Data were analysed with generalized logit mixed-effect models, cross-lagged path, and mediation structural equation models adjusting for cardiometabolic and lifestyle factors. RESULTS: Over follow-up, LVH prevalence increased from 3.6% to 7.2% and LVDD from 11.1 to 16.3%. High cfPWV progression was associated with worsening LVH [Odds ratio 1.23 (1.13-1.35); p < 0.001] in the total cohort, males, overweight/obese, and normotensive. High cfPWV progression was associated with worsening hiLVFP in the total cohort, females, and normal weight. Likewise, high cIMT progression was associated with worsening LVH [1.27 (1.26-1.27); p < 0.0001] in the total cohort, overweight/obese and elevated BP/hypertensive. Neither cfPWV nor cIMT progression was associated with worsening hiRWT in the total cohort. In cross-lagged models, higher baseline cfPWV was associated with future LVMI2.7 (ß = 0.06, SE, 5.14, p = 0.035), RWT, LVDF, and LVFP. However, baseline LVMI2.7, RWT, LVDF, and LVFP were not associated with follow-up cfPWV. Baseline cIMT was not associated with follow-up cardiac indices and vice versa. Cumulative increased systolic blood pressure (34.3% mediation) and insulin resistance (15.1% mediation) mediated the direct associations of cumulative cfPWV with cumulative LVMI2.7. CONCLUSIONS: Arterial stiffness progression temporally preceded worsening structural and functional cardiac damage in youth with increased systolic blood pressure and insulin resistance partly mediating the relationships. Future interventions aimed at attenuating premature cardiac damage in adolescents and young adults may consider a simultaneous treatment of both arterial stiffness, elevated blood pressure and insulin resistance.

Effect of exogenous l-carnitine on aortic stiffness in dyslipidemic adolescents: Design of a quadruple-blind, randomized, controlled interventional trial.

Background: Atherosclerotic cardiovascular disease (ASCVD) risk factors including vascular remodeling leading to hypertension and dyslipidemia are prevalent among children and adolescents. Conflicting observational and Mendelian randomization data suggest endogenous carnitine may affect arterial stiffness and lipid traits. Because of this, we developed a study to evaluate the causal role for carnitine in arterial stiffness at a point when the lifecourse trajectory to hypertension can be modified. Methods: This study is a mechanistic, double-blinded, randomized control trial (RCT) in 166 adolescents with dyslipidemia for the effect of 6 months of maximum dose 3 g daily oral l-carnitine supplementation (CS+) versus placebo (CS-) on aortic stiffness measured as carotid-femoral pulse wave velocity (CFPWV) and pulse pressure (PP); lipid concentrations (total cholesterol, HDL-C, triglycerides, and LDL-C) and serum fatty acid oxidation biomarkers by metabolomic analysis. Conclusions: The simultaneous evaluation of endogenous carnitine genetic effects and exogenous l-carnitine supplementation may facilitate future therapies for youth with cardiometabolic derangement to arrest atherosclerotic changes.

Coarctation of the Aorta: Modern Paradigms Across the Lifespan.

While coarctation of the aorta varies greatly in both severity and age at presentation, all patients are at increased risk of hypertension both before and after repair. Despite advances in knowledge about genetic etiologies, pathophysiologic mechanisms, and optimal repair strategies, patients with repaired coarctation of the aorta remain at increased risk of acquired cardiovascular disease. The aims of this review are to describe the management of coarctation of the aorta at all ages before and after repair, highlight pathophysiologic mechanisms of hypertension, and review long-term follow-up considerations.

Double-Trouble: Atherosclerotic Risk Factors and Congenital Heart Disease.

PURPOSE OF REVIEW: Youth with congenital heart disease (CHD) are uniquely vulnerable to genetic and acquired atherosclerotic cardiovascular disease (ASCVD) risk factors. With the increasingly successful management of CHD, it is important to prevent or optimally managed risk factors with the goal of improving outcomes and longevity. RECENT FINDINGS: This review summarizes guidelines for the evaluation and management of obesity, dyslipidemia, and hypertension in youth (< 18 years of age), focusing on the special vulnerabilities associated with the type of repair and the presence of residual disease in those who undergo cardiac surgery. Clinicians must focus on targeting these highly prevalent ASCVD risk factors to protect CHD survivors from preventable ASCVD morbidity and mortality by applying lifestyle, pharmacologic, or surgical therapies as needed. Future work should examine interventions to identify and treat ASCVD risk factors in CHD patients. Given the increased prevalence of ASCVD risk factors in youth and the morbidity and premature mortality associated with CHD, it is important for clinicians to assess global risk factors in these patients frequently, encourage adherence to lifestyle changes, and recommend pharmacotherapy and surgical interventions when clinically indicated. Future efforts should identify barriers and opportunities for improving risk factor assessment and timely intervention as a routine part of clinical care.

Cumulative insulin resistance and hyperglycemia with arterial stiffness and carotid IMT progression in 1,779 adolescents: a 9-yr longitudinal cohort study.

In pediatric population with diabetes and obesity, insulin resistance (HOMA-IR) has been associated with worsening vascular outcomes, however, the cumulative role of HOMA-IR, hyperglycemia, and hyperinsulinemia on repeatedly measured vascular outcomes in asymptomatic youth is unknown. We examined the longitudinal associations of fasting glucose, insulin, and HOMA-IR with carotid-femoral pulse wave velocity (cfPWV) and carotid intima-media thickness (cIMT). From the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort, UK 1,779, 15-yr-old participants were followed up for 9 yr. Glucose, insulin, and HOMA-IR assessed at 15, 17, and 24 yr and sex-specifically dichotomized as ≥75th percentile, indicating high category and <75th percentile as reference. cfPWV and cIMT were measured at ages 17 and 24 yr. Associations were examined using linear mixed-effect models adjusted for cardiometabolic and lifestyle covariates. Among 1,779 participants [49.9% female], glucose, insulin, and HOMA-IR had a J- or U-shaped increase from ages 15 through 24 yr. The cumulative exposures to hyperinsulinemia effect estimate -0.019 mU/L; [95% CI -0.019 to -0.002; P = 0.033] and high HOMA-IR: -0.021; [-0.039 to -0.004; P = 0.019] from 15 to 24 yr of age were negatively associated with the 7-yr cfPWV progression. Only cumulative hyperinsulinemia and high HOMA-IR from ages 15 to 17 yr but not from ages 17 to 24 yr was associated with decreased cfPWV progression. There were no associations between cumulative hyperglycemia and cfPWV or cIMT progression. Hyperinsulinemia and HOMA-IR were not associated with cIMT progression. In conclusion, late adolescence may be an optimal timing for intervention targeted at sustaining the protective effect of the decline of insulin and insulin resistance on arterial stiffness progression.NEW & NOTEWORTHY Fasting plasma glucose, insulin, and insulin resistance had a J- or U-shaped increase from 15 to 24 yr with the base of the curve at age 17 yr. Cumulative high insulin and high insulin resistance from 15 to 24 yr were negatively associated with arterial stiffness progression from ages 17 to 24 yr. Age 17 yr may be an optimal timing for intervention targeted at sustaining the protective effect of the decline of insulin and insulin resistance on arterial stiffness progression.

Ambulatory Blood Pressure Monitoring in Children and Adolescents: 2022 Update: A Scientific Statement From the American Heart Association.

Use of ambulatory blood pressure monitoring in children and adolescents has markedly increased since publication of the last American Heart Association scientific statement on pediatric ambulatory blood pressure monitoring in 2014. In addition, there has also been significant expansion of the evidence base for use of ambulatory blood pressure monitoring in the pediatric population, including new data linking ambulatory blood pressure levels with the development of blood pressure-related target organ damage. Last, additional data have recently been published that enable simplification of the classification of pediatric ambulatory monitoring studies. This scientific statement presents a succinct review of this new evidence, guidance on optimal application of ambulatory blood pressure monitoring in the clinical setting, and an updated classification scheme for the interpretation of ambulatory blood pressure monitoring in children and adolescents. We also highlight areas of uncertainty where additional research is needed.

Causal Inference of Carnitine on Blood Pressure and potential mediation by uric acid: A mendelian randomization analysis.

BACKGROUND: Dietary change alters blood pressure (BP) but the specific causal dietary elements are unclear. Given previous observational data suggesting serum carnitine or uric acid affect BP, we investigated the role of serum carnitine and serum uric acid concentrations on BP, and considered mediation by lipids and insulin resistance using two-sample bi-directional Mendelian randomization (MR) analysis. METHODS: We performed MR to characterize bi-directional causal relationships of carnitine or uric acid on cardiometabolic traits. We performed two-sample MR using genome-wide association summary data from separate large-scale genomic analyses of carnitine, uric acid, BP, lipids, and glycemic traits. We used inverse variance weighted (IVW) meta-analysis and MR Egger regression to test for causal relations in the absence and presence of pleiotropy, respectively, and performed sensitivity analyses to identify confounders and intermediates. RESULTS: In our analysis, carnitine was directly, causally associated with systolic BP (IVW effect = 0.2, causal p-value = 0.03) but not diastolic BP (IVW causal p = 0.1). Our findings additionally support direct and indirect relationships of carnitine on TG and on uric acid. No causal associations of carnitine were found with glycemic traits. Uric acid was not associated with BP, nor TG. CONCLUSION: Two-sample bi-directional MR demonstrated an unconfounded causal effect of carnitine, but not uric acid, on systolic but not diastolic BP, suggesting a role of carnitine in arterial stiffness. Carnitine, but not uric acid, also has direct and indirect effects on TG but are independent of the causal effect of carnitine on systolic BP.

Pediatric Ambulatory Blood Pressure Classification: The Case for a Change.

In 1997, Soergel et al1 published the first set of normative values for ambulatory blood pressure monitoring (ABPM) in children. Since then, the clinical utility of ABPM has increased dramatically, and now, ABPM is accepted as the standard method to confirm the diagnosis of hypertension in children. Despite significant progress in the field of pediatric ABPM, many important questions remain unanswered. One of the most controversial issues is how to define ambulatory hypertension in children. The purpose of this review is to discuss the limitations of the current pediatric ABPM classification scheme and to provide the justification and rationale for a new classification.

Sleep-Disordered Breathing and Cardiovascular Disease in Children and Adolescents: A Scientific Statement From the American Heart Association.

Obstructive sleep apnea (OSA) is a known risk factor for cardiovascular disease in adults. It is associated with incident systemic hypertension, arrhythmia, stroke, coronary artery disease, and heart failure. OSA is common in children and adolescents, but there has been less focus on OSA as a primary risk factor for cardiovascular disease in children and adolescents. This scientific statement summarizes what is known regarding the impact of sleep-disordered breathing and, in particular, OSA on the cardiovascular health of children and adolescents. This statement highlights what is known regarding the impact of OSA on the risk for hypertension, arrhythmia, abnormal ventricular morphology, impaired ventricular contractility, and elevated right heart pressure among children and adolescents. This scientific statement also summarizes current best practices for the diagnosis and evaluation of cardiovascular disease-related complications of OSA in children and adolescents with sleep apnea and highlights potential future research in the area of sleep-disordered breathing and cardiovascular health during childhood and adolescence.

Pediatric Lipid Disorders.

Current scientific evidence has proven that atherosclerosis is a process that begins in childhood and tracks into adulthood, likely culminating in adverse cardiovascular events such as coronary artery disease, peripheral artery disease, and stroke. In addition, the obesity epidemic and increasing awareness of genetic lipid disorders has made the understanding and management of lipid disorders necessary for pediatricians. Childhood offers a unique opportunity for preventing, modifying, or eliminating risk factors and, in doing so, reversing or slowing the process of atherosclerosis. In general, management involves targeted lifestyle interventions such as strict dietary changes and increases in physical activity. In some circumstances, pharmacotherapy, even in childhood, is warranted. [Pediatr Ann. 2021;50(3):e105-e112.].

Pediatric multisystem SARS COV2 with versus without cardiac involvement: a multicenter study from Latin America.

Latin America (LATAM) children offer special insight into Severe Acute Respiratory Syndrome Coronavirus 2 (SARS COV2) due to high-risk race/ethnicity, variability in medical resources, diverse socioeconomic background, and numerous involved organ systems. This multinational study of LATAM youth examined the distinguishing features of acute or late multisystem SARS COV2 with versus without cardiac involvement. A consecutive sample of youth 0-18 years old (N = 98;50% male) presenting with multisystem SARS COV2 to 32 centers in 10 Latin American countries participating in a pediatric cardiac multi-imaging society were grouped as with versus without cardiac involvement, defined as abnormal echocardiographic findings or arrhythmia. Collected clinical data were analyzed by Student's t-test or Fisher's exact test. Cardiac (N = 48, 50% male) versus no cardiac (N = 50, 50% male) were similar in age; weight; nonrespiratory symptoms; and medical history. The cardiac group had 1 death and symptoms including coronary artery dilation, ejection fraction <50%, pericardial effusion, peripheral edema, arrhythmia, and pulmonary artery thrombus. The cardiac group had higher risk of ICU admission (77% vs 54%, p = 0.02); invasive ventilation (23% vs 4%,p = 0.007); vasoactive infusions (27% vs 4%, p = 0.002); prominent respiratory symptoms (60% vs 36%, p < 0.03); abnormal chest imaging (69% vs 34%, p = 0.001); troponin (33% vs 12%, p = 0.01); alanine aminotransferase (33% vs 12%, p = 0.02); and thrombocytopenia (46% vs 22%, p = 0.02). Receiver operating curve analysis showed that abnormal laboratories had 94% sensitivity and 98% negative predictive value on the need for ICU interventions.Conclusion: In LATAM children with multisystem SARS COV2, cardiac involvement was prevalent. Cardiac involvement was more likely to require ICU interventions, certain abnormal labs, and respiratory involvement. What is Known: • SARS COV2 can be asymptomatic in children but in some cases can have serious multisystemic involvement. • Hispanic ethnicity is purportedly at high risk of SARS COV2 in nations where they are often disadvantaged minority populations. What is New: • Latin American children presenting with multisystem SARS COV2 frequently have cardiac involvement which was associated with ICU interventions; prominent respiratory symptoms; abnormal chest X-ray; elevated troponin, ALT, and thrombocytopenia. • Elevated troponin, ALT or thrombocytopenia had high sensitivity and negative predictive value on the need for intensive care interventions.

Biological Pathways in Adolescent Aortic Stiffness.

Background Aortic stiffening begins in youth and antedates future hypertension. In adults, excess weight, systemic inflammation, dyslipidemia, insulin resistance, neurohormonal activation, and altered adipokines are implicated in the pathogenesis of increased aortic stiffness. In adolescents, we assessed the relations of comprehensive measures of aortic stiffness with body mass index (BMI) and related but distinct circulating biomarkers. Methods and Results A convenience sample of 246 adolescents (mean age, 16±2 years; 45% female, 24% Black, and 43% Hispanic) attending primary care or preventive cardiology clinics at 2 tertiary hospitals was grouped as normal weight (N=98) or excess weight (N=148, defined as BMI ≥age- and sex-referenced 85th percentile). After an overnight fast, participants underwent anthropometry, noninvasive arterial tonometry, and assays for serum lipids, CRP (C-reactive protein), glucose, insulin, renin, aldosterone, and leptin. We used multivariable linear regression to relate arterial stiffness markers (including carotid-femoral pulse wave velocity) to BMI z score and a biomarker panel. Carotid-femoral pulse wave velocity was higher in excess weight compared with normal weight group (5.0±0.7 versus 4.6±0.6 m/s; P<0.01). After multivariable adjustment, carotid-femoral pulse wave velocity was associated with BMI z score (0.09 [95% CI, 0.01-0.18]; P=0.04) and with low-density lipoprotein cholesterol (0.26 [95% CI, 0.03-0.50]; P=0.03). Conclusions Higher BMI and low-density lipoprotein cholesterol were associated with greater aortic stiffness in adolescents. Maintaining optimal BMI and lipid levels may mitigate aortic stiffness.

Lipid temporal trends in normal-weight youth.

Atherosclerosis begins in youth, partly driven by excess weight (EW) and abnormal lipids. Despite pediatric obesity worsening, lipids improved. Given the relation between EW and abnormal lipids, changes in normal-weight (NW) youth may be relevant. We examined the proportions and temporal trends of youth with abnormal lipids who were NW versus EW. METHODS: Analysis was done from National Health and Nutrition Examination Surveys 1988-2016. Data were extracted for 10- to 20-year-olds measured with anthropometrics and laboratory testing to determine proportions of NW versus EW with total cholesterol >190 mg/dL, high-density lipoprotein cholesterol (HDL-C) <40 mg/dL, and calculated non-HDL-C >145 mg/dL (N = 14,785). In survey-weighted regression analysis, a weight-status interaction term was used to examine effect modification in the lipid temporal trend. RESULTS: Over time, EW prevalence increased, whereas dyslipidemia decreased (trend P value < .001 for both). For the pooled sample, EW more than doubled the risk of each lipid disorder (P < .0001 for each). However, for each abnormal lipid, 26%-63% were NW. As the temporal trend in abnormal lipids declined, the proportion with abnormal lipids who were NW also declined. On regression analysis, temporal declines in NW and EW differed for HDL-C. CONCLUSIONS: NW constituted more than a quarter to half of youth with abnormal lipids. Over time, youth with abnormal lipids were less often NW. The novel observation that a high proportion of youth with abnormal lipids are NW is relevant to debates on universal lipid screening, the focus on weight reduction in youth lipid management, and conventional wisdom in cardiometabolic health.

Pediatric Obesity, Hypertension, Lipids.

PURPOSE OF REVIEW: The rise of the pediatric obesity pandemic over the past 40 years has sharpened focus on the management of obesity, hypertension and lipid abnormalities in children. Multiple studies demonstrate that these risk factors track from childhood into adulthood predisposing individuals to premature atherosclerotic cardiovascular disease and putting them at risk for early morbidity and mortality. RECENT FINDINGS: Importantly, obesity, hypertension and lipid problems are individual risk factors that can occur independently. Multiple studies have shown that each risk factor causes target organ damage in children. Intensive and focused lifestyle modifications can improve a child's subclinical disease and decrease the risk for future morbidity. SUMMARY: Childhood offers a unique opportunity at primordial and primary prevention of atherosclerotic cardiovascular disease. Clinicians must focus on targeting these highly prevalent conditions and applying lifestyle modification and then pharmacologic or surgical therapies as needed.

The relationship between payer type and lipid outcomes in response to clinical lifestyle interventions in youth with dyslipidemia.

BACKGROUND: Payer-type (government-sponsored health coverage versus private health insurance) has been shown to influence a variety of cardiovascular disease outcomes in adults. However, it is unclear if the payer-type impacts the response to a lifestyle intervention in children with dyslipidemia. METHODS: We analyzed data prospectively collected from patients under the age of 25 years who were referred to a large regional preventive cardiology clinic from 2010 to 2016 in Massachusetts. We compared baseline high density lipoprotein cholesterol (HDL-C), triglycerides (TG), non-HDL-C, and low density lipoprotein cholesterol (LDL-C) by payer-type. Further, we analyzed the change in lipid values in response to a clinic-based multidisciplinary intervention over a nearly six-year period by payer-type with multi-variable adjusted linear regression models. We also tested for effect modifications by age, sex, race, and body mass index (BMI) category. RESULTS: Of the 1739 eligible patients (mean age 13 years, 52% female, 60% overweight and obese, 59% White), we found that patients with government-sponsored coverage (n = 354, 20%) presented to referral lipid clinic with lower HDL-C (- 3.5 mg/dL [1.0], p < 0.001) and higher natural log-transformed TG (+ 0.14 [0.04], p < 0.001) as compared to those with private insurance; however, the association was attenuated to the null after additionally adjusting for BMI category (- 1.1 [0.9], p = 0.13, and + 0.05 [0.04], p = 0.2 for HDL-C and natural log-transformed TG, respectively). We found no difference in baseline LDL-C between payer-types (+ 3.4 mg/dL [3.0], p = 0.3). However, longitudinally, we found patients with private insurance and a self-reported race of White to have a clinically meaningful additional improvement in LDL-C, decreasing 12.8 (5.5) mg/dL (p = 0.02) between baseline and first follow-up, as compared to White patients with government-sponsored health coverage, after adjusting for age, sex, time between visits, and baseline LDL-C. CONCLUSIONS: Our results suggest that youth with government-sponsored coverage are referred with poorer lipid profiles than those with private insurance, although this is largely explained by higher rates of overweight and obesity in the government-sponsored health coverage group. White patients with private insurance had substantially better improvement in LDL-C longitudinally, suggesting that higher socioeconomic status facilitates improvement in LDL-C, but is less beneficial for HDL-C and triglyceride levels.