Childhood Psychosocial Determinants of Cardiovascular Health

Understanding risk and protective factors that impact cardiovascular health is of utmost importance. There is ample evidence that cardiovascular health begins in childhood, tracks over time, and is subject to adverse social influences. This paper reviews key studies examining the relations of psychosocial factors in childhood to cardiovascular health in adulthood. The existing literature provides evidence for both individual and cumulative effects of childhood psychosocial factors on adult cardiovascular health across the population, although the specific mechanisms underlying these relationships are not yet fully understood. This paper also includes a discussion of evidence-based strategies for prevention and treatment of childhood psychosocial problems. The extent to which these programs lead to improved cardiovascular health in high-risk groups or across the population by impacting psychosocial factors has not yet been studied, but is a clear future direction for research and policy

Causes and Mechanisms, an Interview with Dr. Jeremiah Stamler

Dr. Jeremiah Stamler began his career in New York City and moved to Chicago in 1947 with his wife Rose, to accept a basic research position with Dr. Louis N. Katz. Early animal studies convinced him of the role of dietary factors, particularly cholesterol and salt, in the etiology of atherosclerotic vascular disease. Because of a strong interest in public health, he began the first of many population based cohort studies in the 1950s that subsequently defined the role of health behaviors (adverse nutrition choices, tobacco use, low physical activity) and associated measurable biologic traits, now called risk factors, in the causation of the cardiovascular disease epidemic then at its peak in the United States. He began his professional work in preventive medicine with the City of Chicago Health Department and subsequently developed the Department of Preventive Medicine at Northwestern University Medical School where he now serves as professor emeritus. His research, leadership, and teaching have been critical in defining the contemporary roles of both the American Heart Association (AHA) and the National Heart, Lung, and Blood Institute. He remains an active investigator at age 85. I interviewed Dr. Stamler at his home

Familial Hypercholesterolemia: A Decade of Progress

Natural history studies of familial hypercholesterolemia (FH), a genetic disorder associated with elevated cholesterol and premature coronary artery disease, and with a frequency of about 1:500 in the general population, were first conducted in the 1970s. 1 Homozygotes, with cholesterol levels in excess of 500 mg/dl experience coronary events as early as adolescence and heterozygotes (with one normal and one abnormal gene) are affected prematurely in middle age. The first major breakthrough in understanding the disease came with the discovery of the low density lipoprotein (LDL) receptor by Brown and Goldstein, work that won the Nobel prize

Childhood obesity and blood pressure: back to the future?

The prevalence of childhood hypertension is increasing.1, 2 Studies that apply the 95th percentile definition and repeat measurements on three separate visits, report a pediatric hypertension prevalence of approximately 3.5%3, 4, and among obese children and adolescents the prevalence of both hypertension and prehypertension is even greater. The recently documented increase in hypertension among the young is due largely to the childhood obesity epidemic and possibly other secular changes in lifestyles. These publications and others confirm that hypertension is a prevalent child health condition, especially among overweight and obese children. A consistent positive association between body size and blood pressure level has been observed throughout childhood and adulthood. The report in this issue by Tu et al5 add additional insights on the impact of excess adiposity on blood pressure levels in childhood

Screening for familial hypercholesterolaemia in primary care: Time for general practice to play its part

Fifty per cent of first-degree relatives of index cases with familial hypercholesterolemia (FH) inherit the disorder. Despite cascade screening being the most cost-effective method for detecting new cases, only a minority of individuals with FH are currently identified. Primary care is a key target area to increase identification of new index cases and initiate cascade screening, thereby finding close relatives of all probands. Increasing public and health professional awareness about FH is essential. In the United Kingdom and in Australia, most of the population are reviewed by a General Practitioner (GP) at least once over a three-year period, offering opportunities to check for FH as part of routine clinical consultations. Such opportunistic approaches can be supplemented by systematically searching electronic health records with information technology tools that identify high risk patients. GPs can help investigate and implement results of this data retrieval. Current evidence suggests that early detection of FH and cascade testing meet most of the criteria for a worthwhile screening program. Among heterozygous patients the long latent period before the expected onset of coronary artery disease provides an opportunity for initiating effective drug and lifestyle changes. The greatest challenge for primary care is to implement an efficacious model of care that incorporates sustainable identification and management pathways

Adolescent and adult African Americans have similar metabolic dyslipidemia.

BACKGROUND: African Americans (AAs) have lower triglyceride (TG) and higher high-density lipoprotein cholesterol (HDL-C) than other ethnic groups; yet, they also have higher risk for developing diabetes mellitus despite the strong relationship of dyslipidemia with insulin resistance. No studies directly compare adolescents and adults with regard to relationships among dyslipidemia, high-sensitivity C-reactive protein (hs-CRP), and insulin resistance. Here, we compare AA adolescents to adults with regard to the relationships of adiposity-related lipid risk markers (TG-to-HDL ratio and non-HDL-C) with body mass index (BMI), waist circumference (WC), homeostasis model of insulin resistance (HOMA), and hs-CRP. METHODS: Two cohorts of healthy AA were recruited from the same urban community. Participants in each cohort were stratified by TG-to-HDL ratio (based on adult tertiles) and non-HDL-C levels. BMI, WC, HOMA, and hs-CRP were compared in adolescents and adults in the low-, middle-, and high-lipid strata. RESULTS: Prevalence of TG-to-HDL ratio greater than 2.028 (high group) was 16% (44 of 283) in adolescents and 33% (161 of 484) in adults; prevalence of non-HDL-C above 145 and 160, respectively, was 8% (22 of 283) in adolescents and 12% (60 of 484) in adults. Values of hs-CRP were lower, and HOMA values were higher in adolescents (both P \u3c .01). As both TG-to-HDL ratio and non-HDL-C strata increased, BMI, WC, HOMA, and hs-CRP increased in both adolescents and adults. In the high TG-to-HDL ratio and non-HDL-C groups, BMI and WC were similar in adolescents vs adults (BMI, 34 kg/m(2) vs 32 kg/m(2); WC, 101 cm vs 101 cm). After adjusting for non-HDL-C and other covariates, a 2-fold increase in TG-to-HDL ratio was associated with increases of 10.4% in hs-CRP (95% CI, 1.1%-20.5%) and 24.2% in HOMA (95% CI, 16.4%-32.6%). Non-HDL-C was not significant in models having TG-to-HDL ratio. CONCLUSION: The elevated TG-to-HDL ratio is associated with similar inflammation and metabolic risk relationships in adolescent and adult AAs

Associations of cardiac structure with obesity, blood pressure, inflammation, and insulin resistance in African-American adolescents.

To determine if obesity, blood pressure (BP), markers of inflammation, and insulin resistance are associated with cardiac structure in African-American adolescents, a cross-sectional study was performed on a cohort oversampled for high BP and obesity. Measurements included the following: anthropometrics, BP, homeostasis model assessment (HOMA) to assess insulin resistance, high-sensitivity C-reactive protein, and plasma adipokines (adiponectin, interleukin-6, plasminogen activator inhibitor-1). Echocardiogram measurements were left-ventricular mass index (LVMI) (g/m(2.7)), LV relative wall thickness (LVRWT), left-atrial diameter index [LADI (mm/m)], and LV diastolic time intervals. LADI (r (2) = 0.25) was associated with body mass index (BMI) systolic BP (SBP) and female sex. LVMI (r (2) = 0.35) variation was associated with BMI SBP, heart rate, age, and male sex. LVRWT (r (2) = 0.05) was associated with HOMA. Tissue diastolic intervals were not associated with any risk factor. Inflammatory markers and adipokines were associated with BMI but were not independently associated with any echocardiographic measures. In African-American adolescents, BMI and SBP, but not inflammatory markers or adipokines, are important correlates of LA size and LVM

Serum Non-high-density lipoprotein cholesterol concentration and risk of death from cardiovascular diseases among U.S. adults with diagnosed diabetes: the Third National Health and Nutrition Examination Survey linked mortality study

<p>Abstract</p> <p>Background</p> <p>Non-high-density lipoprotein cholesterol (non-HDL-C) measures all atherogenic apolipoprotein B-containing lipoproteins and predicts risk of cardiovascular diseases (CVD). The association of non-HDL-C with risk of death from CVD in diabetes is not well understood. This study assessed the hypothesis that, among adults with diabetes, non-HDL-C may be related to the risk of death from CVD.</p> <p>Methods</p> <p>We analyzed data from 1,122 adults aged 20 years and older with diagnosed diabetes who participated in the Third National Health and Nutrition Examination Survey linked mortality study (299 deaths from CVD according to underlying cause of death; median follow-up length, 12.4 years).</p> <p>Results</p> <p>Compared to participants with serum non-HDL-C concentrations of 35 to 129 mg/dL, those with higher serum levels had a higher risk of death from total CVD: the RRs were 1.34 (95% CI: 0.75-2.39) and 2.25 (95% CI: 1.30-3.91) for non-HDL-C concentrations of 130-189 mg/dL and 190-403 mg/dL, respectively (<it>P </it>= 0.003 for linear trend) after adjustment for demographic characteristics and selected risk factors. In subgroup analyses, significant linear trends were identified for the risk of death from ischemic heart disease: the RRs were 1.59 (95% CI: 0.76-3.32) and 2.50 (95% CI: 1.28-4.89) (<it>P </it>= 0.006 for linear trend), and stroke: the RRs were 3.37 (95% CI: 0.95-11.90) and 5.81 (95% CI: 1.96-17.25) (<it>P </it>= 0.001 for linear trend).</p> <p>Conclusions</p> <p>In diabetics, higher serum non-HDL-C concentrations were significantly associated with increased risk of death from CVD. Our prospective data support the notion that reducing serum non-HDL-C concentrations may be beneficial in the prevention of excess death from CVD among affected adults.</p

LV Mass Assessed by Echocardiography and CMR, Cardiovascular Outcomes, and Medical Practice

The authors investigated 3 important areas related to the clinical use of left ventricular mass (LVM): accuracy of assessments by echocardiography and cardiac magnetic resonance (CMR), the ability to predict cardiovascular outcomes, and the comparative value of different indexing methods. The recommended formula for echocardiographic estimation of LVM uses linear measurements and is based on the assumption of the left ventricle (LV) as a prolate ellipsoid of revolution. CMR permits a modeling of the LV free of cardiac geometric assumptions or acoustic window dependency, showing better accuracy and reproducibility. However, echocardiography has lower cost, easier availability, and better tolerability. From the MEDLINE database, 26 longitudinal echocardiographic studies and 5 CMR studies investigating LVM or LV hypertrophy as predictors of death or major cardiovascular outcomes were identified. LVM and LV hypertrophy were reliable cardiovascular risk predictors using both modalities. However, no study directly compared the methods for the ability to predict events, agreement in hypertrophy classification, or performance in cardiovascular risk reclassification. Indexing LVM to body surface area was the earliest normalization process used, but it seems to underestimate the prevalence of hypertrophy in obese and overweight subjects. Dividing LVM by height to the allometric power of 1.7 or 2.7 is the most promising normalization method in terms of practicality and usefulness from a clinical and scientific standpoint for scaling myocardial mass to body size. The measurement of LVM, calculation of LVM index, and classification for LV hypertrophy should be standardized by scientific societies across measurement techniques and adopted by clinicians in risk stratification and therapeutic decision making

A double-blind randomized trial of fish oil to lower triglycerides and improve cardiometabolic risk in adolescents.

OBJECTIVES: To determine the efficacy of 4 g/day fish oil to lower triglycerides and impact lipoprotein particles, inflammation, insulin resistance, coagulation, and thrombosis. STUDY DESIGN: Participants (n = 42, age 14 ± 2 years) with hypertriglyceridemia and low-density lipoprotein (LDL) cholesterol/dL were enrolled in a randomized, double-blind, crossover trial comparing 4 g of fish oil daily with placebo. Treatment interval was 8 weeks with a 4-week washout. Lipid profile, lipoprotein particle distribution and size, glucose, insulin, high-sensitivity C-reactive protein, interleukin-6, fibrinogen, plasminogen activator inhibitor-1, and thrombin generation were measured. RESULTS: Baseline lipid profile was total cholesterol 194 (5.4) mg/dL (mean [SE]), triglycerides 272 (21) mg/dL, high-density lipoprotein cholesterol 39 (1) mg/dL, and LDL cholesterol 112 (3.7) mg/dl. LDL particle number was 1614 (60) nmol/L, LDL size was 19.9 (1.4) nm, and large very low-density lipoprotein/chylomicron particle number was 9.6 (1.4) nmol/L. Triglycerides decreased on fish oil treatment but the difference was not significant compared with placebo (-52 ± 16 mg/dL vs -16 ± 16 mg/dL). Large very low-density lipoprotein particle number was reduced (-5.83 ± 1.29 nmol/L vs -0.96 ± 1.31 nmol/L; P \u3c .0001). There was no change in LDL particle number or size. There was a trend towards a lower prothrombotic state (lower fibrinogen and plasminogen activator inhibitor-1; .10 \u3e P \u3e .05); no other group differences were seen. CONCLUSIONS: In children, fish oil (4 g/day) lowers triglycerides slightly and may have an antithrombotic effect but has no effect on LDL particles