Waist-to-height ratio and cardiometabolic risk factors in adolescence: findings from a prospective birth cohort

What is already known about this subject In adults, associations between body mass index (BMI), waist-to-height ratio (WHtR) and cardiometabolic outcomes are similar. In children and adolescents, results from cross-sectional studies examining the associations between BMI z scores, WHtR and cardiometabolic outcomes are conflicting and there is a paucity of prospective data.<p></p> What this study adds This is the first study to demonstrate the prospective association between WHtR in childhood and cardiometabolic outcomes in adolescent boys. WHtR is a simple calculation that can be used to identify children and adolescents for cardiometabolic risk without the need for reference growth charts. The WHtR cut-point of ≥0.5 was highly specific in identifying cardiometabolic risk co-occurrence but has poor sensitivity.<p></p> Objective To examine the associations between body mass index (BMI) and waist-to-height ratio (WHtR) measured in childhood and adolescence and cardiometabolic risk factors in adolescence.<p></p> Methods Secondary data analysis of the Avon Longitudinal Study of Parents and Children, a population based cohort. Data from 2858 adolescents aged 15.5 (standard deviation 0.4) years and 2710 of these participants as children aged 7–9 years were used in this analysis. Outcome measures were cardiometabolic risk factors, including triglycerides, low density lipoprotein cholesterol, high density lipoprotein cholesterol, insulin, glucose and blood pressure at 15 years of age.<p></p> Results Both BMI and WHtR measured at ages 7–9 years and at age 15 years were associated with cardiometabolic risk factors in adolescents. A WHtR ≥0.5 at 7–9 years increased the odds by 4.6 [95% confidence interval 2.6 to 8.1] for males and 1.6 [0.7 to 3.9] for females of having three or more cardiometabolic risk factors in adolescence. Cross-sectional analysis indicated that adolescents who had a WHtR ≥0.5, the odds ratio of having three or more cardiometabolic risk factors was 6.8 [4.4 to 10.6] for males and 3.8 [2.3 to 6.3] for females. The WHtR cut-point was highly specific in identifying cardiometabolic risk co-occurrence in male children and adolescents as well as female children (90 to 95%), but had poor sensitivity (17 to 53%). Similar associations were observed when BMI was used to define excess adiposity.<p></p> Conclusions WHtR is a simple alternative to age and sex adjusted BMI for assessing cardiometabolic risk in adolescents

Acute-on-chronic Liver Failure: MELD Score 30-day Mortality Predictability and Etiology in a Pakistani Population

Background: Cirrhosis is a pathological condition that ultimately leads to liver failure. Acute on chronic liver failure (ACLF) has a high short term mortality rate. Viral hepatitis is the most common cause of liver failure in our local population. We carried out this study to identity the 30-day mortality and etiology of patients presenting with ACLF using Model for End-Stage Liver Disease (MELD) score predictability. Methodology: This was a descriptive case series, conducted at Sheikh Zayed Hospital, Lahore, Pakistan from January 31, 2018 to July 30, 2018. One hundred and eighty five patients who met the inclusion criteria were enrolled using 95% confidence level and 4% margin of error. Data was entered and analyzed with SPSS version 23.0. Numerical variables including age was presented by Mean ± S.D. Categorical variables i.e. gender, etiology of acute-on-chronic liver failure and 30-day mortality were presented by frequency and percentage. Data was stratified for age, gender, duration of chronic liver disease and MELD grade to address the effect modifiers. Post-stratification chi-square test was calculated using 95% significance (p≤0.05). Results: Majority of the enrolled patients were male (74.6%) while only 25.4% of the patients were female. One hundred and thirty patients (70.3%) had underlying viral hepatitis while twelve patients (6.5%) and forty three patients (23.2%) presented with alcoholic liver disease and drug-induced ACLF, respectively. Eighty patients (43.2%) died within 30 days of admission.The 30-day mortality with respect to MELD grade was statistically significant (p<0.001) with the highest mortality noted in grade-IV and thirty five patients (43.8%) dying within 30 days of admission (p<0.001). Grade-II and III MELD scores also contributed to the 30-day mortality with twenty three patients (28.8%) and nineteen patients (23.8%) dying within 30 days of admission (p<0.001). Conclusion: MELD scores are able to accurately predict the short-term mortality in patients with ACLF and viral hepatitis was the most common etiology in our population. Early detection and use of appropriate prognostic models may alleviate mortality and morbidity in paitents with ACLF

Hyperglycemia Has a Greater Impact on Left Ventricle Function in South Asians Than in Europeans

OBJECTIVE Diabetes is associated with left ventricular (LV) diastolic and systolic dysfunction. South Asians may be at particular risk of developing LV dysfunction owing to a high prevalence of diabetes. We investigated the role of diabetes and hyperglycemia in LV dysfunction in a community-based cohort of older South Asians and white Europeans. RESEARCH DESIGN AND METHODS Conventional and Doppler echocardiography was performed in 999 participants (542 Europeans and 457 South Asians aged 58–86 years) in a population-based study. Anthropometry, fasting bloods, coronary artery calcification scoring, blood pressure, and renal function were measured. RESULTS Diabetes and hyperglycemia across the spectrum of HbA1c had a greater adverse effect on LV function in South Asians than Europeans (N-terminal-probrain natriuretic peptide β ± SE 0.09 ± 0.04, P = 0.01, vs. −0.04 ± 0.05, P = 0.4, P for HbA1c/ethnicity interaction 0.02), diastolic function (E/e′ 0.69 ± 0.12, P < 0.0001, vs. 0.09 ± 0.2, P = 0.6, P for interaction 0.005), and systolic function (s′ −0.11 ± 0.06, P = 0.04, vs. 0.14 ± 0.09, P = 0.1, P for interaction 0.2). Multivariable adjustment for hypertension, microvascular disease, LV mass, coronary disease, and dyslipidemia only partially accounted for the ethnic differences. Adverse LV function in diabetic South Asians could not be accounted for by poorer glycemic control or longer diabetes duration. CONCLUSIONS Diabetes and hyperglycemia have a greater adverse effect on LV function in South Asians than Europeans, incompletely explained by adverse risk factors. South Asians may require earlier and more aggressive treatment of their cardiometabolic risk factors to reduce risks of LV dysfunction

Postprandial Vascular Dysfunction Is Associated With Raised Blood Pressure and Adverse Left Ventricular Remodeling in Adolescent Adiposity

BACKGROUND: Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular disease, including heart failure. Although linked to obesity and hypertension, its pathogenesis is multifactorial. Blunted postprandial sympathetic regulation of gut blood flow has been observed in overweight animals and suggested as a promotor of hypertension and LVH. We hypothesized that blunted postprandial superior mesenteric blood flow responses would be more common in overweight humans and associated with increased blood pressure and LVH. METHODS: Left ventricular dimensions and hemodynamic responses to a standardized high-calorie liquid meal were measured in healthy adolescents (n=82; 39 overweight/obese) by magnetic resonance imaging. Covariates such as body mass index, blood pressure, Tanner score, and an index of insulin resistance were included in multiple regression models to examine the independent associations of mesenteric flow response with blood pressure status and LVH. RESULTS: Food ingestion increased cardiac output (Δmean, 0.45 [SD, 0.62] L·min-1; P=3.8×10-8) and superior mesenteric artery flow (Δmean, 0.76 [SD, 0.35] L·min-1; P=4.2×10-31). A blunted mesenteric flow response was associated with increased left ventricular mass (B=-12.7 g·m-2.7 per L·min-1·m-0.92; P=6×10-5) and concentric LVH (log likelihood, -9.9; P=0.001), independently of known determinants of LVH, including body mass index. It was also associated with elevated systolic blood pressure (B=-18.0 mm Hg per L·min-1·m-0.92; P=0.001), but this link did not explain the association with left ventricular mass. CONCLUSIONS: Postprandial mesenteric vascular dysfunction is associated with LVH and hypertension, independently of common risk factors for those conditions. These findings highlight a new, independent marker of cardiovascular risk in the young

Cardiovascular biomarkers and vascular function during childhood in the offspring of mothers with hypertensive disorders of pregnancy: findings from the Avon Longitudinal Study of Parents and Children

&lt;p&gt;&lt;b&gt;Aims:&lt;/b&gt; It is uncertain if the higher blood pressure (BP) observed in the offspring of hypertensive pregnancies is an isolated abnormality or one that is accompanied by impaired vascular function and alterations in lipid and inflammation markers that would be indicative of a more general cardiometabolic disturbance of the type observed in the mother during pre-eclampsia.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods and results:&lt;/b&gt; In a large UK cohort of maternal-offspring pairs (n = 3537–4654), assessed at age 9–12 years, we examined the associations of maternal gestational hypertension and pre-eclampsia with offspring BP, endothelial function assessed by brachial artery flow-mediated dilatation; arterial stiffness assessed by carotid to radial pulse wave velocity; brachial artery distensibility and BP (vascular outcomes); as well as markers of inflammation, lipids and apolipoproteins A1 and B. Offspring of women with pre-eclampsia or gestational hypertension had higher systolic blood pressure by 2.04 mmHg (95% CI: 1.33, 2.76) and 1.82 mmHg (95% CI: 0.03, 3.62), respectively, and higher diastolic blood pressure by 1.10 mmHg (95% CI: 0.47, 1.73) and 1.26 mmHg (95% CI: −0.32, 2.85), respectively, in analyses adjusted for maternal and offspring body mass index (BMI), offspring dietary sodium intake and other potential confounders. However, we found no associations of either hypertensive disorder of pregnancy with the other vascular outcomes or with inflammatory markers, lipids, and apolipoproteins.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusion:&lt;/b&gt; Pre-eclampsia and gestational hypertension are associated with higher offspring BP in childhood in the absence of other vascular alterations or metabolic derangements. The findings support the existence of shared mother-offspring risk factors that are specific for higher BP, rather than the additional cardiometabolic abnormalities of hypertensive disorder of pregnancy having long-term consequences for offspring.&lt;/p&gt

Effect of statins on atrial fibrillation: collaborative meta-analysis of published and unpublished evidence from randomised controlled trials

Objective To examine whether statins can reduce the risk of atrial fibrillation. Design Meta-analysis of published and unpublished results from larger scale statin trials, with comparison of the findings against the published results from smaller scale or shorter duration studies. Data sources Medline, Embase, and Cochrane's CENTRAL up to October 2010. Unpublished data from longer term trials were obtained through contact with investigators. Study selection Randomised controlled trials comparing statin with no statin or comparing high dose versus standard dose statin; all longer term trials had at least 100 participants and at least six months' follow-up. Results In published data from 13 short term trials (4414 randomised patients, 659 events), statin treatment seemed to reduce the odds of an episode of atrial fibrillation by 39% (odds ratio 0.61, 95% confidence interval 0.51 to 0.74; P&lt;0.001), but there was significant heterogeneity (P&lt;0.001) between the trials. In contrast, among 22 longer term and mostly larger trials of statin versus control (105 791 randomised patients, 2535 events), statin treatment was not associated with a significant reduction in atrial fibrillation (0.95, 0.88 to 1.03; P=0.24) (P&lt;0.001 for test of difference between the two sets of trials). Seven longer term trials of more intensive versus standard statin regimens (28 964 randomised patients and 1419 events) also showed no evidence of a reduction in the risk of atrial fibrillation (1.00, 0.90 to 1.12; P=0.99). Conclusions The suggested beneficial effect of statins on atrial fibrillation from published shorter term studies is not supported by a comprehensive review of published and unpublished evidence from larger scale trials

Ethnic Differences in Carotid Intima-Media Thickness Between UK Children of Black African-Caribbean and White European Origin.

BACKGROUND AND PURPOSE: UK black African-Caribbean adults have higher risks of stroke than white Europeans and have been shown to have increased carotid intima-media thickness (cIMT). We examined whether corresponding ethnic differences in cIMT were apparent in childhood and, if so, whether these could be explained by ethnic differences in cardiovascular risk markers. METHODS: We conducted a 2-stage survey of 939 children (208 white European, 240 black African-Caribbean, 258 South Asian, 63 other Asian, 170 other ethnicity), who had a cardiovascular risk assessment and measurements of cIMT at mean ages of 9.8 and 10.8 years, respectively. RESULTS: Black African-Caribbean children had a higher cIMT than white Europeans (mean difference, 0.014 mm; 95% CI, 0.008-0.021 mm; P<0.0001). cIMT levels in South Asian and other Asian children were however similar to those of white Europeans. Among all children, cIMT was positively associated with age, systolic and diastolic blood pressure and inversely with combined skinfold thickness and serum triglyceride. Mean triglyceride was lower among black African-Caribbeans than white Europeans; blood pressure and skinfold thickness did not differ appreciably. However, adjustment for these risk factors had little effect on the cIMT difference between black African-Caribbeans and white Europeans. CONCLUSIONS: UK black African-Caribbean children have higher cIMT levels in childhood; the difference is not explained by conventional cardiovascular risk markers. There may be important opportunities for early cardiovascular prevention, particularly in black African-Caribbean children

Genetic affinities of Fusarim spp. and their correlation with origin and pathogenicity

Random amplified polymorphic DNA (RAPD) analyses was used in combination with pathogenicity assays to study the taxonomic kinships among five Fusarium species. A total of 46 isolates of Fusarium spp. obtained from diseased cotton seedlings showing typical root rot and dampping-off symptoms were characterized. Of 10 primers tested, four primers produced polymorphic amplification patterns with taxon-specific bands, in addition to individual-specific bands. Genetic analysis indicated into 2 main clusters, with the minor cluster included all F. moniliforme and F. solani at the genetic similarity of GS=57.82%. The major cluster consisted of all F. oxysporum, F. avenaceum and F. chlamydosporum clustered at 71% similarity. There was no clear-cut relationship between clustering in the RAPD dendrogram, pathogenicity test and geographic origin of tested isolates. The results suggest that RAPD-PCR is a useful method for analysing genetic variation within and between Fusarium spp. (African Journal of Biotechnology: 2003 2(5): 109-113

Evaluation of C-reactive protein prior to and on-treatment as a predictor of benefit from atorvastatin: observations from the Anglo-Scandinavian Cardiac Outcomes Trial

&lt;p&gt;&lt;b&gt;Aims:&lt;/b&gt; We tested whether on-statin C-reactive protein is associated with cardiovascular (CV) outcome in the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT).&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods and results:&lt;/b&gt; ASCOT randomized a subset of 4853 patients with total cholesterol ≤6.5 mmol/L (250 mg/dL) to atorvastatin or placebo. In a case–control study during 5.5-year follow-up, 485 CV cases were age- and sex-matched with 1367 controls. Baseline LDL-cholesterol (LDL-c) and log-transformed C-reactive protein predicted CV events [odds ratio (OR) per 1 standard deviation (SD) 1.31 (95% confidence interval {CI}: 1.10, 1.56), P = 0.002 and OR 1.19 (1.05, 1.34), P = 0.006, respectively]. Including baseline C-reactive protein into a Framingham risk model very modestly improved risk prediction. Baseline C-reactive protein did not indicate the magnitude of the atorvastatin effect on CV outcome (P = 0.54). At 6 months, atorvastatin reduced median LDL-c by 40.3% and median C-reactive protein by 27.4%. In those randomized to atorvastatin, lower on-treatment LDL-c at 6 months was associated with a significant reduction in subsequent CV events [OR 0.41 (0.22, 0.75), P = 0.004] comparing those above and below the median (2.1 mmol/L). In contrast, C-reactive protein below the median (1.83 mg/L) compared with C-reactive protein above the median was not associated with a significant reduction in CV events [OR 0.86 (0.49, 1.51), P = 0.60]. Consequently, addition of on-treatment C-reactive protein to LDL-c did not improve prediction of statin efficacy.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusion:&lt;/b&gt; Among these hypertensive patients selected on the basis of traditional CV risk factors, C-reactive protein did not usefully improve the prediction of CV events and, critically, reduction in C-reactive protein associated with statin therapy was not a predictor of CV outcome alone or in combination with LDL-c.&lt;/p&gt