This study aimed to systematically review and appraise evidence on the short-term (e.g. morbidity, mortality) and long-term (obesity and non-communicable diseases, NCDs) health consequences of catch-up growth (vs. no catch-up growth) in individuals with a history of low birth weight (LBW).We searched MEDLINE, EMBASE, Global Health, CINAHL plus, Cochrane Library, ProQuest Dissertations and Thesis and reference lists. Study quality was assessed using the risk of bias assessment tool from the Agency for Health Care Research and Quality, and the evidence base was assessed using the GRADE tool. Eight studies in seven cohorts (two from high-income countries, five from low-middle-income countries) met the inclusion criteria for short-term (mean age: 13.4 months) and/or longer-term (mean age: 11.1 years) health outcomes of catch-up growth, which had occurred by 24 or 59 months. Of five studies on short-term health outcomes, three found positive associations between weight catch-up growth and body mass and/or glucose metabolism; one suggested reduced risk of hospitalisation and mortality with catch-up growth. Three studies on longer-term health outcomes found catch-up growth were associated with higher body mass, BMI or cholesterol. GRADE assessment suggested that evidence quantity and quality were low. Catch-up growth following LBW may have benefits for the individual with LBW in the short term, and may have adverse population health impacts in the long-term, but the evidence is limited. Future cohort studies could address the question of the consequences of catch-up growth following LBW more convincingly, with a view to informing future prevention of obesity and NCDs. © 2016 John Wiley & Sons Ltd.

Adherence to WHO infant feeding recommendations has short-term benefits and may also help in the prevention of non-communicable diseases (NCDs). This study reviewed the evidence on whether adherence to all elements of the WHO infant feeding recommendations (comparison group those exclusively breastfed to 6 months, introduced to appropriate complementary feeding from 6 months, with continued breastfeeding to at least 24 months; exposure group characterised by non-adherence to any of the three recommendations) is associated with reduced risk of later obesity or cardiometabolic disease. The population of interest was children not classified as very low weight (weight-for-age z-score >-3.0). MEDLINE, EMBASE, Global Health, CINAHL plus, ProQuest Dissertations and Thesis were systematically searched from 2001 to July 2014, manual reference searching of a birth cohort register (http://www.birthcohorts.net/) as well as papers identified in the search and selected journals was carried out. The database search yielded 9050 records, 275 English-language full-text articles were screened, but no studies were eligible, failing to meet the following criteria: comparison (213); exposure (14); population (3); relevant outcome (5); outcome before 24 months (9); insufficient information provided (30); plus one study was qualitative. Eight studies met the inclusion criterion of exclusive breastfeeding to 6 months, but did not meet the other inclusion criteria. The present study has revealed an important gap in the evidence on NCD prevention, and suggestions for addressing this evidence gap are provided.

Troponins are thin myofilament proteins that regulate the contraction of cardiac and skeletal muscle. The cardio-specific troponin I (TnI) and T (TnT) proteins are sensitive and specific biomarkers of myocardial injury which over the past twenty years have revolutionised the diagnosis and management of myocardial infarction. With the advent of high sensitivity assays the role for cardiac troponins is possibly expanding. Elevated levels are associated with adverse cardiovascular events and mortality in heart failure and the general population. Studies in cardiomyopathies are generally small with <200 patients, but serum troponin levels can be chronically raised and detect subclinical myocyte damage. This review examines all major published studies of cardiac troponin measurement in cardiomyopathies. There is considerable variability among studies regarding assays used and definitions of abnormal results but elevated troponin levels are almost invariably related to poor prognosis and their negative predictive value is important.

Background ESC guidelines recommend measurement of troponin T in patients with hypertrophic cardiomyopathy (HCM) because high concentrations are associated with cardiovascular events, heart failure and death. The cardiac Troponin I subunit is not expressed in skeletal muscle making it a cardio-specific isoform. The use of troponin biomarkers in management of patients HCM is limited because concentrations only weakly correlate with clinical parameters. Most studies are small, and few have examined their relation with genotype and mortality. Purpose To assess the relationship between high-sensitive troponin I (hsTnI) and characteristics of adults with HCM. Methods Patients included were adults with an established diagnosis of HCM referred to a single centre for genetic testing. Demographic, clinical and imaging data were recorded at baseline. Echocardiography and cardiac magnetic resonance (CMR) were performed according to EACVI standards. Quantification of late gadolinium enhancement (LGE) was performed using the 5 SD quantitative threshold. Genotype was evaluated using a 16 gene panel in an accredited UK laboratory. Pathogenic and likely pathogenic variants were considered as a positive genotype. Serum hsTnI was measured by a two-site electrochemiluminescence immunoassay on a Roche E170 analyser. Normal values for the assay 0–34 ng/L for males and 0–16 ng/L for females. Results 313 patients (n=200, 64% male) median age 57 (IQR 47–68) years were included. hsTnI concentration was abnormal in 69 (22%) patients. An abnormal hsTnI was more common in females (n=36, 32%) compared to males (n=33, 17%, c2 9.9, p&lt;0.05). A pathogenic variant in a sarcomere gene was identified in 95 (30%) individuals. An abnormal hsTnI concentration was associated with higher left ventricular (LV) wall thickness (20mm v 18mm, p&lt;0.05) and LV outflow tract (LVOT) gradient (34 v 22 mmHg) on echocardiography (n=313). Of the patients (n=204) who had a CMR, an abnormal hsTnI concentration was associated with higher LV mass (183 v 156g, p&lt;0.05) and greater % LGE (30 v 16%, p&lt;0.01, n=129). There was no difference in hsTnI between those with a positive or negative genotype. During follow-up, 18 patients died. Of the 9 patients that died with a normal hsTnI, two died suddenly. Conclusions In HCM, patients with abnormal hsTnI concentration have higher LV mass and LVOT gradient and more fibrosis. Whilst mortality is higher in those with abnormal hsTnI, sudden cardiac death may occur with a normal hsTnI. It may not be appropriate to extrapolate hsTnI sex-specific thresholds used in the diagnosis of myocardial infarction to HCM. Funding Acknowledgement Type of funding source: None