METHODS: This cross-sectional study was performed at Hue Central Hospital from 2012-2016 on 176 CKD and 64 control subjects. ADMA levels were measured by using the enzyme linked immunosorbent assay (ELISA) method.
RESULTS: Mean ADMA level was markedly higher (p<0.001) in all patients combined (0.73±0.24μmol/L) than in control subjects (0.47±0.13μmol/L). Mean ADMA levels in advanced kidney disease were higher than control subjects. ADMA levels correlated inversely and relatively strictly to estimated glomerular filtration rate (eGFR) (r = -0.689; p<0.001), haemoglobin (r = -0.525; p<0.001) and haematocrit (r = - 0.491; p<0.001); correlated favourably and relatively strictly to serum creatinine (r = 0.569; p<0.001) and serum urea (r = 0.642; p<0.001). ADMA elevation was predicted simultaneously by eGFR<60 mL/min/1.73m2 (p<0.001), anaemia (p=0.002), body mass index (BMI) (p=0.011) and high sensitivity C-reactive protein (hs-CRP) (p=0.041). Cutoff of ≥0.68μmol/L, ADMA levels predict reduction of eGFR<60 mL/min/1.73m2, sensitivity of 86.9 %, specificity of 82.6%, area under ROC 92.4% (95%CI: 88.6-96.1%).
METHOD: This cross-sectional study involved eighty-three (n=83) adults attending a health screening program at Universiti Putra Malaysia (UPM). Demographic data, anthropometric measurements and blood samples for fasting blood glucose (FBG), fasting lipid profile (FSL), glycated haemoglobin (HbA1c) and hsCRP were taken. Respondents were grouped according to FRS and the Joint Interim Statement into 10-year CVD risk categories (low, intermediate and high) and MetS, respectively.
RESULTS: hsCRP was significantly increased in patients with high body mass index (BMI) (p=0.001), at-risk waist circumference (WC) (p=0.001) and MetS (p=0.009). Spearman's correlation coefficient showed a significant positive correlation between hsCRP level and total FRS score (r=0.26, p<0.05) and HDL-C score (r=0.22, p<0.05).
CONCLUSION: The significant difference of hsCRP levels across obesity levels and MetS with its modest correlation with FRS scores supported the adjunctive role of hsCRP in CVD risk prediction, most likely capturing the inflammatory pathological aspect and thus partly accounting for the residual CVD risk.
Methods: A total of 80 NT and 80 PreHT healthy subjects aged between 18-45 years were recruited in Kuantan, Pahang, Malaysia using an observational cross-sectional study approach. DNA methylation level of IL-6 promoter in peripheral leukocytes were measured using bisulphite conversion and MethyLight assay.
Results: There was no significant difference in age between NT and PreHT (P = 0.655). The mean blood pressure was 110(8)/73(5) mmHg in NT and 125(7)/82(5) mmHg in PreHT subjects. The IL-6 promoter methylation level was significantly lower in PreHT compared to NT subjects (P < 0.001).
Conclusion: The current study demonstrates that hypomethylation of IL-6 promoter was associated with pre-hypertension in young adults. Thus, IL-6 methylation could be used as an early indicator for predicting hypertension and related risk of cardiovascular diseases in prehypertensive subjects. Gene expression and longitudinal studies are warranted to examine the methylation effect on IL-6 expression over time.
Methods: A pretest-posttest experimental design was employed. Fifty subjects, diagnosed with T2DM, attending the Diabetes Clinic of the University of Nigeria Teaching Hospital, Enugu, were conveniently recruited, gender and age-matched, and randomised into exercise and control groups. The intervention included an eight-week aerobic exercise at 60%-79% HRmax for 45 min-60 min, 3-days per week. The FBS, SpO2, BMI, resting heart rate (RHR), and systolic (SBP) and diastolic blood pressure (DBP) of the subjects were measured before and after the intervention. The paired and independent t-test(s) were used for the analyses within and between the groups, respectively (P ≤ 0.05).
Results: The exercise group had a significantly lower SBP (15.0 mmHg, P = 0.001), DBP (7.9 mmHg, P = 0.001), RHR (4.8 bpm, P = 0.001), FBS (34.9 mg/dl, P = 0.001), and BMI (2.3, P = 0.001), while the SpO2 improved by 3.9% with P = 0.001, relative to the control group.
Conclusion: Aerobics is an efficacious adjunct therapy in controlling the FBS level, blood pressure, BMI, and improving SpO2 among T2DM subjects.
METHODS: Forty-two adult male Sprague-Dawley rats were equally assigned into 6 groups.The first group was fed with normal rat chow as the control group, and the subsequent groups were fed with rat chow fortified with 15% weight/weight of the following: fresh palm olein, palm olein heated once, palm olein heated twice, palm olein heated 5 times, or palm olein heated 10 times. The duration of feeding was 6 months. Fatty acid analyses of oil were performed using gas chromatography. Peroxide values were determined using standard titration. Plasma was collected for biochemical analyses.
RESULTS: Repeatedly heated palm olein increased the levels of peroxide, angiotensin-converting enzyme, and lipid peroxidation as well as reduced the level of heme oxygenase. Fresh palm olein and palm olein heated once had lesser effects on lipid peroxidation and a better effect on the activity of blood pressure-regulating enzymes than repeatedly heated palm olein.
CONCLUSION: Repeatedly heated palm olein may negatively affect the activity of blood pressure-regulating enzymes and increase lipid peroxidation.
METHODS: In this multinational, prospective cohort study, we studied 157 436 adults aged 35-70 years who were enrolled in the PURE study in countries with ambient PM2·5 estimates, for whom follow-up data were available. Cox proportional hazard frailty models were used to estimate the associations between long-term mean community outdoor PM2·5 concentrations and cardiovascular disease events (fatal and non-fatal), cardiovascular disease mortality, and other non-accidental mortality.
FINDINGS: Between Jan 1, 2003, and July 14, 2018, 157 436 adults from 747 communities in 21 high-income, middle-income, and low-income countries were enrolled and followed up, of whom 140 020 participants resided in LMICs. During a median follow-up period of 9·3 years (IQR 7·8-10·8; corresponding to 1·4 million person-years), we documented 9996 non-accidental deaths, of which 3219 were attributed to cardiovascular disease. 9152 (5·8%) of 157 436 participants had cardiovascular disease events (fatal and non-fatal incident cardiovascular disease), including 4083 myocardial infarctions and 4139 strokes. Mean 3-year PM2·5 at cohort baseline was 47·5 μg/m3 (range 6-140). In models adjusted for individual, household, and geographical factors, a 10 μg/m3 increase in PM2·5 was associated with increased risk for cardiovascular disease events (hazard ratio 1·05 [95% CI 1·03-1·07]), myocardial infarction (1·03 [1·00-1·05]), stroke (1·07 [1·04-1·10]), and cardiovascular disease mortality (1·03 [1·00-1·05]). Results were similar for LMICs and communities with high PM2·5 concentrations (>35 μg/m3). The population attributable fraction for PM2·5 in the PURE cohort was 13·9% (95% CI 8·8-18·6) for cardiovascular disease events, 8·4% (0·0-15·4) for myocardial infarction, 19·6% (13·0-25·8) for stroke, and 8·3% (0·0-15·2) for cardiovascular disease mortality. We identified no consistent associations between PM2·5 and risk for non-cardiovascular disease deaths.
INTERPRETATION: Long-term outdoor PM2·5 concentrations were associated with increased risks of cardiovascular disease in adults aged 35-70 years. Air pollution is an important global risk factor for cardiovascular disease and a need exists to reduce air pollution concentrations, especially in LMICs, where air pollution levels are highest.
FUNDING: Full funding sources are listed at the end of the paper (see Acknowledgments).
METHODS: In this international, community-based cohort study, we prospectively enrolled adults aged 35-70 years who had no intention of moving residences for 4 years from rural and urban communities across 17 countries. A portable spirometer was used to assess FEV1. FEV1 values were standardised within countries for height, age, and sex, and expressed as a percentage of the country-specific predicted FEV1 value (FEV1%). FEV1% was categorised as no impairment (FEV1% ≥0 SD from country-specific mean), mild impairment (FEV1% <0 SD to -1 SD), moderate impairment (FEV1% cardiovascular disease outcomes (including myocardial infarction, stroke, sudden death, or congestive heart failure), and respiratory hospitalisations (from chronic obstructive pulmonary disease, asthma, pneumonia, tuberculosis, or other pulmonary conditions). Fully adjusted hazard ratios (HRs) were calculated by multilevel Cox regression.
FINDINGS: Among 126 359 adults with acceptable spirometry data available, during a median 7·8 years (IQR 5·6-9·5) of follow-up, 5488 (4·3%) deaths, 5734 (4·5%) cardiovascular disease events, and 1948 (1·5%) respiratory hospitalisation events occurred. Relative to the no impairment group, mild to severe FEV1% impairments were associated with graded increases in mortality (HR 1·27 [95% CI 1·18-1·36] for mild, 1·74 [1·60-1·90] for moderate, and 2·54 [2·26-2·86] for severe impairment), cardiovascular disease (1·18 [1·10-1·26], 1·39 [1·28-1·51], 2·02 [1·75-2·32]), and respiratory hospitalisation (1·39 [1·24-1·56], 2·02 [1·75-2·32], 2·97 [2·45-3·60]), and this pattern persisted in subgroup analyses considering country income level and various baseline risk factors. Population-attributable risk for mortality (adjusted for age, sex, and country income) from mildly to moderately reduced FEV1% (24·7% [22·2-27·2]) was larger than that from severely reduced FEV1% (3·7% [2·1-5·2]) and from tobacco use (19·7% [17·2-22·3]), previous cardiovascular disease (5·5% [4·5-6·5]), and hypertension (17·1% [14·6-19·6]). Population-attributable risk for cardiovascular disease from mildly to moderately reduced FEV1 was 17·3% (14·8-19·7), second only to the contribution of hypertension (30·1% [27·6-32·5]).
INTERPRETATION: FEV1 is an independent and generalisable predictor of mortality, cardiovascular disease, and respiratory hospitalisation, even across the clinically normal range (mild to moderate impairment).
FUNDING: Population Health Research Institute, the Canadian Institutes of Health Research, Heart and Stroke Foundation of Ontario, Ontario Ministry of Health and Long-Term Care, AstraZeneca, Sanofi-Aventis, Boehringer Ingelheim, Servier, and GlaxoSmithKline, Novartis, and King Pharma. Additional funders are listed in the appendix.
METHODS: In this large-scale prospective cohort study, we recruited adults aged between 35 years and 70 years from 367 urban and 302 rural communities in 20 countries. We collected data on families and households in two questionnaires, and data on cardiovascular risk factors in a third questionnaire, which was supplemented with physical examination. We assessed socioeconomic status using education and a household wealth index. Education was categorised as no or primary school education only, secondary school education, or higher education, defined as completion of trade school, college, or university. Household wealth, calculated at the household level and with household data, was defined by an index on the basis of ownership of assets and housing characteristics. Primary outcomes were major cardiovascular disease (a composite of cardiovascular deaths, strokes, myocardial infarction, and heart failure), cardiovascular mortality, and all-cause mortality. Information on specific events was obtained from participants or their family.
FINDINGS: Recruitment to the study began on Jan 12, 2001, with most participants enrolled between Jan 6, 2005, and Dec 4, 2014. 160 299 (87·9%) of 182 375 participants with baseline data had available follow-up event data and were eligible for inclusion. After exclusion of 6130 (3·8%) participants without complete baseline or follow-up data, 154 169 individuals remained for analysis, from five low-income, 11 middle-income, and four high-income countries. Participants were followed-up for a mean of 7·5 years. Major cardiovascular events were more common among those with low levels of education in all types of country studied, but much more so in low-income countries. After adjustment for wealth and other factors, the HR (low level of education vs high level of education) was 1·23 (95% CI 0·96-1·58) for high-income countries, 1·59 (1·42-1·78) in middle-income countries, and 2·23 (1·79-2·77) in low-income countries (pinteraction<0·0001). We observed similar results for all-cause mortality, with HRs of 1·50 (1·14-1·98) for high-income countries, 1·80 (1·58-2·06) in middle-income countries, and 2·76 (2·29-3·31) in low-income countries (pinteraction<0·0001). By contrast, we found no or weak associations between wealth and these two outcomes. Differences in outcomes between educational groups were not explained by differences in risk factors, which decreased as the level of education increased in high-income countries, but increased as the level of education increased in low-income countries (pinteraction<0·0001). Medical care (eg, management of hypertension, diabetes, and secondary prevention) seemed to play an important part in adverse cardiovascular disease outcomes because such care is likely to be poorer in people with the lowest levels of education compared to those with higher levels of education in low-income countries; however, we observed less marked differences in care based on level of education in middle-income countries and no or minor differences in high-income countries.
INTERPRETATION: Although people with a lower level of education in low-income and middle-income countries have higher incidence of and mortality from cardiovascular disease, they have better overall risk factor profiles. However, these individuals have markedly poorer health care. Policies to reduce health inequities globally must include strategies to overcome barriers to care, especially for those with lower levels of education.
FUNDING: Full funding sources are listed at the end of the paper (see Acknowledgments).
METHODS: We assessed use of antiplatelet, cholesterol, and blood-pressure-lowering drugs in 8492 individuals with self-reported cardiovascular disease from 21 countries enrolled in the Prospective Urban Rural Epidemiology (PURE) study. Defining one or more drugs as a minimal level of secondary prevention, wealth-related inequality was measured using the Wagstaff concentration index, scaled from -1 (pro-poor) to 1 (pro-rich), standardised by age and sex. Correlations between inequalities and national health-related indicators were estimated.
FINDINGS: The proportion of patients with cardiovascular disease on three medications ranged from 0% in South Africa (95% CI 0-1·7), Tanzania (0-3·6), and Zimbabwe (0-5·1), to 49·3% in Canada (44·4-54·3). Proportions receiving at least one drug varied from 2·0% (95% CI 0·5-6·9) in Tanzania to 91·4% (86·6-94·6) in Sweden. There was significant (p<0·05) pro-rich inequality in Saudi Arabia, China, Colombia, India, Pakistan, and Zimbabwe. Pro-poor distributions were observed in Sweden, Brazil, Chile, Poland, and the occupied Palestinian territory. The strongest predictors of inequality were public expenditure on health and overall use of secondary prevention medicines.
INTERPRETATION: Use of medication for secondary prevention of cardiovascular disease is alarmingly low. In many countries with the lowest use, pro-rich inequality is greatest. Policies associated with an equal or pro-poor distribution include free medications and community health programmes to support adherence to medications.
FUNDING: Full funding sources listed at the end of the paper (see Acknowledgments).
METHODS: A pragmatic randomised controlled trial was conducted on 29 healthy sedentary adults (seven males and 22 females) in a 12-week exercise program. They were randomly assigned to group A (75 min/week, N.=15) or group B (150 min/week, N.=14) of moderate intensity aerobic exercise groups. HRR at 1-minute (HRR1), HRR at 2-minute (HRR2), and peak oxygen uptake (VO2peak) were measured pre- and post-intervention.
RESULTS: The improvements of HRR1 and HRR2 were seen in both groups but was only significant (P<0.05) for group A with HRR1, -4.07 bpm (post 24.47±6.42 - pre 20.40±5.51, P=0.018) and HHR2, -3.93 bpm (post 43.40±13.61 - pre 39.47±10.68, P=0.046). Group B showed increment of HRR1, -1.14 bpm (post 21.14±5.35 - pre 20.00±6.30, P=0.286) and HRR2, -2.5 bpm, (post 39.36±8.01 - pre 36.86±9.57, P=0.221). Improvement of the VO2peak was only significant in group B with an increment of 1.52±2.61 (P=0.049).
CONCLUSIONS: In conclusion, our study suggests that improvements in heart rate recovery (HRR1 and HRR2) among sedentary healthy adults can be achieved by engaging in moderate intensity exercise at a dose lower than the current recommended guidelines. The lower dose seems to be more attainable and may encourage exercise compliance. Future studies should further explore the effects of different exercise volumes on HRR in a larger sample size and also by controlling for BMI or gender.
STUDY DESIGN: A systematic search was performed using the MEDLINE, EMBASE, PsycINFO, CINAHL, and Web of Science databases to identify English-language articles published through June 2018. Articles were included if they were longitudinal studies in community-based populations, the primary exposure occurred during childhood, and the primary outcome was either a measure of subclinical CVD or a clinical CVD event occurring in adulthood. Two independent reviewers screened determined whether eligibility criteria were met.
RESULTS: There were 210 articles that met the predefined criteria. The greatest number of publications examined associations of clinical risk factors, including childhood adiposity, blood pressure, and cholesterol, with the development of adult CVD. Few studies examined childhood lifestyle factors including diet quality, physical activity, and tobacco exposure. Domains of risk beyond "traditional" cardiovascular risk factors, such as childhood psychosocial adversity, seemed to have strong published associations with the development of CVD.
CONCLUSIONS: Although the evidence was fairly consistent in direction and magnitude for exposures such as childhood adiposity, hypertension, and hyperlipidemia, significant gaps remain in the understanding of how childhood health and behaviors translate to the risk of adulthood CVD, particularly in lesser studied exposures like glycemic indicators, physical activity, diet quality, very early life course exposure, and population subgroups.