Higher Risk Of Coronary Heart Disease Research Articles

Food additive monosodium glutamate and risk of cardiovascular diseases - NutriNet-Santé cohort

Abstract Background One may add monosodium glutamate (MSG) to food for its flavour-enhancing properties. However, its implication in long-term cardiovascular health is uncertain due to a lack of precise epidemiological evidence. This study aimed to investigate the associations between food additive glutamate exposures and cardiovascular disease (CVD) risk, including cerebrovascular disease (CVA) and coronary heart disease (CHD) risks in a large prospective cohort of French adults. Methods Participants (n = 108,932, 79.3% women, mean age=42.4 years, SD = 14.5) were 15 years old and above from the French NutriNet-Santé prospective cohort (2009-2023). We assessed dietary intakes using repeated 24h-dietary records and exposure to food additive glutamate using food composition databases and laboratory assays. We characterised associations between cumulative time-dependent continuous exposures to total glutamate, natural glutamic acid, MSG and risk of CVD, CVA, and CHD using multivariable proportional hazards Cox models adjusted for known risk factors for standardised increments of glutamate intake. Results During follow-up (median 7.92 years), 2397, 1113, and 1284 participants were diagnosed with CVD, CVA, and CHD respectively. Higher intakes of naturally occurring glutamic acid (HR per 3000 mg/d increment=1.08, 95% CI [1.01-1.16], p-value=0.03), food additive MSG (HR per 200 mg/d increment=1.05, 95% CI [1.01-1.09], p-value=0.03), and total glutamate (HR per 3000 mg/d increment=1.09, 95% CI [1.01-1.17], p-value=0.02) were associated with higher risks of CHD (p-value for non-linearity>0.6). Conclusions This large prospective cohort study revealed positive associations between exposure to the widely used glutamate food additives, especially MSG (E621) and CVD, CVA, and CHD risks. Key messages • This large prospective cohort study revealed positive associations between exposure to the widely used glutamate food additives, especially MSG (E621) and CVD, CVA, and CHD risks. • If confirmed, our findings regarding MSG could lead to a re-evaluation of the safety of these food additives by European and international public health agencies to improve consumer protection.

Visceral and subcutaneous adiposity and cardiovascular disease: Unravelling associations and prognostic value.

The distribution pattern of abdominal adiposity may help determine cardiovascular disease (CVD). Waist circumference (WC) is the most common but imprecise method for measuring abdominal adiposity, as it fails to differentiate between visceral adipose tissue (VAT) and abdominal subcutaneous adipose tissue (ASAT). This study aimed to determine whether elevated VAT or ASAT provides greater prognostic value for CVD events compared to elevated WC in the general population using data from the UK Biobank. In this secondary analysis of UK Biobank study, 24 265 participants with available abdominal magnetic resonance imaging data were included. The primary outcome of the study was coronary heart disease (CHD), and secondary outcomes included stroke, heart failure (HF) and atrial fibrillation (AF). Cox regressions for VAT, ASAT and WC were examined in relation to the predefined outcomes on continuous scales using standard deviation (SD) changes and by categories of concordant and discordant values defined by medians. During a mean follow-up period of 12.9 ± 1.8 years, 2641 participants developed CVD events (1296 CHD, 165 stroke, 286 HF and 894 AF) Each 1 SD increase in VAT yielded a hazard ratio (HR) of 1.15 (95% confidence interval [CI]: 1.09-1.22) for CHD risk, whereas ASAT had a HR of 1.10 (95% CI: 1.04-1.18). Further adjustment for WC eliminated the association between ASAT and CHD risk, in contrast to the association between VAT and CHD risk, which remained almost unaffected. Discordant VAT above the median with WC below presented a HR of 1.43 (95% CI: 1.15-1.78) for CHD, compared with concordant VAT and WC below the median. Similar results were found for discordant WC above the median with VAT below, with a HR of 1.46 (95% CI: 1.18-1.81). In contrast, discordant ASAT above the median with WC below was not associated with an increased risk of CHD. Similarly, discordant ASAT above the median with VAT below was not associated with an increased risk of CHD. Additionally, there was no observed association between VAT or ASAT and the risks of stroke, HF or AF after further adjustment for WC. Additionally, there was no observed association between VAT or ASAT and the risks of stroke, HF or AF after further adjustment for WC. Incorporating VAT measurements alongside WC data improved the ability to identify individuals at high risk for CHD compared to using WC alone. Both VAT and WC proved to be more accurate indicators of CHD risk than ASAT. However, VAT alone did not fully account for the CHD risk associated with elevated WC levels. Neither VAT nor ASAT showed an association with the risk of stroke, HF and AF.

The association between the single-nucleotide polymorphism of site rs1333040 in region 9p21 and the risk of coronary heart disease in Chinese population

Background Rs1333040 is the single-nucleotide polymorphisms (SNP) related with coronary heart disease (CHD). The aim of the present study is to examine the association between rs1333040 polymorphism genotypes and CHD and to further explore the molecular mechanism in Chinese population. Methods A case-control study was used in this study, including 500 CHD patients and 500 control subjects. CHD patients and controls were distinguished by coronary angiography. Genotypes of rs1333040 were determined on the Agena MassARRAY system. Statistical analysis was conducted by SPSS (Ver 16.0) and plink (Ver. 1.07, Shaun Purcell). Results Fisher’s exact test by plink indicated a significant difference in the allele distribution between cases and controls, the allele T may be associated with a higher risk of CHD (p = 0.012, odds ratio (OR) = 1.258). The serum levels of low-density lipoprotein cholesterol (LDL-C) (p = 0.029) and Gensini score (p = 0.008) distributed differently in patients with various alleles. In the recessive model, the levels of high-density lipoprotein (HDL) and apolipoprotein A (ApoA) were higher in the TC + CC genotype than in the TT genotype. The TC + TT genotype was found to be risk factors against CHD in a dominant model (OR = 1.278, p = 0.014). The TC + TT genotype along with multiple risk factors significantly positively correlated with the risk of CHD. Conclusions The present study investigates the association between the rs1333040 polymorphism genotypes and CHD. The T allele of rs1333040 is the susceptibility site of CHD. The interaction between SNP and various risk factors plays an important role in the development of CHD.

The relationship between system inflammation response index and coronary heart disease: a cross-sectional study (NHANES 2007-2016).

Coronary heart disease (CHD) is one of the common chronic diseases in clinical practice, often accompanied by inflammatory reactions. In recent years, the system inflammation response index (SIRI) has aroused researchers' interest as a novel inflammatory biomarker. This study aims to explore the relationship between the SIRI and CHD through the National Health and Nutrition Examination Survey (NHANES) database. We conducted a cross-sectional study and analyzed participants aged 40 and above with complete data from the NHANES survey years 2007-2016. Logistic regression analysis was used in this study to explore the relationship between the risk of CHD and SIRI. Stratified subgroup analysis was conducted based on age, gender, race, education level, body mass index (BMI), smoking status, drinking, hypertension, diabetes and angina pectoris to evaluate the relationship between SIRI and CHD in different populations. Additionally, restricted cubic spline (RCS) analysis was employed to investigate whether there is a nonlinear association between SIRI and CHD. A total of 6374 eligible participants were included, among whom 387 were diagnosed with CHD. The SIRI levels in the CHD group were significantly higher than those in the non-CHD group. After adjusting for potential confounders, an elevated SIRI level was associated with an increased risk of CHD, with an odds ratio of 1.12, 95% CI: (1.03, 1.22), P = 0.008. Subgroup analysis results indicated a significant interaction between SIRI and CHD among genders (P for interaction <0.05), especially in females. In contrast, no significant interaction was observed among age, race, education level, BMI, smoking status, drinking, hypertension, diabetes and angina pectoris (P for interaction >0.05). The RCS analysis showed a significant linear relationship between SIRI and CHD (P for non-linearity >0.05), with an inflection point at 2.86. Our study indicates that an elevated system inflammation response index is associated with a higher risk of CHD. Particularly among women.

Gut-Microbiota-Related Metabolite Phenylacetylglutamine and Risk of Incident Coronary Heart Disease among Women.

Phenylacetylglutamine (PAGln) is a novel metabolite derived from gut microbial metabolism of dietary proteins, specifically phenylalanine, which may be linked to risks of adverse cardiovascular events. We investigated whether higher plasma levels of PAGln were associated with a greater risk of incident coronary heart disease (CHD) and tested whether adherence to a plant-based diet, which characterizes habitual dietary patterns of animal and plant food intake, modified the associations. We examined associations between plasma PAGln and risk of incident CHD over 11-16 years in a nested case-control study of 1520 women (760 incident cases and 760 controls) from the Nurses' Health Study. Separately, we analyzed relations between PAGln and dietary intakes measured through dietary records in the Women's Lifestyle Validation Study (n=725). Higher PAGln levels were related to a greater risk of CHD (p <0.05 for dose-response relationship). Higher PAGln was associated with greater red/processed meat intake and lower vegetable intake (p <0.05 for all). We found a significant interaction between PAGln and adherence to plant-based diet index (PDI) on CHD (Pinteraction=0.008); higher PAGln levels were associated with an increased risk of CHD (relative risk per 1 SD: 1.22 [95% CI: 1.05, 1.41]) among women with low PDI but not among those with high PDI. Higher PAGln was associated with higher risk of CHD, particularly in women with dietary patterns of eating more animal foods and fewer plant-based foods. Adherence to plant-based diets might attenuate unfavorable associations between a novel microbial metabolite and CHD risk.

Contemporary algorithms for diagnosing obstructive coronary artery disease in real clinical practice

Background. Despite the high evidence level of the currently existing international recommendations on stable coronary heart disease (CHD) and chronic coronary syndrome, their implementation in domestic clinical practice is insufficient.The aim of the work. To analyze the choice of diagnostic tactics (non-invasive and invasive) in patients with suspected obstructive coronary heart disease in real clinical practice.Methods. The study included outpatients with suspected obstructive CHD, in whom the pre-test probability (PTP) of obstructive CHD was determined; if PTP = 5–15 %, clinical probability was assessed based on CHD risk factors. Based on the results of coronary angiography, the following groups were identified: group I – obstructive lesion of the coronary arteries (≥ 70 %) (n = 50); group II – non-obstructive lesion of the coronary arteries (&lt; 70 %) (n = 32); group III – intact coronary arteries (n = 40). Results. According to the results of coronary angiography, the frequency of detection of obstructive lesion of the coronary arteries was 42 % (in patients without past medical history of myocardial infarction – 31 %). Before performing coronary angiography, non-invasive tests were performed in 2.5 % of cases. Pain in the chest was represented by typical angina in 74 % of patients, with no difference in frequency in all groups. PTP values were statistically significantly higher in the group with obstructive CHD (median – 32 %), however, in the other two groups, PTP values corresponded to a high risk of obstructive CHD (median – 27 % and 21 %, respectively). PTP was an independent predictor for obstructive CHD and subsequent myocardial revascularization.Conclusion. In the cohort of outpatients with suspected coronary heart disease we examined during invasive coronary angiography, the frequency of obstructive lesion of the coronary arteries remains low. Non-invasive tests were performed in isolated cases, while PTP was an independent predictor for obstructive CHD and subsequent myocardial revascularization. To increase the frequency of detection of obstructive coronary heart disease, we should adhere to the diagnostic algorithms of the European Society of Cardiology and make wider use of non-invasive imaging tests.

Correlation Between Blood Cadmium Levels and Platelet Characteristics, As Well As Their Impact on Susceptibility to Coronary Heart Disease: Findings from NHANES 2005-2018 Data.

Investigating the correlation between blood cadmium levels, platelet characteristics, and susceptibility to coronary heart disease (CHD). Utilized NHANES 2005-2018 data with covariates such as age, sex, race, marital status, and socio-economic status. Blood cadmium served as the independent variable, while platelet count (PC) and mean platelet volume (MPV) were dependent variables. The average age of the participants was 68.77 ± 11.03 years, and 67.4% of them were male. The mean values for WBC, MPV, PC, and blood cadmium were 7.53 ± 3.36 × 103 cells/µL, 11.33 ± 0.27fL, 57.61 ± 5.34 × 103 cells/µL, and 2.58 ± 0.61 µg/L, respectively. Adjusting for other variables revealed increased MPV and PC with rising blood cadmium levels in cardiac patients, indicating a higher risk of CHD in those with elevated blood cadmium. The average age of the participants was 68.77 ± 11.03 years, and 67.4% of them were male. The mean values for WBC, MPV, PC, and blood cadmium were 7.53 ± 3.36 × 103 cells/µL, 11.33 ± 0.27fL, 57.61 ± 5.34 × 103 cells/µL, and 2.58 ± 0.61 µg/L, respectively. Adjusting for other variables revealed increased MPV and PC with rising blood cadmium levels in cardiac patients, indicating a higher risk of CHD in those with elevated blood cadmium. This study enhances understanding of how cadmium impacts platelet characteristics, contributing to increased CHD risk, providing insights for primary prevention strategies.

Microvascular Disease, Cardiovascular Health, and Risk of Coronary Heart Disease in Type 2 Diabetes: A UK Biobank Study.

The interplay between cardiovascular health metrics (CVHMs) and microvascular disease (MVD) in relation to the risk of incident coronary heart disease (CHD) among individuals with type 2 diabetes mellitus (T2DM) remains to be evaluated. To investigate the role of MVD and CVHMs in the development of CHD among T2DM. We included 19 664 participants with T2DM from the UK Biobank who had CVHM data and were free of CHD during recruitment. CVHMs were defined based on 5 behavioral (body mass index, diet, sleep duration, smoking, and regular exercise) and 3 biological (glycemic control, hyperlipidemia, and hypertension) factors. MVD was defined as the presence of retinopathy, peripheral neuropathy, or chronic kidney disease. Hazard ratio (HR) and 95% CI of CHD were estimated by multivariable Cox regression models. There were 3252 incident cases of CHD recorded after a median follow-up of 12.3 years. After multivariable adjustment, each MVD was separately associated with risk of CHD, and those who had 1 or ≥ 2 MVD had a 27% and an 87% increased risk of developing CHD, respectively. Each unfavorable CVHM was associated with a higher risk of CHD. As compared with MVD-free participants who had ideal CVHMs, those who had ≥ 2 MVD and had poor CVHMs were at particularly high risk of incident CHD (HR = 4.58; 95% CI: 3.58, 5.86), similarly when considering behavioral CVH or biological CVH separately. On an additive scale, there was a positive statistically significant interaction between number of MVD and CVHMs. Coexistence of multiple MVDs was associated with a substantially higher risk of CHD among individuals with T2DM. Such association may be amplified by unfavorable CVHMs.

Association Between HDL2-C and HDL3-C with Cardiovascular Disease: A Nested Case-Control Study in an Iranian Population.

The contribution of high-density lipoprotein cholesterol (HDL-C) subclasses to incident cardiovascular disease (CVD) and coronary heart disease (CHD) remains a subject of debate. The objective of this study was to investigate these associations in a population with a high prevalence of dyslipidemia and CVD. In a nested case-control study, HDL-C and its subclasses (HDL2-C and HDL3-C) in 370 age and gender-matched case and control subjects were determined. This study employed multivariable-adjusted conditional logistic regression to calculate the odds ratios (ORs) for the associations between HDL-C, HDL2-C, HDL3-C, and HDL2-C/HDL3-C (both as continuous and categorical variables) with incident CVD and CHD. The present study models were adjusted for a comprehensive set of confounders, including body mass index, current smoking, hypertension, type 2 diabetes mellitus, use of lipid-lowering drugs, family history of premature CVD, non-HDL-C, and triglycerides. In multivariate analysis, when considering lipoprotein parameters as continuous variables, a 1-unit increase in HDL-C and HDL3-C was associated with a reduced risk of incident CVD and CHD. For CVD, the ORs (95% confidence intervals [CI]) were 0.95 (0.92 - 0.98) and 0.95 (0.93 - 0.98) for HDL-C and HDL3-C, respectively. The corresponding values for CHD were 0.94 (0.91 - 0.97) and 0.94 (0.91 - 0.97). In the categorical approach to lipoprotein parameters, higher quartiles of HDL-C and HDL3-C, compared to the first quartile, were significantly associated with a lower risk of incident CVD and CHD. The ORs (95% CI) for the fourth quartiles were 0.43 (0.25 - 0.74, P for trend = 0.003) and 0.46 (0.27 - 0.78, P for trend = 0.005) for HDL-C and HDL3-C regarding CVD and 0.32 (0.17 - 0.59) and 0.32 (0.18 - 0.59) (all P for trend = 0.001) regarding CHD, respectively. Paradoxically, across quartiles of HDL2-C/HDL3-C, this lipid ratio was associated with a higher risk of CHD (92% higher risk in the fourth quartile). The results showed that HDL3-C, but not HDL2-C, was primarily responsible for the protective effect of HDL-C against CVD, particularly CHD, in Iranian adults.

Development and Validation of a Novel Model for Predicting Coronary Heart Disease in Snoring Hypertensive Patients with Hyperhomocysteinemia.

Hypertensive patients with snoring and elevated plasma homocysteine levels are common. When these factors are combined, the risk of coronary heart disease (CHD) is high. Herein, we developed and validated an easy-to-use nomogram to predict high-risk CHD in snoring hypertensive patients with elevated plasma homocysteine.Snoring patients (n = 1,962) with hyperhomocysteinemia and hypertension were divided into training (n = 1,373, 70%) and validation (n = 589, 30%) sets. We extracted CHD predictors using multivariate Cox regression analysis, then constructed a nomogram model. Internal validation using 1,000 bootstrap resampling was performed to assess the consistency and discrimination of the predictive model using the area under the receiver operating characteristic curve (AUC) and calibration plots.We constructed a nomogram model with the extracted predictors, including age, waist-height ratio, smoking, and low-density lipoprotein cholesterol levels. The AUCs of the training and validation cohorts at 80 months were 0.735 (95% CI: 0.678-0.792) and 0.646 (95% CI: 0.547-0.746), respectively. The consistency between the observed CHD survival and the probability of CHD survival in the training and validation sets was acceptable based on the calibration plots. A total of more than 151 points in the nomogram can be used in the identification of high-risk patients for CHD among snoring hypertensive patients with elevated plasma homocysteine.We developed a CHD risk prediction model for snoring hypertension patients with hyperhomocysteinemia. Our findings provide a useful clinical tool for the rapid identification of high-risk CHD at an early stage.

Utility of a polygenic risk score for incident CHD: interplay with lifestyle in a multi-ethnic cohort of more than 60,000 individuals

Abstract Background The degree to which benefits of healthy eating, physical activity and not smoking are protective for coronary heart disease (CHD) based on levels of polygenic risk remains an important question. We set out to investigate whether and to what degree a favorable lifestyle could reduce the effect of high genetic risk. Methods We utilized data from the Genetic Epidemiology Resource in Adult Health and Aging (GERA) Multi-Ethnic cohort of 60,682 (mean ± SD age = 59 ± 9 years; 67% female; 18% non-European ancestry) Kaiser Permanente of Northern California (KPNC) members. We characterized the cohort at baseline in 2003-2007 by smoking status (never, former or current smoker), Mediterranean-pattern diet (MedDiet) and meeting current AHA physical activity recommendations (PAR) of at least 150 min of moderate activity or 75 min of vigorous activity per week. We stratified the cohort into three groups of CHD genetic risk (low: quintile 1, intermediate: quintiles 2, 3 and 4 combined, and high: quintile 5) using a validated 12-SNP Polygenic Risk Score (PRS) for CHD (CARDIO inCode-Score, GENinCode Plc). Incident CHD consisted of primary in-patient codes for angina pectoris, myocardial infarction, revascularization procedures or CHD death (n=2,220) through 12/31/2014; mean follow-up was 9.5 years. Results Age-adjusted CHD rates per 10,000 person-years were estimated using Poisson regression (accounting for death and health plan disenrollment) by number of favorable lifestyle factors (LF) and, within each level, by genetic risk groups (see Figure below). Genetic background provided further CHD risk stratification within each lifestyle group. The most favorable lifestyle (never smoking, MedDiet, meeting PAR) reduced the effect of high genetic risk by 59% (age-adjusted rates per 10,000 person-years 40 vs. 99) and similar reductions were observed at intermediate or low genetic risk. Conclusions Our results are consistent with an additive model of genetic risk and lifestyle as determinants of CHD. These results underscore the importance of favorable lifestyle and the need to prioritize those individuals with the highest CHD risk (most unfavorable lifestyle and high genetic risk), who will benefit the most from lifestyle advice.

Clustering of vascular aging manifestations and incident cardiovascular events. The Paris Prospective Study III

Abstract Background Vascular aging is a key contributor to cardiovascular disease (CVD). Manifestations of vascular aging are heterogeneous and include atherosclerosis, arterial stiffening, increased arterial wall stress and arterial diameter enlargement. These manifestations have different pathophysiological mechanisms and likely require different prevention strategies. How the different vascular aging manifestations co-exist, or cluster, at the individual level and the association of any such clusters with incident CVD is unknown. Purpose To examine how vascular aging manifestations cluster and whether any such clusters are associated with incident CVD. Methods In the Paris Prospective Study III, a French community-based prospective study on novel determinants of CVD, 10,157 participants underwent a high-resolution carotid echotracking (Artlab, Esaote) between 2008 and 2012, and were thereafter monitored every two years for CVD events up to end 2020 . Hospitalized stroke and coronary heart disease (CHD) events were validated after the review of all medical records. Hierarchical clustering analysis was employed to identify patterns of vascular aging. Hazard ratios (HRs) were quantified in Cox models. Results The study sample included 8,360 participants (39% women, mean age 59.6 years) without prevalent CVD. Three clusters of vascular aging manifestations were identified: - Cluster 1 included 3,995 (47.8%) participants and was characterized by low prevalence of carotid plaques, low carotid intima-media thickness (IMT), low carotid artery stiffness, small carotid diameter and low carotid circumferential wall stress (healthy vascular aging cluster). - Cluster 2 included 2,109 (25.2%) participants and was characterized by high carotid artery stiffness and high carotid circumferential wall stress (arterial stiffness vascular aging cluster). - Cluster 3 included 2,256 (27.0%) participants, and was characterized by high prevalence of carotid plaques and high carotid IMT(atherosclerosis vascular aging cluster). After a median follow-up of 8.5 years, 108 incident stroke events, 218 CHD events and 192 deaths occurred. Compared with cluster 1, cluster 2 (HR 1.76, [95%CI, 1.06-2.94]), but not cluster 3 (HR 1.57, [0.94-2.62]), was associated with a higher risk of stroke. In addition, compared to cluster 1, cluster 3 (HR 1.53, [1.08-2.16]), but not cluster 2 (HR 1.38, [95% CI, 0.96-1.98]), was associated with higher risk of CHD. Both cluster 2 and 3 were associated with higher all-cause mortality (HR for cluster 2: 1.50, [1.02-2.21]; HR for cluster 3: 1.48, [1.01-2.17]). Internal validation using bootstrapping methods (n=1000 samples) provided consistent findings. Conclusion The simultaneous analysis of carotid-echotracking vascular aging parameters identified three patterns of vascular aging that are differentially associated with CHD and stroke in the community.Carotid properties by clustersKM survival curves by clusters

PECULIARITIES OF ANTITHROMBOTIC THERAPY IN THE PATIENTS WITH CORONARY HEART DISEASE WITH CONMINANT TRAUMATOLOGICAL PATHOLOGY. HOW TO KEEP THE BALANCE BETWEEN THROMBOSIS AND BLEEDING?

The selection of antithrombotic therapy for patients with coronary heart disease (CHD) and concomitant pathology, despite clinical recommendations and scales defining the risk of thrombosis and bleeding may be difficult in some cases. Each doctor may face a clinical situation that does not fit within the general recommendations. Practical experience and determination of indications for the use of anticoagulants depending on the dosage in each specific case will help in the faultless choice of a combination of antithrombotic therapy. A clinical example of a very high-risk CHD patient with concomitant traumatological pathology requiring the selection of antithrombotic therapy is presented.

Associations of dietary sugar types with coronary heart disease risk: a prospective cohort study

BackgroundHigher intake of total sugar has been linked with coronary heart disease (CHD) risk, but the role of individual sugars, particularly fructose, is uncertain. ObjectivesThis study aimed to investigate the associations of individual dietary sugars with CHD risk. MethodsIn prospective cohort studies, we followed 76,815 women (Nurses’ Health Study, 1980-2020) and 38,878 men (Health Professionals Follow-up Study, 1986-2016). Sugar and carbohydrate intake, including total fructose equivalents ([TFE] from fructose monosaccharides and sucrose), total glucose equivalents ([TGE] from glucose monosaccharides, disaccharides, and starch), and other sugar types, was measured every 2 to 4 y by semiquantitative food frequency questionnaires. ResultsWe documented 9,723 incident CHD cases over 40 years. In isocaloric substitution models with total fat as a comparison nutrient, comparing extreme quintiles of intake, hazard ratios (HRs), 95% confidence interval [CI]) for CHD risk were 1.31 (1.20 to 1.42; Ptrend < 0.001) for TGE and 1.03 (0.94 to 1.11; Ptrend = 0.25) for TFE. TFE from fruits and vegetables was not associated with CHD risk (Ptrend = 0.70), but TFE from added sugar and juice was associated with CHD risk (HR: 1.12, 95% CI: 1.04 to 1.20; Ptrend < 0.01). Intakes of total sugars and added sugar were positively associated with CHD risk (HRs: 1.16, 95% CI: 1.07 to 1.26, Ptrend < 0.001; 1.08, 95% CI: 0.99 to 1.16, Ptrend = 0.04). ConclusionsIntakes of TGE, total sugar, added sugar, and fructose from added sugar and juice were associated with higher CHD risk, but TFE and fructose from fruits and vegetables were not.

Coronary heart disease risk factors among academic workers based on the Jakarta Cardiovascular Score: A cross-sectional study.

Change in lifestyle leads to change in disease patterns from infectious diseases and malnutrition to degenerative diseases, such as coronary heart disease (CHD). The increasing prevalence of cardiovascular diseases among Indonesian workers and the general public will not only burden medical care expenses but also reduce work productivity, leading to more work-related injuries and work-related losses. The aim of this study was to determine the risk factors for CHD (age, sex, blood pressure, smoking, diabetes mellitus, body mass index, and weekly physical activity) and the CHD risk level among university workers. A cross-sectional study was conducted at workers at School of Medicine, Universitas Malikussaleh, Lhokseumawe, Indonesia. The risk level of CHD was calculated using Jakarta Cardiovascular Score and predicting model analyzed with multiple logistic regression model. Our data found that 58.2%, 25.5% and 16.3% of the university workers had low-, medium- and high-risk to have CHD. The final model indicted that the risk of heart disease was determined by gender, age, and the presence of hypertension and diabetes mellitus. Being male had odds ratio (OR) 30.84, aged >41 years old had OR 11.52, having hypertension had OR 4.87 and having diabetes mellitus had OR 13.99 for having high risk of CHD compared to female, those younger than 41 years old, having no hypertension and having no diabetes mellitus, respectively. In conclusion, our data suggests that more than 15% the respondents (university employees) have high risk of CHD and being male and older, and having hypertension and diabetes mellitus are associated with risk of CHD. Implantation of the preventive measures is therefore important to be implemented at the universities.

Abstract P1045: Replacement Of Wearable-device-measured Sedentary Time By Physical Activity, Genetic Susceptibility, And Risk Of Coronary Heart Disease

Backgrounds: Excess sedentary time (ST) is recognized as an important modifiable risk factor for coronary heart disease (CHD). However, whether the associations of genetic susceptibility with CHD incidence can be modified by replacing wearable-device-measured ST with physical activity (PA) is unknown. This study aims to examine the combined associations of genetic susceptibility to CHD, and wearable-device-measured ST replaced by moderate-to-vigorous PA (MVPA) or light PA in relation to incident CHD. Methods and Findings: This study included 75,545 white British (57% female) with valid wrist-worn accelerometer data and without prevalent CHD/stroke from UK Biobank. Genetic susceptibility to CHD was quantified through weighted polygenic risk scores for CHD based on 300 single-nucleotide polymorphisms. Wrist-worn accelerometer data were used to derive ST, light PA and MVPA. The hazard ratio of CHD was 1.36 (95% CI: 1.03-1.80) for every-30-minute/day-increase in ST relative to other movement behaviors, after adjusting for genetic risk and confounders. Reallocation of any amount of ST (as little as 1 minute/day) into the same MVPA time (but not light PA) was associated with lower CHD hazards overall and within strata of genetic risk: no evidence of interaction between genetic risk and ST (p-value: 0.739). However, differences in absolute risk of CHD for ST replaced by MVPA were greater at high genetic risk versus low genetic risk. Limitations of our study include no causal evidence derived, limited generalizability to individuals of other ethnic groups or with sub-clinical symptoms, and potential residual confounding. Conclusions: Replacing any amount of ST with an equal amount of MVPA time is associated with a lower relative risk of developing CHD at all levels of genetic susceptibility to CHD. Potential reductions in absolute risk of CHD through replacement of ST by MVPA in equivalent amounts may be greater in individuals at high genetic risk of CHD.

Prediction of Coronary Heart Disease Events in Blood or Marrow Transplantation Recipients.

The long-term risk of coronary heart disease (CHD) and clinical models that predict this risk remain understudied in blood or marrow transplantation (BMT) recipients. This study sought to examine the risk of CHD after BMT and identify the associated risk factors. Participants included patients transplanted between 1974 and 2014 at City of Hope, University of Minnesota, or University of Alabama at Birmingham and those who survived≥2 years after BMT. Multivariable logistic regression models assessed CHD risk in BMT survivors compared with a sibling cohort. A self-reported questionnaire and medical records provided information regarding sociodemographics, comorbidities, and therapeutic exposures, which were used to develop a CHD risk prediction nomogram. Overall, 6,677 BMT recipients participated; the mean age at BMT was 43.9 ± 17.7 years, 58.3% were male, and 73.3% were non-Hispanic Whites. The median length of follow-up was 6.9 years (range: 2-46.2 years) from BMT. CHD was reported in 249 participants, with a 20-year cumulative incidence of 5.45% ± 0.39%. BMT survivors had a 1.6-fold greater odds of CHD compared with a sibling cohort (95% CI: 1.09-2.40). A nomogram was then developed to predict the risk of CHD at 10 and 20 years after BMT including age at BMT (HR: 1.06/y; 95% CI: 1.04-1.08), male sex (HR: 1.89; 95% CI: 1.15-3.11), a history of smoking (HR: 1.61; 95% CI: 1.01-2.58), diabetes (HR: 2.45; 95% CI: 1.23-4.89), hypertension (HR: 2.02; 95% CI: 1.15-3.54), arrhythmia (HR: 1.90; 95% CI: 0.89-4.06), and pre-BMT chest radiation (yes vs no: HR: 2.83; 95% CI: 1.20-6.67; unknown vs no: HR: 0.88; 95% CI: 0.34-2.28). The C-statistic was 0.77 in the test set (95% CI: 0.70-0.83). This study identified BMT recipients at high risk for CHD, informing targeted screening for early detection and aggressive control of risk factors.

Mode of transport, genetic susceptibility, and incidence of coronary heart disease

BackgroundCar use has been associated with higher risk of coronary heart disease (CHD). However, whether the associations of transport modes with CHD vary by genetic susceptibility to CHD are unknown. This study aims to investigate the associations of genetic susceptibility and modes of transport with incidence of CHD.MethodsWe included 339,588 white British participants from UK Biobank with no history of CHD or stroke at baseline or within two years of follow-up (52.3% in work). Genetic susceptibility to CHD was quantified through weighted polygenic risk scores derived from 300 single-nucleotide polymorphisms related to CHD risk. Categories of transport mode included exclusive car use and alternatives to the car (e.g., walking, cycling and public transport), separately for non-commuting (e.g., getting about [n=339,588] excluding commuting for work), commuting (in the sub-set in work [n=177,370] who responded to the commuting question), and overall transport (transport mode for both commuting and non-commuting [n=177,370]). We used Cox regression with age as the underlying timescale to estimate hazard ratios (HR) of CHD (n=13,730; median 13.8-year follow-up) and tested the interaction between genetic susceptibility and travel modes with adjustment for confounders.ResultsCompared to those using alternatives to the car, hazards of CHD were higher for exclusive use of cars for overall transport (HR: 1.16, 95% confidence interval (CI): 1.08-1.25), non-commuting (HR: 1.08, 95% CI: 1.04-1.12) and commuting (HR: 1.16, 95% CI: 1.09-1.23), after adjusting for confounders plus genetic susceptibility. HRs of CHD were 1.45 (95% CI: 1.38-1.52) and 2.04 (95% CI: 1.95-2.12) for the second and third tertile of genetic susceptibility to CHD, respectively, compared to the first. There was, in general, no strong evidence of interactions between genetic susceptibility and categories of overall, non-commuting and commuting transport. Estimated 10-year absolute risk of CHD was lower for the alternatives to the car across strata of genetic susceptibility, compared with exclusive use of cars for overall, non-commuting and commuting transport.ConclusionExclusive use of cars was associated with a relatively higher risk of CHD across all strata of genetic susceptibility. Using alternatives to the car should be encouraged for prevention of CHD for the general population including individuals at high genetic risk.

Lung function indices do not affect the incidence of coronary heart disease in patients with sleep-disordered breathing

BackgroundCurrently, it's unclear whether sleep-disordered breathing (SDB) and reduced lung function could synergistically increase the incidence of coronary heart disease (CHD). Furthermore, the predictive value of different lung function indices for the incidence of CHD remains unknown. MethodsWe enrolled 3749 participants from the Sleep Heart Health Study (SHHS) to conduct a retrospective study. The individuals were divided into the SDB and non-SDB subgroups according to Apnoea–Hypopnoea Index (AHI). Cox regression models were used to evaluate the association between lung function and CHD. We also conducted a ROC analysis to assess the predictive value of different lung function indices. Results512 cases of CHD were identified during an average of 10.40 years of follow-up in participants without CVD at baseline. We observed that lung function was a better predictor of CHD in non-SDB participants compared with SDB participants. Reduced lung function was associated with a higher risk of CHD in participants without SDB, while the inverse association became non-significant in participants with SDB. Furthermore, the incremental contribution of lung function to CHD diminished with increasing severity of SDB. ConclusionWe need to focus more on the lung function of individuals without SDB rather than those with SDB to reduce the risk of CHD.

Lifestyle and pharmacological interventions in South America: Potential barriers for recruitment, implementation, and effectiveness

AbstractBackgroundThe study of vascular cognitive impairment and dementia (VCID) risk factors must be reproduced in every community so that disparities may be addressed. In South America, diverse levels of education, mixed ethnicity, genetic and cultural heterogeneity, and the burden of cerebrovascular risk are important features to be investigated for proper interventions.MethodsObservational and interventional VCID studies from South America will be discussed so that issues concerning potential barriers for participant recruitment and research effectiveness may be addressed.ResultsFew South American institutions have studied risk factors for VCID. Older people suffer the effects of restrictions to female education that occurred a century ago. Cross‐sectional studies demonstrated that APOE‐ε4 carrier status predisposes to physical inactivity and has smaller effects over dementia onset than in studies from the Northern Hemisphere, possibly due to ethnical disparities, while the burden of combined cerebrovascular risk factors (and smoking in particular) in this regard is high. Foreigners living in Brazil had later dementia onset, unexplained by common genetic variants. While prevalent in almost half of the older population, and associated with earlier dementia onset particularly in women, depression could be a risk factor or a prodromal symptom. Late life prospective studies verified that cerebrovascular risk factors such as arterial hypertension, hypercholesterolemia and a higher coronary heart disease risk, or increased creatinine clearance for women only, may be neuroprotective against cognitive and functional decline, probably due to enhanced cerebral perfusion. Lifetime sanitary conditions and increasing late life body mass index may protect against frailty, while education is neuroprotective for women and APOE‐ε4 carriers (though associated with faster cognitive decline in some cohorts). Longitudinal pharmacogenetic studies demonstrated that potential benefits of cerebrovascular metabolism modulators such as angiotensin‐converting enzyme inhibitors and lipophilic statins depend upon epistatic interactions among specific genetic variants. Caregiver awareness of the need to control cerebrovascular risk is beneficial for patients.ConclusionsGenomic effects of cognitive reserve, cerebral perfusion, and hormonal changes interact on mechanisms of neurodegeneration. Adherence to lifestyle and pharmacological interventions in South America is highly dependent upon proper funding, public support, harmonization efforts, institutional expertise and leadership, and caregiver education. (Supported by FAPESP grant #2015/10109‐5)