Incidence Of Coronary Heart Disease Research Articles

Sex-Associated Metabolites and Incident Stroke, Incident Coronary Heart Disease, Hypertension, and Chronic Kidney Disease in the REGARDS Cohort.

Sex disparities exist in cardiometabolic diseases. Metabolomic profiling offers insight into disease mechanisms, as the metabolome is influenced by environmental and genetic factors. We identified metabolites associated with sex and determined if sex-associated metabolites are associated with incident stoke, incident coronary heart disease, prevalent hypertension, and prevalent chronic kidney disease. Targeted metabolomics was conducted for 357 metabolites in the REGARDS (Reasons for Geographic and Racial Differences in Stroke) case-cohort substudy for incident stroke. Weighted logistic regression models were used to identify metabolites associated with sex in REGARDS. Sex-associated metabolites were replicated in the HyperGEN (Hypertension Genetic Epidemiology Network) and using the literature. Weighted Cox proportional hazard models were used to evaluate associations between metabolites and incident stroke. Cox proportional hazard models were used to evaluate associations between metabolites and incident coronary heart disease. Weighted logistic regression models were used to evaluate associations between metabolites and hypertension and chronic kidney disease. Fifty-one replicated metabolites were associated with sex. Higher levels of 6 phosphatidylethanolamines were associated with incident stroke. No metabolites were associated with incident coronary heart disease. Higher levels of uric acid and leucine and lower levels of a lysophosphatidylcholine were associated with hypertension. Higher levels of indole-3-lactic acid, 7 phosphatidylethanolamines, and uric acid, and lower levels of betaine and bilirubin were associated with chronic kidney disease. These findings suggest that the sexual dimorphism of the metabolome may contribute to sex differences in stroke, hypertension, and chronic kidney disease.

Family History and Smoking on Coronary Heart Disease

Cases of coronary heart disease in a private hospital in Madiun City in the last year have increased by 41% due to various risk factors. So researchers are interested in examining whether the incidence of coronary heart disease is correlated with family history and smoking. This research design is quantitative with a case-control approach. The population is all CHD sufferers in the period January-November 2022. The total population is 159 subjects, with a sample of 54 case subjects and 54 control subjects. The questionnaire method was used to collect data, and then the Chi-square test was used to analyze the data. The results of this study were that there was a significant relationship between smoking and the incidence of CHD (p-value = 0,034), and there was a family history of CHD incidence (p-value = 0,012) at Hospital X Madiun City. There is a need to provide outreach regarding efforts to prevent CHD to the public in order to reduce cases of CHD.

Very short sleep duration reveals a proteomic fingerprint that is selectively associated with incident diabetes mellitus but not with incident coronary heart disease: a cohort study

BackgroundThe molecular pathways linking short and long sleep duration with incident diabetes mellitus (iDM) and incident coronary heart disease (iCHD) are not known. We aimed to identify circulating protein patterns associated with sleep duration and test their impact on incident cardiometabolic disease.MethodsWe assessed sleep duration and measured 78 plasma proteins among 3336 participants aged 46–68 years, free from DM and CHD at baseline, and identified cases of iDM and iCHD using national registers. Incident events occurring in the first 3 years of follow-up were excluded from analyses. Tenfold cross-fit partialing-out lasso logistic regression adjusted for age and sex was used to identify proteins that significantly predicted sleep duration quintiles when compared with the referent quintile 3 (Q3). Predictive proteins were weighted and combined into proteomic scores (PS) for sleep duration Q1, Q2, Q4, and Q5. Combinations of PS were included in a linear regression model to identify the best predictors of habitual sleep duration. Cox proportional hazards regression models with sleep duration quintiles and sleep-predictive PS as the main exposures were related to iDM and iCHD after adjustment for known covariates.ResultsSixteen unique proteomic markers, predominantly reflecting inflammation and apoptosis, predicted sleep duration quintiles. The combination of PSQ1 and PSQ5 best predicted sleep duration. Mean follow-up times for iDM (n = 522) and iCHD (n = 411) were 21.8 and 22.4 years, respectively. Compared with sleep duration Q3, all sleep duration quintiles were positively and significantly associated with iDM. Only sleep duration Q1 was positively and significantly associated with iCHD. Inclusion of PSQ1 and PSQ5 abrogated the association between sleep duration Q1 and iDM. Moreover, PSQ1 was significantly associated with iDM (HR = 1.27, 95% CI: 1.06–1.53). PSQ1 and PSQ5 were not associated with iCHD and did not markedly attenuate the association between sleep duration Q1 with iCHD.ConclusionsWe here identify plasma proteomic fingerprints of sleep duration and suggest that PSQ1 could explain the association between very short sleep duration and incident DM.

Changes in Sleep Patterns, Genetic Susceptibility, and Incident Cardiovascular Disease in China

The associations of changes in sleep patterns with incident cardiovascular disease (CVD) are not fully elucidated, and whether these associations are modified by genetic susceptibility remains unknown. To investigate the associations of 5-year changes in sleep patterns with incident CVD and whether genetic susceptibility modifies these associations. This prospective cohort study of the Dongfeng-Tongji cohort was conducted from 2008 to 2018 in China. Eligible participants included those with complete sleep information at baseline survey (2008-2010) and the first follow-up survey (2013); participants who had no CVD or cancer in 2013 were prospectively assessed until 2018. Statistical analysis was performed in November 2023. Five-year changes in sleep patterns (determined by bedtime, sleep duration, sleep quality, and midday napping) between 2008 and 2013, and polygenic risk scores (PRS) for coronary heart disease (CHD) and stroke. Incident CVD, CHD, and stroke were identified from 2013 to 2018. Cox proportional hazards regression models were applied to estimate hazard ratios (HRs) and 95% CIs. Among 15 306 individuals (mean [SD] age, 65.8 [7.4] years; 8858 [57.9%] female and 6448 male [42.1%]), 5474 (35.78%) had persistent unfavorable sleep patterns and 3946 (25.8%) had persistent favorable sleep patterns. A total of 3669 incident CVD cases were documented, including 2986 CHD cases and 683 stroke cases, over a mean (SD) follow-up of 4.9 (1.5) years. Compared with those with persistent unfavorable sleep patterns, individuals with persistent favorable sleep patterns over 5 years had lower risks of incident CVD (HR, 0.80; 95% CI, 0.73-0.87), CHD (HR, 0.84; 95% CI, 0.76-0.92), and stroke (HR, 0.66; 95% CI, 0.54-0.82) in the subsequent 5-year period. No significant effect modification by PRS was observed for sleep pattern change and CHD or stroke risk. However, sleep pattern changes and PRS were jointly associated with the CHD and stroke risk in a dose-dependent manner, with the lowest risk being among those with persistent favorable sleep patterns combined with low PRS (HR for CHD, 0.65; 95% CI, 0.52-0.82 and HR for stroke, 0.48; 95% CI, 0.29-0.79). In this cohort study of middle-aged and older Chinese adults, individuals with persistent favorable sleep patterns had a lower CVD risk, even among those with higher genetic risk. These findings highlight the importance of maintaining favorable sleep patterns for CVD prevention.

Differential age-specific associations of LDL cholesterol and body mass index with coronary heart disease

Background and aimsLow‐density lipoprotein cholesterol (LDLc) and body mass index (BMI) are not always correlated and their relationship is probably dependent on age, indicating differential age-specific associations of these factors with health outcomes. We aim to discriminate the roles of LDLc and BMI in coronary heart disease (CHD) across different age groups. MethodsThis is a prospective cohort study of 368,274 participants aged 38–73 years and free of CHD at baseline. LDLc and BMI were measured at baseline, and incident CHD was the main outcome. Cox proportional hazards model and restricted cubic spline (RCS) regression were used to estimate hazard ratio (HR) and 95% confidence interval (CI) of exposure on CHD. ResultsAfter a mean of 12 years of follow-up, similar relationships of LDLc and BMI with CHD risk were observed in the overall population but in differential age-specific patterns. Across the age groups of <50, 50–54, 55–59, 60–64 and ≥ 65 years, the LDLc-CHD association diminished with the adjusted HRs decreasing from 1.35, 1.26, 1.19, 1.11 to 1.08; while no declining trend was found in BMI-CHD relationship with the adjusted HRs of 1.15, 1.11, 1.12, 1.13 and 1.15, respectively. The interaction and mediation between LDLc and BMI on CHD risk were more pronounced at young-age groups. LDLc-CHD but not BMI-CHD association was dependent on sex, metabolic syndrome and lipid-lowering drugs use. ConclusionsThere were differential age-specific associations of LDLc and BMI with the risk of developing CHD, calling for future efforts to discriminate the age-different benefits from lipids management or weight control on the primary prevention for CHD.

Incidence of coronary heart disease among remote workers: a nationwide web-based cohort study

Coronary heart disease (CHD) risk is influenced by socioeconomic status-related parameters, particularly occupation. We investigated occupational gaps in CHD risk and how the introduction of remote work moderated the observed occupational differences in CHD risk during the coronavirus disease 2019 pandemic in Japan. Data from a web-based, nationwide cohort study, comprising 17,640 workers (aged 20–65 years) with baseline data from December 2020, were analyzed. Participants were grouped by occupation as upper-level nonmanual workers (managers/professionals) and others (reference group). The primary outcome was CHD (angina pectoris/myocardial infarction) onset retrospectively confirmed at the 1-year follow-up survey. Upper-level nonmanual workers exhibited a higher CHD incidence than others (2.3% vs. 1.7%). This association was pronounced in the younger (20–49 years) population, with a significant CHD risk (adjusted risk ratio = 1.88). Upper-level nonmanual workers exhibited nearly 15% higher remote work prevalence, with a significant remote work-related CHD risk (adjusted risk ratio = 1.92). The mediating effects of remote work explained an overall disparity of 32% among the younger population. Occupational gaps in CHD incidence in Japan differ from those in Western countries, where upper-level nonmanual workers have lower cardiovascular risk. In Japan, remote work can mediate CHD risk in the younger population of upper-level nonmanual workers.

Polygenic risk and incident coronary heart disease in a large multiethnic cohort

ObjectiveMany studies support the notion that polygenic risk scores (PRS) improve risk prediction for coronary heart disease (CHD) beyond conventional risk factors. However, PRS are not yet considered risk-enhancing factor in guidelines. Our objective was to determine the predictive performance of a commercially available PRS (CARDIO inCode-Score®) compared with the Pooled Cohorts Equations (PCE) in a contemporary, multi-ethnic cohort. MethodsParticipants (n = 63,070; 67 % female; 18 % non-European) without prior CHD were followed from 2007 through 12/31/2022. The association between the PRS and incident CHD was assessed using Cox regression adjusting for genetic ancestry and risk factors. Event rates were estimated by categories of PCE and by low/intermediate/high genetic risk within PCE categories; risk discrimination and net reclassification improvement (NRI) were also assessed. ResultsThere were 3,289 incident CHD events during 14 years of follow-up. Adjusted hazard ratio (aHR) for incident CHD per 1 SD increase in PRS was 1.18 (95 % CI:1.14–1.22), and the aHR for the upper vs lower quintile of the PRS was 1.66 (95 % CI:1.49–1.86). The association was consistent in both sexes, in European participants compared with all minority groups combined and was strongest in the first 5 years of follow-up. The increase in the C-statistic was 0.004 (0.747 vs. 0.751; p < 0.0001); the NRI was 2.4 (0.9–3.8) for the entire cohort and 9.7 (7.5–12.0) for intermediate PCE risk individuals. After incorporating high genetic risk, a further 10 percent of participants at borderline/intermediate PCE risk would be candidates for statin therapy. ConclusionInclusion of polygenic risk improved identification of primary prevention individuals who may benefit from more intensive risk factor modification.

Abstract P105: Blood Lipids, Lipoproteins, and Apolipoproteins With Risk of Coronary Heart Disease: A Prospective Study Among Multi-Racial Populations

Background: Blood lipids, such as total cholesterol (TC), LDL-cholesterol (LDL-C), and triglycerides (TG), are well-known risk factors for coronary heart disease (CHD). However, studies that examined the associations of circulating lipids and apolipoproteins carried by different lipoproteins with incident CHD remain limited, particularly among racially diverse populations. Hypothesis: Potential novel lipoprotein biomarkers, other than TC, TG, LDL-C, and HDL-C, are associated with incident CHD in diverse populations. Methods: We conducted nested case-control studies of CHD among White Americans (542 pairs; n =1084), Black Americans (622 pairs; n =1244), and Chinese adults (557 pairs; n =1114) drawn from the Southern Community Cohort Study and Shanghai Women’s and Men’s Health Studies. We examined the associations of 36 plasma lipids, lipoproteins, and apolipoproteins (measured by Bruker IVDr NMR platform) with incident CHD using conditional logistic regression, adjusted for sociodemographics, lifestyle, family history of CHD, and menopausal status (women only). Race-specific odds ratios (ORs) were pooled using fixed-effect meta-analysis. Results: TC, TG, LDL-C, and HDL-C were associated with incident CHD, with pooled ORs being 1.35, 1.31, 1.26, and 0.79 per 1-SD increase. Sixteen lipoprotein biomarkers showed larger effect sizes than those conventional lipids, with pooled ORs per 1-SD ranged from 1.37 to 1.59 and a negative OR of 0.77 ( Figure 1 ); all associations were significant within each race. Significant associations were observed across subpopulations defined by sociodemographics, lifestyle, and status of obesity, diabetes, hypertension, and dyslipidemia, including among individuals with normal levels of TC, TG, LDL-C, and HDL-C. Conclusion: Our study identified several lipoprotein biomarkers (e.g., ApoB/ApoA1 ratio and LDL-TG) associated with incident CHD among multi-racial populations, suggesting potential clinical utility complementing the current lipid panel.

Abstract MP46: Recurrent Hypertensive Disorders of Pregnancy and Subsequent Maternal Coronary Heart Disease and Stroke

Introduction: Hypertensive disorders of pregnancy (HDP) complicate 5-10% of pregnancies and lead to maternal morbidity and mortality. Prior HDP increases HDP risk in subsequent pregnancies with little known about coronary heart disease (CHD) and stroke in recurrent HDP. We aimed to assess the relationship between recurrent HDP and subsequent CHD and stroke. Methods: This retrospective cohort study included women aged 12-49 with one or more singleton, live birth in South Carolina from 2004-2016. Deliveries were evaluated for HDP (preeclampsia, eclampsia, gestational hypertension) defined by birth certificate and/or hospitalization/emergency department (ED) visit data. Women were classified as having no, one, or two or more pregnancies with HDP. Hospitalization/ED visit and death certificate data defined incident CHD and stroke. Extended Cox models with time varying covariates were used to evaluate the association of recurrent HDP with CHD and stroke controlling for sociodemographic, behavioral, and clinical characteristics. Results: The 163,598 women (non-Hispanic White (NHW; 57.8%), non-Hispanic Black (NHB; 33.9%), and Hispanic (8.3%) had two or more (3.3%), one (12.0%), or no (84.7%) HDP pregnancies. Women with recurrent HDP were more likely to develop subsequent CHD or stroke after covariable adjustment (Table 1). Having one or two or more HDP pregnancies compared with no HDP pregnancies increased the subsequent risk of CHD (HR=2.25; 95% CI: 1.97-2.56 and HR=2.98; 95% CI: 2.43-3.67, respectively). Having one or two or more HDP pregnancies compared with no HDP pregnancies increased the subsequent risk of stroke (HR=2.05; 95% CI: 1.61-2.61 and HR=2.97; 95% CI: 2.04-4.32, respectively). Discussion: Women with recurrent HDP are at higher risk of subsequent CHD and stroke. Higher incident CHD and stroke risk appears to persist into the next pregnancy with accumulated HDP conferring higher risk.

Abstract MP73: The Association of Urinary Metals With Cardiovascular Disease Incidence and All-Cause Mortality in the Multi-Ethnic Study of Atherosclerosis (MESA)

Background: Environmental exposure to metals is widespread yet preventable and has been associated with cardiovascular disease (CVD) endpoints, although evidence from prospective studies with racial and ethnic diversity is limited. Objective: We assessed the prospective association of urinary metals with incident coronary heart disease (CHD) and CVD and all-cause mortality in a diverse population of adults from the Multi-Ethnic Study of Atherosclerosis (MESA). Methods: We included 6,638 MESA participants (mean (SD) age 62.1(10.2) years, 53% female, 39% non-Hispanic white, 27% non-Hispanic Black, 22% Hispanic/Latino, 12% Chinese). Urinary non-essential metals (cadmium, tungsten, and uranium), and essential metals (cobalt, copper, and zinc) were assessed at baseline (2000-2001). We used Cox proportional hazards regression to estimate adjusted (table footnote) hazard ratios (HR) for the association between urine metals with incident CHD, CVD, and all-cause mortality through 2019. Results: Over 17.7 years median follow up (IQR: 12.4, 18.5), 749 (11%) participants developed CHD, 1,162 (17%) developed CVD, and 1,844 (28%) died. In the models adjusted by sociodemographic and behavioral factors (Table 1, [Model 1]), one IQR increase in urinary cadmium, tungsten, cobalt, copper, and zinc at baseline was significantly associated with higher risk of incident CHD, incident CVD and all-cause mortality. Uranium levels were significantly associated with all-cause mortality and incident CVD, but not CHD. The magnitude of the association was attenuated when adjusting the models for clinical risk factors (Table 1, [Model 2]). A linear trend was identified for cadmium and copper and all endpoints. Conclusion: Our findings among a large and ethnically diverse US population support that metal exposure is associated with incident CVD and premature mortality. These findings can inform the development of novel preventive strategies to improve cardiovascular health.

Abstract 44: Soluble CD14 and Risk of Incident Cognitive Impairment: The Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study

Introduction: Black adults in the U.S. experience a greater burden of systemic inflammation and cognitive impairment and dementia compared with White adults. Increasing evidence suggests peripheral inflammation is a risk factor for cognitive decline, however few longitudinal studies have investigated these relationships. CD14 is a pattern recognition receptor expressed by monocytes and macrophages that promotes inflammation. Concentrations of the soluble form of CD14 (sCD14) vary by race, and higher sCD14 was associated with incident coronary heart disease (CHD) and stroke in Black but not White participants in the REGARDS cohort study. We hypothesized higher sCD14 would also be more strongly associated with incident cognitive impairment (ICI) in Black compared to White adults. Methods: We performed a nested case-control study of ICI in the REGARDS study, a biracial cohort of 30,239 American adults ≥45 years old. Cases were 495 participants without cognitive impairment or stroke at baseline who developed ICI during a median 3.5 years of follow-up based on abnormal scores on ≥2 of 3 cognitive tests. 587 controls were selected from a cohort random sample and free of cognitive impairment or stroke at baseline. Logistic regression models estimated odds ratios (OR) of ICI by concentration of sCD14 measured from stored baseline serum samples. We tested for a sCD14-by-race interaction a priori. Results: The sCD14-by-race interaction term was statistically significant in each model (p-interaction &lt;0.05). In analyses stratified by race, adjusting for demographic factors (age, sex, and region), a 1-SD increment sCD14 was associated with a 40% higher odds of ICI among Black adults (OR: 1.40; 95% CI: 1.07, 1.95) with no association among White adults (OR: 1.08; 95% CI: 0.90, 1.28). In models adjusted for cognitive and vascular risk factors (income, education, systolic blood pressure, hypertension medication use, dyslipidemia, BMI, history of heart disease, atrial fibrillation, diabetes, smoking, and alcohol use), the relationship was attenuated in Black participants (OR: 1.33; 95% CI: 0.96, 1.84) and remained null among White participants (OR: 0.99; 95% CI: 0.81, 1.22). Comparing those with sCD14 concentration &gt;90th percentile to below, adjusted for risk factors, Black participants had a 2.47 (95% CI: 1.08, 5.67) higher odds of ICI with no association in White participants (OR: 0.91; 95% CI: 0.46, 1.80). Discussion: Higher sCD14 was associated with ICI risk in Black but not White adults, similar to prior observations for stroke. Results suggest that sCD14-associated inflammatory responses may be a risk factor for ICI among Black adults.

Abstract 19: Time-Varying Exposure to Food Retailers and Cardiovascular Disease Incidence and Mortality in the Netherlands: A Nationwide Prospective Cohort Study

Background: The food environment is suggested as a risk factor of cardiovascular disease (CVD), but current evidence is inconsistent and does not account for changes in the food environment. We aimed to explore if time-varying exposure to the food environment was associated with hospitalisation and mortality due to total and specific types of CVD in The Netherlands. We hypothesized that favourable time-varying trends in food environment exposure would be associated with decreased risk of CVD, stroke, heart failure (HF), and coronary heart disease (CHD) morbidity and mortality among the Dutch general population. Methods: A prospective cohort study was performed among all Dutch residents aged 35+ years who did not change residence in 2002-2018 without CVD in 2004, identified through registry data from Statistics Netherlands (n=4,641,435; 51.3% female, 91.2% Dutch). Time-varying Food Environment Healthiness Index (FEHI) scores (range: -5 to 5) and time-varying Kernel density of six specific food retailers (food delivery outlets, fast food outlets, restaurants, local food shops, supermarkets and convenience stores) around the home location were based on bi-annual updates between 2004-2018. Hospitalisation and mortality due to overall CVD, stroke, HF, and CHD occurring between 2004 and 2020 were used as outcomes, based on hospital and death registries. Models were adjusted for age, sex, ethnic origin, household composition, income, marital status and neighbourhood urbanisation level and effect modification by age, sex, urbanization and income was studied. Results: Each unit increase in the FEHI, representing a 10% improvement, was associated with a lower hospitalisation and mortality of CVD (hospitalization Hazard Ratio (HR h )=0.90, 0.89-0.91, mortality Hazard Ratio (HR m )=0.85, 0.82-0.89), CHD (HR h =0.88, 0.85-0.91, HR m =0.80, 0.75-0.86), stroke (HR h =0.89, 0.84-0.93, HR m =0.89, 0.82-0.98), and HF (HR h =0.90, 0.84-0.96, HR m =0.84, 0.76-0.92). Increased density of local food shops, fast food outlets, supermarkets and convenience stores, and decreased density of food delivery outlets and restaurants were associated with a higher risk of CVD, CHD, stroke and HF incidence and mortality, albeit with small effect sizes. Stratified analyses suggest slightly stronger associations in highly urbanized areas, younger adults and those with higher incomes. Conclusions: Favourable trends in time-varying food retailer exposure were associated with a risk reduction in CVD hospitalisation and mortality, in particular in urbanized areas and for younger adults and those with higher incomes.

Abstract P277: Adherence to Time-Restricted Eating, Plasma Metabolomic Signatures, and Risk of Coronary Heart Disease

Introduction: Early time-restricted eating (TRE) has been recently suggested as an effective dietary intervention strategy to improve risk factors of coronary heart disease (CHD), whereas late TRE may be related to poor cardiometabolic health. Metabolomic pathways linking the adherence to habitual TREs depending on the time of the day and CHD risk are unknown. Hypothesis: We tested whether adherence to early or late TRE was related to distinct metabolomic signatures (including those in pathways of energy/purine pyrimidine metabolism, lipids, carbohydrates, and acylcarnitines). We then tested whether TRE-related plasma metabolites were associated with the risk of incident CHD among women without prior CHD. Methods: This study included 674 women without cardiovascular disease who completed 7-day food records and measurements of untargeted plasma metabolomics in a sub-study of the Nurses’ Health Studies (NHS/NHSII). TRE was indicated by 4-12 hours of daily eating window. The adherence to TRE was assessed by summing up the TRE days in a week (0-7 days). We analyzed two TRE habits: early TRE (starting before 9 a.m./ending no later than 9 p.m.) and late TRE (beginning after 9 a.m.). Separately, plasma metabolites were measured in a prospective nested case-control of 762 incident cases of CHD and 762 matched controls identified over 10-14 years of follow-up in the NHS. A metabolomic risk score for predicting adherence to late TRE (MRS-TRE late ) was created based on metabolites selected through the elastic net procedure with a 10-fold cross-validation. Results: Adherence to late TRE was positively associated with greater adiposity, insulin/proinsulin, uric acid, and medium-chain fatty acids/acylcarnitines; the late TRE habit was inversely related to metabolites in the TCA cycle/pyruvate metabolism and specific PC species ( P FDR &lt;0.05). On the other hand, metabolites in lipid pathways (including diglyceride DG 38:5) and glucose were inversely related to the adherence to early TRE. Individual levels of late-TRE-related metabolites in energy/phosphatidylcholine /acylcarnitine pathways were significantly associated with an increased risk of CHD. Every 1 SD increment of MRS-TRE late , based on 21 metabolites in various metabolic pathways, was associated with a relative risk (RR) of 1.24 (95% CI: 1.11, 1.38) for CHD in a model adjusted for matching factors, and a RR of 1.15 (1.02, 1.29) after adjusting for covariates, such as demographic factors, diet quality, alcohol, lifestyle factors, and BMI. Women in the top tertile of MRS-TRE late had a 1.44-fold (1.10, 1.89) increased risk of CHD as compared to those in the lowest tertile after adjusting for the covariates. Conclusions: TRE habit, depending on the timing, was related to distinct metabolomic pathways, and adherence to late TRE may be associated with metabolic reliance linked to the risk of incident CHD among women.

Plasma Biomarker Profiles for Premature and Nonpremature Coronary Heart Disease in Women.

Premature coronary heart disease (CHD) is a major cause of death in women. We aimed to characterize biomarker profiles of women who developed CHD before and after age 65 years. In the Women's Health Study (median follow-up 21.5 years), women were grouped by age and timing of incident CHD: baseline age <65 years with premature CHD by age 65 years (25 042 women; 447 events) and baseline age ≥65 years with nonpremature CHD (2982 women; 351 events). Associations of 44 baseline plasma biomarkers measured using standard assays and a nuclear magnetic resonance (NMR)-metabolomics assay were analyzed using Cox models adjusted for clinical risk factors. Twelve biomarkers showed associations only with premature CHD and included lipoprotein(a), which was associated with premature CHD [adjusted hazard ratio (HR) per SD: 1.29 (95% CI 1.17-1.42)] but not with nonpremature CHD [1.09(0.98-1.22)](Pinteraction = 0.02). NMR-measured lipoprotein insulin resistance was associated with the highest risk of premature CHD [1.92 (1.52-2.42)] but was not associated with nonpremature CHD (Pinteraction <0.001). Eleven biomarkers showed stronger associations with premature vs nonpremature CHD, including apolipoprotein B. Nine NMR biomarkers showed no association with premature or nonpremature CHD, whereas 12 biomarkers showed similar significant associations with premature and nonpremature CHD, respectively, including low-density lipoprotein (LDL) cholesterol [1.30(1.20-1.45) and 1.22(1.10-1.35)] and C-reactive protein [1.34(1.19-1.50) and 1.25(1.08-1.44)]. In women, a profile of 12 biomarkers was selectively associated with premature CHD, driven by lipoprotein(a) and insulin-resistant atherogenic dyslipoproteinemia. This has implications for the development of biomarker panels to screen for premature CHD.

Fish - a scoping review for Nordic Nutrition Recommendations 2023.

The aim of this scoping review was to conduct evidence-based documentation between fish intake and health outcomes for food-based dietary guidelines (FBDGs) in the Nordic Nutrition Recommendations (NNR) 2023. For most health outcomes, the evidence for fish oil and n-3 long chain (LC) polyunsaturated fatty acids (PUFA) supplementation was included when examining evidence between fish intake and health. In this review, conclusions from qualified systematic reviews (qSR) approved by NNR2023 are included. In addition, conclusions of a de novo systematic reviews on the topic of n-3 LC-PUFA, asthma, and allergy are included. Finally, a systematic literature search was performed limited to systematic reviews and meta-analysis published between 2011 and September 2021. In total, 21 papers from the systematic literature search, four qSR, and eight reports were included addressing the association between fish intake, fish oil, and n-3 LC-PUFA supplementation on several health outcomes. These included cardiovascular disease (CVD), type 2 diabetes, cancers (colorectal, breast, and prostate), metabolic syndrome, obesity, mortality, cognition and mental health, pregnancy-related outcomes (preterm birth and birth weight), and outcomes specific for children (neurodevelopment, and risk of food allergies, and asthma). In addition, intermediate risk factors such as blood lipids, glucose, C-reactive protein, and blood pressure were reviewed. Based on current evidence, fish consumption can have beneficial effects to prevent coronary heart disease (CHD) and stroke incidence, and lower mortality from CVD, CHD, myocardial infarction (MI), and stroke, as well as total mortality risk. In addition, fish consumption is beneficial for preventing cognitive decline in adults (e.g. dementia and Alzheimer's disease). Fish intake may also prevent metabolic syndrome, supported by an observed association between fish intake and reduction in plasma triglycerides and increase in high-density lipoprotein (HDL) cholesterol levels. Data from fish oil and n-3 LC-PUFA supplementation studies supports the conclusions on the effects of fish consumption on most of the health outcomes.

Hubungan Efek Gabungan Hipertensi dan Obesitas dengan Penyakit Jantung Koroner Pada Analisis Data IFLS 5 Tahun 2014

Background: Coronary heart disease is a non-communicable disease. Risk factors for coronary heart disease include hypertension, smoking, high cholesterol, obesity, and low consumption of fruits and vegetables.Methods: The aim of this study was to determine the relationship between the combined effects of hypertension and obesity and the incidence of coronary heart disease. This study uses the 2014 Indonesia Family Life Survey (IFLS). This analysis uses univariate analysis to determine the proportion of research variables, bivariate analysis to determine the relationship between variables, and stratification analysis to determine the presence of confounding and modification effects. Multivariate analysis to determine the final model. This study used a cross-sectional design.Results: coronary heart disease variable 1.44%, hypertension and obesity 9.77%, hypertension and not obesity 9.64%, not hypertension and obesity 22.04%, not hypertension and not obesity 58.55%. And the relationship of hypertension and obesity to coronary heart disease after controlling for age and gender variables.Conclusion: The relationship of the combined effect of hypertension and obesity with the incidence of coronary heart disease after controlling for age and gender variables.

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.

Characterization of cardiac fibroblast-extracellular matrix crosstalk across developmental ages provides insight into age-related changes in cardiac repair.

Heart failure afflicts an estimated 6.5 million people in the United States, driven largely by incidents of coronary heart disease (CHD). CHD leads to heart failure due to the inability of adult myocardial tissue to regenerate after myocardial infarction (MI). Instead, immune cells and resident cardiac fibroblasts (CFs), the cells responsible for the maintenance of the cardiac extracellular matrix (cECM), drive an inflammatory wound healing response, which leads to fibrotic scar tissue. However, fibrosis is reduced in fetal and early (<1-week-old) neonatal mammals, which exhibit a transient capability for regenerative tissue remodeling. Recent work by our laboratory and others suggests this is in part due to compositional differences in the cECM and functional differences in CFs with respect to developmental age. Specifically, fetal cECM and CFs appear to mitigate functional loss in MI models and engineered cardiac tissues, compared to adult CFs and cECM. We conducted 2D studies of CFs on solubilized fetal and adult cECM to investigate whether these age-specific functional differences are synergistic with respect to their impact on CF phenotype and, therefore, cardiac wound healing. We found that the CF migration rate and stiffness vary with respect to cell and cECM developmental age and that CF transition to a fibrotic phenotype can be partially attenuated in the fetal cECM. However, this effect was not observed when cells were treated with cytokine TGF-β1, suggesting that inflammatory signaling factors are the dominant driver of the fibroblast phenotype. This information may be valuable for targeted therapies aimed at modifying the CF wound healing response and is broadly applicable to age-related studies of cardiac remodeling.

Associations of Abdominal Muscle Density and Area and Incident Cardiovascular Disease, Coronary Heart Disease, and Stroke: The Multi-Ethnic Study of Atherosclerosis.

Muscle density is inversely associated with all-cause mortality, but associations with cardiovascular disease (CVD) risk are not well understood. This study evaluated the association between muscle density and muscle area and incident total CVD, coronary heart disease (CHD), and stroke in diverse men and women. Adult participants (N=1869) in the Multi-Ethnic Study of Atherosclerosis Ancillary Body Composition Study underwent computer tomography scans of the L2-L4 region of the abdomen. Muscle was quantified by density (Hounsfield units) and area in cm2. Sex-stratified Cox proportional hazard models assessed associations between incident total CVD, incident CHD, and incident stroke across sex-specific percentiles of muscle area and density, which were entered simultaneously into the model. Mean age for men and women at baseline were 64.1 and 65.1 years, respectively, and median follow-up time was 10.3 years. For men, associations between muscle density and incident CVD were inverse but not significant in fully adjusted models (P trend=0.15). However, there was an inverse association between density and CHD (P trend=0.02; HR, 0.26 for 95th versus 10th percentile), and no association with stroke (P trend=0.78). Conversely, for men, there was a strong positive association between muscle area and incident CVD (HR, 4.19 for 95th versus 10th percentile; P trend<0.001). Associations were stronger for CHD (HR, 6.18 for 95th versus 10th percentile; P trend<0.001), and null for stroke (P trend=0.67). Associations for women were mostly null. For men, abdominal muscle density is associated with lower CHD risk, whereas greater muscle area is associated with markedly increased risk of CHD.

Association of plasma proteomics with incident coronary heart disease in individuals with and without type 2 diabetes: results from the population-based KORA study.

Coronary heart disease (CHD) is a major global health concern, especially among individuals with type 2 diabetes (T2D). Given the crucial role of proteins in various biological processes, this study aimed to elucidate the aetiological role and predictive performance of protein biomarkers on incident CHD in individuals with and without T2D. The discovery cohort included 1492 participants from the Cooperative Health Research in the Region of Augsburg (KORA) S4 study with 147 incident CHD cases (45 vs. 102 cases in the group with T2D and without T2D, respectively) during 15.6 years of follow-up. The validation cohort included 888 participants from the KORA-Age1 study with 70 incident CHD cases (19 vs. 51 cases in the group with T2D and without T2D, respectively) during 6.9 years of follow-up. We measured 233 plasma proteins related to cardiovascular disease and inflammation using proximity extension assay technology. Associations of proteins with incident CHD were assessed using Cox regression and Mendelian randomization (MR) analysis. Predictive models were developed using priority-Lasso and were evaluated on top of Framingham risk score variables using the C-index, category-free net reclassification index (cfNRI), and relative integrated discrimination improvement (IDI). We identified two proteins associated with incident CHD in individuals with and 29 in those without baseline T2D, respectively. Six of these proteins are novel candidates for incident CHD. MR suggested a potential causal role for hepatocyte growth factor in CHD development. The developed four-protein-enriched model for individuals with baseline T2D (ΔC-index: 0.017; cfNRI: 0.253; IDI: 0.051) and the 12-protein-enriched model for individuals without baseline T2D (ΔC-index: 0.054; cfNRI: 0.462; IDI: 0.024) consistently improved CHD prediction in the discovery cohort, while in the validation cohort, significant improvements were only observed for selected performance measures (with T2D: cfNRI: 0.633; without T2D: ΔC-index: 0.038; cfNRI: 0.465). This study identified novel protein biomarkers associated with incident CHD in individuals with and without T2D and reaffirmed previously reported protein candidates. These findings enhance our understanding of CHD pathophysiology and provide potential targets for prevention and treatment.