Incidence Of Coronary Heart Disease Research Articles

Abstract P194: Proteomic Profiling of Pulmonary Function Decline and Cardiovascular Disease Risk in the Atherosclerosis Risk in Communities (ARIC) Study

Introduction: Measures of pulmonary function are associated with cardiovascular disease risk; however, the underlying mechanism remains unclear. Hypothesis: We hypothesize that protein biomarkers are associated with pulmonary function decline, as well as the risk of subsequent incident coronary heart disease (CHD), heart failure (HF), and mortality. Methods: We included participants from the Atherosclerosis Risk in Communities (ARIC) study with plasma proteome measured by SOMAscan and spirometric measures (forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC)) at both visits 2 (1990-1992) and 5 (2011-2013). Cross-sectional associations of protein levels with FEV1 and FVC at both visits were assessed using multivariable linear regression. The decline of FEV1 was evaluated among proteins related to cross-sectional FEV1 and FVC measures. The FEV1-decline-related proteins were further probed into the effects on incident CHD, HF, and mortality, using Cox proportional hazard models post-visit 2. Results: Out of 4,677 proteins, 364 were cross-sectionally associated with both FEV1 and FVC at visit 2 (n=11,354, age 57, 23% blacks, and 56% women) and 5 (n=3,517, age 75, 17% blacks, and 58% women) at FDR <0.05. Twenty-seven of 364 proteins were associated with FEV1 decline between visits (FDR <0.05). The protein effects were more predominant in women than men (p <0.001). Among 27 FEV1 decline-related proteins, 25 and 27 were associated with incident HF and mortality during an average of 29 years follow-up (FDR <0.05, Figure ). Gamma-aminobutyric acid receptor-associated protein showed the greatest effect with FEV1 decline, and its per SD increase was associated with 20% higher risk of HF and mortality. Compared to HF and mortality, FEV1 decline-related proteins were less associated with incident CHD. Conclusions: Twenty-seven proteins related to pulmonary function decline were heavily associated with the risk of HF and mortality, suggesting shared etiology between those conditions.

Abstract P406: Association Between Perceived Interpersonal Racism and Incident Coronary Heart Disease Among Black Women

Background: Racism is highly prevalent in our society and has disproportionate impact on Black individuals. However, little data exists about whether perceived interpersonal racism are associated with risk of coronary heart disease (CHD). Methods: We followed 48,297 participants in the Black Women’s Health Study from 1997, when they provided information on perceived interpersonal racism and were free of cardiovascular disease and cancer, until the end of 2019. We averaged participant’s responses to the five questions about perceived interpersonal racism in everyday activities, such as “people act as if they think you are dishonest.” We summed up the positive responses to the three questions for perceived racism in interactions that involved jobs, housing, and police; score ranged from 0 (No to all) to 3 (Yes to all). We used Cox proportional hazard models to assess the relation of perceived interpersonal racism with incident CHD, adjusting for major confounders. Results: During 22 years of follow-up, we identified 1,036 incident CHD cases. Women who were in the highest quartile of perceived interpersonal racism in daily life had a 21% increased risk of incident CHD (multivariable hazard ratios (HR)=1.21, 95% confidence interval (CI): 0.99-1.48, p trend=0.05), compared to women in the lowest quartile. Women who reported experience of racism in employment, housing, and the criminal justice system had a 29% increased risk (multivariable adjusted HR=1.29, 95%CI: 1.03-1.63, p trend=0.05) of CHD relative to those who reported no such perceived racism. Conclusion: Perceived experiences of racism in the context of employment, housing and the criminal justice system were associated with increased incidence of CHD among Black women. These findings support the hypothesis that experiences of racism may explain some of the disproportionately high incidence of CHD in the Black population.

Abstract 16: Maternal Coronary Heart Disease and Mortality Within 5 Years of Delivery Among Women With Hypertensive Disorders of Pregnancy and/or Diabetes

Introduction: Pre-pregnancy hypertension (HTN), hypertensive disorders of pregnancy (HDP), and diabetes are linked to increased risk of post-pregnancy coronary heart disease (CHD) and all-cause mortality, but the cumulative impact of pre-pregnancy HTN, HDP, and diabetes has yet to be fully investigated. We aimed to examine associations between HDP and diabetes with CHD and mortality ≤5 years of delivery stratified by race/ethnicity. Methods: This retrospective cohort study included women aged 12-49 with ≥1 singleton, live birth in South Carolina (2004-2016). After exclusions, 431,839 women remained: non-Hispanic White [NHW; 58.8%], non-Hispanic Black [NHB; 31.7%], and Hispanic [9.5%]. Birth certificates defined pre-pregnancy HTN, HDP (preeclampsia, eclampsia, gestational hypertension), and diabetes (pre-pregnancy, gestational); hospitalization/ED visit data also defined pre-pregnancy HTN and HDP. Hospitalization/ED visit data and death certificates defined incident CHD and all-cause mortality. Cox proportional hazard models adjusted for covariates assessed associations by condition and race/ethnicity. Results: Incident CHD risk was increased ≤5 years of delivery for women with diabetes (HR=1.79, CI: 1.40-2.29), HDP (HR=2.91, CI: 1.98-2.65), diabetes and HDP (HR=3.95 CI:3.09-5.05), pre-pregnancy HTN and HDP (HR=3.94, CI: 3.11-5.00), and all three conditions (HR=5.78, CI: 4.41-8.06) compared to none. All-cause mortality risk was increased for HDP (HR=1.31, CI: 1.08-1.58), diabetes and HDP (HR=1.93, CI: 1.30-2.87), pre-pregnancy HTN and HDP (HR=2.20, CI: 1.54-3.15), and all three conditions (HR=2.88, CI: 1.61-5.16), but not with diabetes. The table shows overall and race/ethnic-specific event rates and model results. Discussion: Women with HDP (regardless of pre-pregnancy HTN) and/or diabetes experienced higher incident CHD and all-cause mortality risk ≤5 years of delivery. Event rates were highest for women with two or three conditions, with all event rates higher for NHB than NHW women.

Abstract MP65: Magnesium-Rich Diet Score is Inversely Associated With Incident Cardiovascular Disease: The Atherosclerosis in Communities (ARIC) Study

Background: Numerous studies have shown inverse associations between serum magnesium (Mg) levels and risk of cardiovascular disease (CVD), but studies of dietary Mg have not been consistent. Aim: The association of a Mg-rich diet score with risks of incident CVD, coronary heart disease (CHD), and ischemic stroke in the Atherosclerosis Risk in Communities (ARIC) study was examined. Methods: There were 15,022 Black and White adults without prevalent CVD included in this analysis. Diet was assessed at two visits using an interviewer-administered 66-item food frequency questionnaire. A Mg-rich diet score was created including whole grain products, nuts, fruits, vegetables, legumes, coffee, and tea. Cox proportional hazard regression evaluated the associations of incident CVD, CHD and stroke through 2019 across quintiles of Mg-rich diet score adjusted for demographic characteristics, lifestyle factors, and clinical characteristics. Results: Participants in the highest quintile of Mg-rich diet score compared to the lowest quintile consumed more servings of Mg-rich foods and fiber and less refined grains, red and processed meat, total fat and saturated fat. Over 30 years of follow up, a Mg-rich diet score was inversely associated with incident CVD (HR Q5 vs Q1 =0.88, 95% CI 0.78-0.99, p trend =0.03) and CHD (HR=0.83, 95% CI 0.72-0.96, p trend =0.01); however the diet-stroke association was null (HR=1.08, 95% CI 1.07-1.09, p trend =0.93) (Table). Conclusions: Consuming a diet rich in whole grains, nuts, fruits and vegetables, legumes, coffee and tea is consistent with a lower long-term risk of CVD and CHD.

Abstract MP62: Fatty Acid Biomarkers of 15:0, 17:0 and Trans 16:1n-7 and Incident Coronary Heart Disease and Stroke: A Pooling Project of 15 Prospective Cohorts in the Fatty Acids and Outcomes Research Consortium

Introduction: Previous studies have reported inverse associations of circulating and tissue levels of pentadecanoic acid (15:0), heptadecanoic acid (17:0) and trans -palmitoleic acid ( trans 16:1n-7), which have been proposed as potential biomarkers of dairy fat intake, with risk of type-2 diabetes and certain cardiovascular outcomes. Hypothesis: We assessed the hypothesis that circulating and tissue levels of 15:0, 17:0, trans 16:1n-7 are inversely associated with risk of incident coronary heart disease (CHD) and stroke in a global consortium of prospective studies. Methods: We used data from 15 prospective cohorts in the Fatty Acids and Outcomes Research Consortium. We included adults (age≥18 years) who were free of cardiovascular diseases and had blood or adipose tissue measurements of 15:0, 17:0 or trans 16:1n-7. We used a harmonized analysis protocol with each exposure standardized to the interquintile range (IQR): difference between the 10 th and 90 th percentiles of each fatty acid to conduct new individual participant-level analyses. We harmonized covariate definitions across studies to include demographic, lifestyle and health variables, and levels of other fatty acids associated with CHD or stroke. We used inverse-variance meta-analysis to calculate the pooled relative risks (RR) and 95% confidence intervals (CI) for each outcome. We also calculated Spearman correlation coefficients between levels of each fatty acid exposure and potential dietary determinants of their levels (intakes of total, high-fat and low-fat dairy, meat from ruminant animals, fish and dietary fiber) among 6 studies with dietary data. Results and Conclusions: Among 34,187 participants, 5,790 incident CHD and 3,098 stroke cases were documented during a maximum follow-up of 23.3 years. We did not observe significant associations of any of the fatty acid biomarkers with risk of CHD or stroke. The pooled multivariate RR and 95% CI of CHD per IQR were 0.97 (0.92, 1.02) for 15:0, 0.97 (0.92, 1.02) for 17:0, 1.11 (0.97, 1.26) for trans 16:1n-7, and 0.98 (0.92, 1.04) for the sum of the fatty acids. The respective RR and 95% of stroke were 1.01 (0.93, 1.09) for 15:0, 0.91 (0.81, 1.03) for 17:0, 0.99 (0.83, 1.18) for trans 16:1n-7, and 0.93 (0.85, 1.04) for the summed fatty acids. Additionally, we did not observe significant heterogeneity by age, sex, race/ethnicity, world region, baseline hypertension status or lipid compartment. Circulating and tissue levels of 15:0, 17:0 and trans 16:1n-7 were weakly correlated with intakes of total or high-fat dairy (Spearman correlations [ r = 0.05 to 0.37]) but were not correlated with intakes of low-fat dairy, ruminant meat, fish or dietary fiber [ r = -0.08 to 0.09]. In conclusion, circulating and tissue levels of 15:0, 17:0, trans 16:1n-7 were not associated with risk of CHD or stroke. Our study suggests a limited role for these fatty acids in the etiology of cardiovascular disease.

Abstract MP11: Ultra-Processed Food Consumption and Cardiovascular Disease in the European Prospective Investigation Into Cancer and Nutrition Study

Introduction: Diets containing many ultra-processed foods (UPF) are linked to unfavourable health. UPF are defined by the NOVA classification as industrial food and drinks made from substances not used in domestic culinary preparations, such as hydrogenated fats, modified starches, and other food additives. There is evidence suggesting a link between UPF consumption and cardiovascular disease (CVD) incidence, but this association has not been tested in a large European cohort. Using data from the pan-European Prospective Investigation into Cancer and nutrition (EPIC) study, we assessed the hypothesis that higher consumption of UPF is associated with an increased risk of incident fatal and non-fatal CHD and stroke in the EPIC-Heart cohort. Methods: Case-cohort design nested in the EPIC cohort including 36,415 adults from Denmark, Germany, Italy, the Netherlands, Spain, Sweden, and the UK. Socio-demographic, lifestyle factors and usual dietary intake were assessed at time of recruitment (1992 - 2000) using country-specific validated questionnaires. Consumption of UPF was expressed in percentage of grams per day. CVD cases ascertainment varied across EPIC centres and included hospital admissions, linkage to registers, self-report and mortality data. Proportion of missing values ranged from 0.95% for smoking status to 14.2% for history of diabetes. We performed multiple imputation on all covariates with missing values. Cox proportional hazard models with age as the underlying time variable stratified by sex, centre and age were used to test the longitudinal association between UPF consumption and coronary heart disease (CHD) and stroke incidence adjusted for confounders. We applied prentice weights to our cox proportional hazard models to account for the case-cohort design. Results: The mean contribution of UPF to the overall diet in grams was 14.2% in men and 12.8% in women. After a median follow-up time of 9.7 years, it was documented 11,973 non-fatal and 2,281 fatal CHD events, and 6,765 non-fatal and 899 fatal stroke events. In models adjusted for education, smoking, physical activity, body mass index, height, diabetes, high blood pressure, alcohol, energy, and sodium intake, and the Mediterranean diet score, each 10% increase in the consumption of grams from UPF was associated with an increased risk of non-fatal CHD (HR 1.13, 95%CI 1.02 - 1.26), fatal CHD (HR 1.33, 95%CI 1.09 - 1.62) and fatal stroke (HR 1.40, 95%CI 1.07 - 1.85), but not with non-fatal stroke (HR 1.11, 95%CI 0.98 - 1.24). Complete-case analysis showed similar results. Conclusion: In this large prospective cross-European study we found that higher proportion of UPF in the diet was associated with an increased risk of non-fatal CHD and fatal CHD and stroke. These findings corroborate other large-scale cohort studies indicating that the increasing consumption of ultra-processed intake may contribute to higher CVD incidence.

Abstract MP24: Atherogenic Gut Microbial Metabolite Scores and Risk of Coronary Heart Disease Among Women in the Nurses’ Health Study

Introduction: Recent evidence suggests that dietary proteins modulate the microbial composition and metabolite production to influence host physiology. Gut-microbiota-related metabolites, such as trimethylamine N-oxide (TMAO) and its precursors, phenylacetylglutamine (PAGln) and p-tolyl (cresol) sulfate, have been recently implicated as atherogenic metabolites derived from the microbial metabolism of protein foods (such as red meat) and amino acids. Hypothesis: We tested a hypothesis that combined effects of atherogenic gut microbiota-related metabolites may be strongly related to the risk of incident coronary heart disease (CHD) among women. Methods: We conducted a prospective nested case-control study of 762 incident cases of CHD (fatal CHD and nonfatal myocardial infarction) and 762 matched controls identified over 10-14 years of follow-up. Plasma metabolites (TMAO, N,N,N-trimethyllysine, PAGln, and p-tolyl (cresol) sulfate) were measured at baseline. We regressed the CHD outcome against metabolites using conditional logistic regression and then calculated an atherogenic microbial metabolite score (AMMS) of CHD by summing the β effects of metabolites. Results: Every 1 SD increment of AMMS was associated with a matching factor-adjusted RR of 1.28 (95% CI: 1.15, 1.44) and a multivariable-adjusted RR of 1.26 (1.12, 1.42) for CHD controlling for demographic, dietary, and lifestyle factors, postmenopausal hormone use, and body mass index. Dose-response analysis showed a linear relation between AMMS and the risk of CHD ( P <0.001). In addition, there was a 1.20 (1.06, 1.36) times increased risk of CHD per 1 SD of AMMS after adjusting for common metabolic comorbidities (diabetes, hypertension, and dyslipidemia). The highest quintile (Q5) group had an adjusted RR of 1.60 (1.08, 2.37) for CHD, as compared to the lowest quintile (Q1) ( Fig ). Conclusions: Atherogenic gut microbiota-related metabolite scores were significantly associated with risk of incident CHD among women without prior CHD.

Abstract 41: Comprehensive Plasma Metabolomic Risk Scores to Predict Incident Coronary Heart Disease Events

Introduction: Integrating multiple metabolomics signatures related to coronary heart disease (CHD) into a metabolomic risk score (MRS) may contribute to improving the risk prediction beyond traditional risk factors, although applications of the MRS remain underdetermined, especially in people at usual risk. Hypothesis: We analyzed associations of plasma metabolites with the risk of CHD to develop MRS for predicting risk of incident CHD by incorporating comprehensive metabolic pathways among women at usual risk from the Nurses’ Health Study (NHS). We also tested whether changes in CHD-related plasma metabolites were associated with significant reductions in atherosclerotic cardiovascular disease (ASCVD) risk scores among participants in the POUNDS Lost trial. Methods: Untargeted metabolomics profiling was performed to measure plasma metabolites at baseline in a prospective nested case-control of 762 incident cases of CHD (fatal CHD and nonfatal myocardial infarction) and 762 matched controls identified over 10-14 years of follow-up time in NHS. An MRS of CHD risk was created based on metabolites that were selected through conditional logistic regression with the elastic net procedure. The POUNDS Lost trial included adults with overweight/obesity who consumed weight-loss diets with different macronutrient intakes. We measured untargeted plasma metabolomics signatures at baseline, 6 months, and 2 years to calculate changes in response to the dietary interventions. The primary outcome in the POUNDS Lost trial was the reduction of 10-year ASCVD risk scores calculated by the validated pooled cohort equations. Results: Various plasma metabolites (such as gut-microbiota-related and others in the pathways of ceramides, phospholipids, and polyamine metabolism) were associated with the risk of incident CHD ( P FDR <0.05). We developed MRS for CHD combining 122 metabolites and found that the highest quartile (Q4) was associated with 11.3 times (95% CI: 6.88, 18.6) higher risk of CHD, as compared to the lowest quartile (Q1), even after adjusting for covariates including common CHD risk factors (such as a family history of MI, lifestyle factors, obesity, diabetes, hypertension, and dyslipidemia). Every 1 SD increment of MRS was associated with an adjusted RR of 3.23 (95% CI 2.62, 3.97) for CHD events. In the POUNDS Lost, diet-intervention-induced changes in CHD-related metabolites, particularly those in ceramide pathways, were significantly associated with reductions in the ASCVD risk score at 6 months and 2 years. Conclusions: Comprehensive metabolomic scores were strongly related to the risk of incident CHD among women without prior CHD. Dietary interventions may modify the unfavorable relations between CHD-risk-related metabolites and ASCVD risk. Further studies in other populations are warranted to validate the performance of MRS in predicting ASCVD events.

Abstract MP60: Prediabetes and Undiagnosed Diabetes Predisposing Women to Excess Risk of Cardiovascular Disease

Objective: Women with type 2 diabetes (T2DM) have a 25-50% higher risk of cardiovascular disease (CVD) than their men counterparts. The reasons for this sex disparity are incompletely understood. We sought to examine if pre-diabetes (preDM) and undiagnosed T2DM are associated with a greater magnitude of CVD risk in women than in men. Methods: We pooled CVD-free individuals (N=18,745) from the Atherosclerosis Risk in Communities, the Multi-Ethnic Study of Atherosclerosis, and the Jackson Heart Study. CVD outcomes included incident coronary heart disease (CHD) (myocardial infarction, CHD death, or cardiac procedures including percutaneous coronary interventions, bypass surgery, or coronary revascularization), stroke (ischemic or hemorrhagic stroke), and a composite atherosclerotic CVD (ASCVD) (any CHD condition or stroke). Multivariable Cox models examined the outcomes associated with preDM (fasting glucose [FG] 100-125 mg/dL or HbA1c 5.7-6.4%) or undiagnosed T2DM (FG ≥126 mg/dL or HbA1c ≥6.5% and without a DM diagnosis or anti-diabetes medication use) adjusted for age, race/ethnicity, education, BMI, blood pressure, total cholesterols, smoking, anti-hypertensive and lipid-lowering medications, and cohort indicator. An interaction term sex x preDM or undiagnosed DM was added to models to test the sex modifying effect. We consider p-interaction<0.2 as significant. Results: During a median follow-up of 17 years, the adjusted model showed that preDM was significantly associated with a higher risk of CHD (Hazard ratio 1.09, 95%CI 1.04-1.14), stroke (1.08, 1.04-1.13), and ASCVD (1.09, 1.04-1.14) in women, but not in men (1.04, 0.99-1.1 for CHD, 1.03, 0.98-1.08 for stroke, and 1.03, 0.98-1.09 for ASCVD, respectively). Undiagnosed T2DM was significantly associated with the risk of CHD (1.27, 1.16-1.4 in women and 1.17, 1.05-1.3 in men), stroke (1.32, 1.21-1.45 in women and 1.2, 1.09-1.32 in men), and ASCVD (1.27, 1.16-1.4 in women and 1.15, 1.03-1.29 in men) in both sexes but with more pronounced effect in women (P-interactions ≤0.11). In racial-stratified analysis, a higher magnitude of CVD risk associated with preDM or undiagnosed DM was also found in non-Hispanic (NH) white women and NH-black women than in their men counterparts. Conclusions: PreDM and undiagnosed DM predispose women to excess CVD risk, possibly due to women’s higher susceptibility to metabolic dysfunction at a lower glucose level and the prolonged unmanaged time for risk factors relative to men. T2DM screening and risk factor control should be enhanced in both sexes to reduce future CVD risk, particularly in women.

Pregnancy loss and risk of incident CVD within 5 years: Findings from the Women's Health Initiative.

Previous studies have demonstrated an increased risk of cardiovascular disease (CVD) in women with a history of pregnancy loss. Less is known about whether pregnancy loss is associated with age at the onset of CVD, but this is a question of interest, as a demonstrated association of pregnancy loss with early-onset CVD may provide clues to the biological basis of the association, as well as having implications for clinical care. We conducted an age-stratified analysis of pregnancy loss history and incident CVD in a large cohort of postmenopausal women aged 50-79 years old. Associations between a history of pregnancy loss and incident CVD were examined among participants in the Women's Health Initiative Observational Study. Exposures were any history of pregnancy loss (miscarriage and/or stillbirth), recurrent (2+) loss, and a history of stillbirth. Logistic regression analyses were used to examine associations between pregnancy loss and incident CVD within 5 years of study entry in three age strata (50-59, 69-69, and 70-79). Outcomes of interest were total CVD, coronary heart disease (CHD), congestive heart failure, and stroke. To assess the risk of early onset CVD, Cox proportional hazard regression was used to examine incident CVD before the age of 60 in a subset of subjects aged 50-59 at study entry. After adjustment for cardiovascular risk factors, a history of stillbirth was associated with an elevated risk of all cardiovascular outcomes in the study cohort within 5 years of study entry. Interactions between age and pregnancy loss exposures were not significant for any cardiovascular outcome; however, age-stratified analyses demonstrated an association between a history of stillbirth and risk of incident CVD within 5 years in all age groups, with the highest point estimate seen in women aged 50-59 (OR 1.99; 95% CI, 1.16-3.43). Additionally, stillbirth was associated with incident CHD among women aged 50-59 (OR 3.12; 95% CI, 1.33-7.29) and 60-69 (OR 2.06; 95% CI, 1.24-3.43) and with incident heart failure and stroke among women aged 70-79. Among women aged 50-59 with a history of stillbirth, a non-significantly elevated hazard ratio was observed for heart failure before the age of 60 (HR 2.93, 95% CI, 0.96-6.64). History of stillbirth was strongly associated with a risk of cardiovascular outcomes within 5 years of baseline in a cohort of postmenopausal women aged 50-79. History of pregnancy loss, and of stillbirth in particular, might be a clinically useful marker of cardiovascular disease risk in women.

The importance of sleep patterns in the incidence of coronary heart disease: a 6-year prospective study in Mashhad, Iran

Chronic shortened sleep can increase several cardiovascular risk factors, including depression, anxiety, metabolic syndrome, diabetes and hypertension. In the current study, we aimed to investigate the relationship between sleep patterns and the incidence of coronary heart disease (CHD). A total of 9704 healthy participants were recruited for the MASHAD cohort study. Within 6 years of follow-up, participants were categorized into four groups based on their number of hours of nightly sleep. Cox’s proportional hazard model was used to assess relative risks (RRs) and 95% confidence intervals (CIs). During the study, 235 heart problems, including myocardial infarction, stable angina and unstable angina, were confirmed. There were significant differences between men and women who had short and long nightly sleep (p < 0.05). The incidence of CHD was significantly higher in participants with very short night sleep durations than in those with longer hours of night sleep. The subjects with very short nightly sleep were more susceptible to unstable angina (RR: 2.614 (CI 1.354–5.047)) (p < 0.05). We found that shortened nightly sleep was associated with an increased incidence of coronary heart disease in an Iranian population. These findings suggest that sleep disorders, especially shortened night sleep, can be a risk factor for CHD.

Risk factors and characteristics of new-onset coronary heart disease in adults with physical disabilities: A retrospective cohort study

ObjectivesThere is limited information about coronary heart disease (CHD) in adults with physical disabilities. This study was performed to assess the incidence and predictors of the new development of CHD in adults with physical disabilities. MethodsA retrospective cohort study was performed on 3902 physically disabled people in Shanghai, China. Baseline information was collected in January 2012, and participants were followed-up with for 7.5 years for CHD events. Risk factors for demographic characteristics, disease history, electrocardiography, and blood biochemical indicators were evaluated using a Cox proportional hazard model. Subgroup analyzes were performed according to gender and level of physical disability. ResultsOut of the total 3902 adults with physical disabilities (average age 55.9 ± 8.5 years), 468 (12.0%) developed CHD, during a median follow-up period of 7 years. Independent predictors of CHD included the following: age (HR = 1.411, 95% CI = 1.255–1.587, p＜0.001), gender (HR = 0.773, 95% CI = 0.637–0.940, p = 0.010), abnormal electrocardiogram(HR = 1.396, 95% CI = 1.088–1.792, p = 0.009), hypertension (HR = 1.657, 95% CI = 1.369–2.006, p＜0.001), diabetes (HR = 1.649, 95% CI = 1.307–2.081, p＜0.001), serum uric acid (HR = 1.001, 95% CI = 1.000–1.002, p = 0.046), and total cholesterol (HR = 1.416, 95% CI = 1.054–1.902, p = 0.021). In addition to the risk factors of the total population with physical disability, triglyceride was also a significant risk factor for CHD in the subgroup with women and mild disability. ConclusionsDuring a 7.5 years period, the CHD incidence rate among physically disabled people was 12.0%. We identified the role of CHD risk factors such as age, gender, hypertension, diabetes, serum uric acid, total cholesterol, and abnormal electrocardiogram.

Associations of genetic and infectious risk factors with coronary heart disease.

Coronary heart disease (CHD) is one of the most pressing health problems of our time and a major cause of preventable death. CHD results from complex interactions between genetic and environmental factors. Using multiplex serological testing for persistent or frequently recurring infections and genome-wide analysis in a prospective population study, we delineate the respective and combined influences of genetic variation, infections, and low-grade inflammation on the risk of incident CHD. Study participants are enrolled in the CoLaus|PsyCoLaus study, a longitudinal, population-based cohort with baseline assessments from 2003 through 2008 and follow-up visits every 5 years. We analyzed a subgroup of 3459 individuals with available genome-wide genotyping data and immunoglobulin G levels for 22 persistent or frequently recurring pathogens. All reported CHD events were evaluated by a panel of specialists. We identified independent associations with incident CHD using univariable and multivariable stepwise Cox proportional hazards regression analyses. Of the 3459 study participants, 210 (6.07%) had at least one CHD event during the 12 years of follow-up. Multivariable stepwise Cox regression analysis, adjusted for known cardiovascular risk factors, socioeconomic status, and statin intake, revealed that high polygenic risk (hazard ratio [HR] 1.31, 95% CI 1.10-1.56, p=2.64 × 10-3) and infection with Fusobacterium nucleatum (HR 1.63, 95% CI 1.08-2.45, p=1.99 × 10-2) were independently associated with incident CHD. In a prospective, population-based cohort, high polygenic risk and infection with F. nucleatum have a small, yet independent impact on CHD risk.

Nuts and Cardiovascular Disease Outcomes: A Review of the Evidence and Future Directions.

Nuts are nutrient-rich foods that contain many bioactive compounds that are beneficial for cardiovascular health. Higher consumption of nuts has been associated with a reduced risk of several cardiovascular diseases (CVD) in prospective cohort studies, including a 19% and 25% lower risk of CVD incidence and mortality, respectively, and a 24% and 27% lower risk of coronary heart disease incidence and mortality, respectively. An 18% lower risk of stroke mortality, a 15% lower risk of atrial fibrillation, and a 19% lower risk of total mortality have also been observed. The role of nuts in stroke incidence, stroke subtypes, peripheral arterial disease and heart failure has been less consistent. This narrative review summarizes recommendations for nuts by clinical practice guidelines and governmental organizations, epidemiological evidence for nuts and CVD outcomes, nut-containing dietary patterns, potential mechanisms of nuts and CVD risk reduction, and future research directions, such as the use of biomarkers to help better assess nut intake. Although there are still some uncertainties around nuts and CVD prevention which require further research, as summarized in this review, there is a substantial amount of evidence that supports that consuming nuts will have a positive impact on primary and secondary prevention of CVD.

Lifestyle Factors, Genetic Risk, and Cardiovascular Disease Risk among Breast Cancer Survivors: A Prospective Cohort Study in UK Biobank.

Evidence is limited regarding the association between lifestyles and cardiovascular disease (CVD), and the extent to which healthy lifestyles could offset the genetic risk of CVD in females with breast cancer (BC). Females diagnosed as BC, who were free of CVD at baseline, from UK Biobank were included. Five modifiable lifestyle factors were considered to calculate the healthy lifestyle score, namely body mass index (BMI), smoking, alcohol drinking, dietary habits, and physical activity. The polygenetic risk score (PRS) was derived for coronary heart disease (CHD), ischemic stroke (IS), and heart failure (HF). In 13,348 female BC survivors, there were 986 CVD events (736 CHD, 165 IS, and 353 HF) over a median of 8.01 years of follow-up. Participants with 4-5 healthy lifestyle components were associated with a decreased risk of incident CVD (HR: 0.50; 95%CI: 0.37, 0.66), CHD (HR: 0.49; 95%CI: 0.35, 0.69), IS (HR: 0.35; 95%CI: 0.19, 0.65), and HF (HR: 0.59; 95%CI: 0.36, 0.97), compared with those with 0-1 lifestyle components. Evidence for the genetic-lifestyle interaction was observed for CHD (p = 0.034) and HF (p = 0.044). Among participants at high genetic risk, a healthy lifestyle was associated with a lower risk of CHD (HR: 0.37; 95%CI: 0.24, 0.56), IS (HR: 0.37; 95%CI: 0.15, 0.93) and HF (HR: 0.39; 95%CI: 0.21, 0.73). Our findings suggest that BC survivors with a high genetic risk could benefit more from adherence to a healthy lifestyle in reducing CVD risk.

Therapeutic Effect of Chia Seed Oil‐Based Ice Cream against Coronary Heart Disease in Wister Rat Model

AbstractThe present study is designed to explore the therapeutic effect of chia seed oil (CSO) based ice cream against Coronary heart disease (CHD). CSO based ice cream is developed by using different concentrations of CSO (G2 3%, G3 5%, and G4 7%). The incorporation of CSO improves the DPPH activity of ice cream along with the betterment in the level of total phenolic content (TPC) and total flavonoid contet (TFC) without affecting the sensory attributes. The bio‐evaluation trials are carried out on male Wister rats by feeding them with CSO based ice cream for 45 days. Blood serum of rats is taken and analyzed after 0, 15, 30, and 45 day intervals for the determination of total cholesterol (TC), triglycerides (TG), high density lipoprotein (HDL), and low‐density lipoprotein (LDL). The results show a significant (p &lt; 0.05) decrease (51%) in TG level in G3 (109.88–104.74 mg dL−1). HDL level is increased (25.23–35.78 mg dL−1) and LDL level decreases (29.19–23.18 mg dL−1) for all the groups. It can be concluded that CSO based ice cream has therapeutic effect to improve the incidence of CHD and to better improve the serum lipid profile.

Long-term exposure to air pollution and incidence of coronary heart diseases and stroke in the longitudinal metropolitan studies (LMS) network: the BIGEPI project

to assess the potential of using longitudinal metropolitan studies (LMS) to study the association between long-term exposure to air pollution and the incidence of acute coronary events and stroke. closed cohort. subjects aged >=30 years, who took part in the 2011 census, residents in 5 cities (Turin, Bologna, Rome, Brindisi and Taranto). Annual concentrations of particulate matter (PM10 and PM2.5), nitrogen dioxide (NO2) and warm-season ozone (O3) (annual O3 in Taranto and Brindisi), estimated through satellite (Turin, Bologna, Rome) or photochemical models (Taranto and Brindisi) with a spatial resolution of 1 km2, were assigned to the census address. incidence of coronary heart disease (CHD) and stroke until 31.12.2018 (2019 in Bologna). Cohort-specific Hazard Ratios (HRs), estimated using Cox regression models progressively adjusting for individual and contextual covariates, were pooled with random-effect meta-analysis. there were 71,872 incident CHD cases and 43,884 incident cases of stroke in almost 18 million person-years. No association was observed between the exposures studied and incidence of CHD and stroke, except for an increase in the incidence of CHD associated with warm-season O3 exposure (HR 1.034 per 5 μg/m3 increase). Some positive associations were found in specific cities (both outcomes in Brindisi with PM10 exposure and in Taranto with NO2 exposure, stroke in Rome with both PM10 and PM2.5), although estimates were not significant in some instances. LMS are a high potential tool for the study of comparative medium- and long-term effects of air pollution. Their further development (different definitions of exposure, outcomes, characteristics of the urban areas and extension to other LMS) may make them even more valuable tools for monitoring and planning public health interventions.

Development of a risk score model for the prediction of patients needing percutaneous coronary intervention.

The incidence of coronary heart disease (CHD) is increasing worldwide. The need for percutaneous coronary intervention (PCI) is determined by coronary angiography (CAG). As coronary angiography is an invasive and risky test for patients, it will be of great help to develop a predicting model for the assessment of the probability of PCI in patients with CHD using the test indexes and clinical characteristics. A total of 454 patients with CHD were admitted to the cardiovascular medicine department of a hospital from January 2016 to December 2021, including 286 patients who underwent CAG and were treated with PCI, and 168 patients who only underwent CAG to confirm the diagnosis of CHD were set as the control group. Clinical data and laboratory indexes were collected. According to the clinical symptoms and the examination signs, the patients in the PCI therapy group were further split into three subgroups: chronic coronary syndrome (CCS), unstable angina pectoris (UAP), and acute myocardial infarction (AMI). The significant indicators were extracted by comparing the differences among the groups. A nomogram was drawn based on the logistic regression model, and predicted probabilities were performed using R software (version 4.1.3). Twelve risk factors were selected by regression analysis; the nomogram was successfully constructed to predict the probability of needing PCI in patients with CHD. The calibration curve shows that the predicted probability is in good agreement with the actual probability (C-index=0.84, 95% CI=0.79-0.89). According to the results of the fitted model, the ROC curve was plotted, and the area under the curve was 0.801. Among the three subgroups of the treatment group, 17 indexes were statistically different, and the results of the univariable and multivariable logistic regression analysis revealed that cTnI and ALB were the two most important independent impact factors. cTnI and ALB are independent factors for the classification of CHD. A nomogram with 12 risk factors can be used to predict the probability of requiring PCI in patients with suspected CHD, which provided a favorable and discriminative model for clinical diagnosis and treatment.

Association of Rare Protein-Truncating DNA Variants in APOB or PCSK9 With Low-density Lipoprotein Cholesterol Level and Risk of Coronary Heart Disease

Protein-truncating variants (PTVs) in apolipoprotein B (APOB) and proprotein convertase subtilisin/kexin type 9 (PCSK9) are associated with significantly lower low-density lipoprotein (LDL) cholesterol concentrations. The association of these PTVs with coronary heart disease (CHD) warrants further characterization in large, multiracial prospective cohort studies. To evaluate the association of PTVs in APOB and PCSK9 with LDL cholesterol concentrations and CHD risk. This studied included participants from 5 National Heart, Lung, and Blood Institute (NHLBI) studies and the UK Biobank. NHLBI study participants aged 5 to 84 years were recruited between 1971 and 2002 across the US and underwent whole-genome sequencing. UK Biobank participants aged 40 to 69 years were recruited between 2006 and 2010 in the UK and underwent whole-exome sequencing. Data were analyzed from June 2021 to October 2022. PTVs in APOB and PCSK9. Estimated untreated LDL cholesterol levels and CHD. Among 19 073 NHLBI participants (10 598 [55.6%] female; mean [SD] age, 52 [17] years), 139 (0.7%) carried an APOB or PCSK9 PTV, which was associated with 49 mg/dL (95% CI, 43-56) lower estimated untreated LDL cholesterol level. Over a median (IQR) follow-up of 21.5 (13.9-29.4) years, incident CHD was observed in 12 of 139 carriers (8.6%) vs 3029 of 18 934 noncarriers (16.0%), corresponding to an adjusted hazard ratio of 0.51 (95% CI, 0.28-0.89; P = .02). Among 190 464 UK Biobank participants (104 831 [55.0%] female; mean [SD] age, 57 [8] years), 662 (0.4%) carried a PTV, which was associated with 45 mg/dL (95% CI, 42-47) lower estimated untreated LDL cholesterol level. Estimated CHD risk by age 75 years was 3.7% (95% CI, 2.0-5.3) in carriers vs 7.0% (95% CI, 6.9-7.2) in noncarriers, corresponding to an adjusted hazard ratio of 0.51 (95% CI, 0.32-0.81; P = .004). Among 209 537 individuals in this study, 0.4% carried an APOB or PCSK9 PTV that was associated with less exposure to LDL cholesterol and a 49% lower risk of CHD.

The Metabolic Score for Insulin Resistance (METS-IR) Predicts Cardiovascular Disease and Its Subtypes in Patients with Hypertension and Obstructive Sleep Apnea.

We aimed to evaluate the METS-IR (metabolic score for insulin resistance) index for the prediction of incident cardiovascular disease (CVD) and its subtypes (coronary artery disease and stroke) in patients with hypertension and obstructive sleep apnea (OSA). A retrospective cohort study was conducted with 2031 adults with hypertension and OSA, participants from the Urumqi Research on Sleep Apnea and Hypertension study (UROSAH). The hazard ratios and 95% CIs (credibility interval) for CVD and its subtypes were estimated using multivariate Cox proportional hazards regression models. After a median follow-up of 6.80 years (interquartile range: 5.90-8.00 years), a total of 317 (15.61%) participants developed new-onset CVD, including 198 (9.75%) incident coronary heart disease (CHD) and 119 (5.86%) incident stroke. After adjusting for as many relevant confounding factors as possible, each SD increase in METS-IR was associated with a 30% increased risk of new onset overall CVD events, a 32% increased risk of new onset CHD, and a 27% increased risk of new onset stroke. When METS-IR was assessed as tertiles, after adjustment for fully confounding factors, the highest tertiles versus the lowest tertiles were associated with a greater hazard of CVD (HR 2.05; 95% CI 1.52,-2.77), CHD (HR 1.96; 95% CI 1.35-2.84), and stroke (HR 2.24; 95% CI 1.35-3.72). The results of various subgroups and sensitivity analyses were similar. When METS-IR was added, CVD predictions were reclassified and identified more accurately than baseline models for the C-index, continuous net reclassification improvement, and integrated discrimination index. CHD and stroke showed similar results. METS-IR is a powerful predictor of CVD and its subtypes in patients with hypertension and OSA, which can facilitate the identification of high-risk individuals and provide individualized CVD prevention.