Incidence Of Coronary Heart Disease Research Articles

Impact of the COVID-19 pandemic on incidence of coronary heart disease in Bavaria, Germany: an analysis of health claims data

BackgroundInconsistent findings about the impact of the COVID-19 pandemic on cardiovascular disease diagnosis and consultations have been reported internationally. The objective of this study was to analyse the impact of...

Abstract 4119535: Aspirin Use and Cardiovascular Disease Incidence in Adults with High Lipoprotein(a): A Multi-Cohort Study

Introduction: There is an active debate about who may benefit from taking aspirin to reduce their incidence of cardiovascular disease (CVD). Some prior cohort studies with small sample size suggest that aspirin use may be associated with a lower incidence of CVD or coronary heart disease (CHD) in adults with Lp(a) ≥50 mg/dL but not in those with Lp(a) <50 mg/dL, a hypothesis that needs confirmation. Research question: Does the association of aspirin use with incident CVD or CHD vary by Lp(a) among US adults? Methods: We analyzed publicly available data from adults without CVD at baseline in the ARIC (n=13,085, mean age 54 years), CHS (n=3,956, mean age 72 years), and MESA (n=6,324, mean age 62 years) studies. Lp(a) ≥50 mg/dL was defined as high. Participants were followed for incident CVD (myocardial infarction, stroke, or CVD death) and CHD (myocardial infarction or CHD death; median follow-up: ARIC 26 years, CHS 12 years, MESA 14 years). Hazard ratios associated with aspirin use were calculated after propensity score matching (primary analysis) and in all participants using multivariable adjustment (secondary analysis). Mixed-effects models were used to obtain pooled hazard ratios. Results: Aspirin use was 25.1% in ARIC, 29.6% in CHS, and 19.9% in MESA. In MESA, adults taking aspirin were older, had higher blood pressure, and were more likely to have diabetes and a low estimated glomerular filtration rate and to be taking antihypertensive medication and a statin versus those not taking aspirin. These differences were attenuated or not present in ARIC and CHS. The CVD incidence rate per 1,000 person-years (95%CI) was higher in adults with versus without high Lp(a): 16.3 (15.3-17.4) and 12.5 (12.1-13.0), respectively, in ARIC, 35.8 (31.5-40.1) and 32.3 (30.6-34.0) in CHS, and 10.8 (9.1-12.4) and 8.2 (7.5-8.9) in MESA. Aspirin use was not associated with CVD or CHD incidence in adults with or without high Lp(a) in the primary analysis ( Figure ). No association between aspirin use and CVD or CHD incidence was present in the secondary analysis using multivariable adjustment (data not shown). Conclusion: The association of aspirin use with CVD and CHD incidence did not differ by Lp(a) in this multi-cohort study.

Abstract 4137836: Association of AHA PREVENT Risk Score with Cardiovascular Mortality Across Social Determinants of Health: A Nationwide Retrospective Cohort Study

Introduction/Background: The AHA PREVENT risk calculator was recently developed to accurately predict the risk of cardiovascular disease (CVD) risk, including incident heart failure, stroke, and coronary heart disease. However, the risk prediction of this tool for CVD mortality overall and among groups with increasing social determinants of health (SDOH) burden in a multi-ethnic nationally representative cohort of American adults is unclear. Methods: This retrospective study included adult NHANES participants (age > 30 years) from 1998-2018 cycles without known CVD. Individuals without data for risk estimation were excluded. AHA PREVENT risk was scored from 0 to 100. Multivariable-adjusted Cox regression models were used to estimate the risk of CVD mortality, accounting for 7 SDOH measures (employment, family income, food security, health access, health insurance, housing instability, and being married or living with partner). Population was stratified based on cumulative SDOH burden (1, 2, 3, 4, 5, > 5 unfavorable SDOH markers). Model discrimination was assessed using C-statistics in these groups. Results: Among 19,887 participants (median age 53 years, 49% Female, 54% White, 19% Black), a 1% increase in AHA PREVENT Risk score calculation was associated with 13% higher risk of CVD mortality (HR adj 1.13, 95% CI: 1.12-1.14) with C-statistic of 0.91. While AHA PREVENT Risk score was predictive of CVD mortality across the SDOH burden strata, there was a decline in C-statistic from 0.91 among those without any unfavorable SDOH to 0.81 among those with > 5 unfavorable SDOH measures. Conclusion: The AHA PREVENT Risk score is predictive of CVD mortality even when accounting for SDOH measures. However, the risk discrimination decreases among individuals with a higher SDOH burden. Further investigation is needed to identify means to improve CVD risk prediction among disadvantaged people with high unfavorable SDOH burden.

Abstract 4119941: Identification of individuals who benefit from omega-3 fatty acid supplementation to prevent coronary heart disease: A machine-learning analysis of the VITAL

Backgrounds: Randomized controlled trials (RCTs) have demonstrated benefits of marine omega-3 polyunsaturated fatty acids (omega-3 FA) supplementation for the prevention of coronary heart disease (CHD). However, it has not been clear which individuals would benefit the most from the supplementation. We sought to predict the individual treatment effect of omega-3 FA supplementation on CHD prevention and to develop an omega-3 effect score to stratify individuals according to their expected benefit from the supplementation. Methods: Among the 25,871 randomized participants without history of CVD in the VITamin D and OmegA-3 TriaL (VITAL), we applied machine-learning (ML) approaches to predict individual treatment effect of omega-3 FA supplementation on 5-year CHD risk (a composite of myocardial infarction, coronary revascularization, and CHD death) using 11 covariates pre-specified in the VITAL trial protocol. A 10-fold cross-validation was used and held-out test dataset was used for the evaluation. An omega-3 effect score was developed such that each covariate contributed linearly, and utility of the score was further evaluated by transportability analysis using the National Health and Nutrition Examination Survey (NHANES) data as the target population. Results: Omega-3 FA intervention led to absolute 0.48% [SE: 0.20] reduction in CHD in the total population. ML algorithms effectively stratified participants by their expected benefit according to individual factors; decreased CHD risk was observed in those with quintile 1 and 2 of the expected benefit (absolute CHD risk reduction %: 1.30 % [0.55] and 1.32 % [0.51] in quintile 1 and 2, respectively). Race, diabetes, and fish intake most contributed to the omega-3 effect score. CHD incidence rates per 1000 person-year were 5.5 [0.44] if treated and 8.5 [0.55] if not treated (35.3% reduction) in individuals with the score ≥11 (upper 40th percentile), and 3.9% [0.31] if treated and 3.4% [0.55] if not treated (14.7% increase) in those with the score <11, respectively. The transportability of the utility of the score to baseline NHANES data was confirmed. Conclusion: In VITAL, ML approaches identified individuals who experienced greater CHD reduction from the omega-3 FA intervention, and an omega-3 effect score stratified the expected benefit. Although it warrants testing in a new RCT, the omega-3 effect score holds promise for guiding the indication of omega-3 FA supplementation in US primary prevention population.

AGE-RELATED CHARACTERISTICS OF ISCHEMIC HEART DISEASE INCIDENCE IN UKRAINE: A TWO-CENTER STUDY

Purpose of this study is to investigate the age-related characteristics of the incidence of coronary heart disease in Ukraine, considering sex differences. Materials and Methods: The study included patients with coronary heart disease who underwent coronary artery bypass surgery on a beating heart (n = 3,674), comprising 3,061 males and 613 females. The average age of the participants was 60.6 ± 0.8 years. The analysis was based on data obtained from primary medical documentation, including medical histories, anamnestic information, and extracts from patients’ outpatient cards. The research design categorized participants by age group according to the World Health Organization age classification and by sex. Results: The article presents the incidence rates of coronary artery disease based on patient age groups, classified according to the World Health Organization, and sex. The distribution of patients by age groups was analyzed while considering sex, and the frequencies and average ages of the patients were determined. It was found that the incidence of coronary artery disease was highest among the most prevalent age groups in Ukraine's population: middle-aged and elderly patients. The frequency of early postoperative mortality was 0.6%, and it correlated with age-related incidence rates of coronary heart disease. Notably, early postoperative mortality was significantly higher in age groups with the highest incidence of coronary heart disease, specifically among middle-aged and elderly patients (p = 0.03, χ² = 4.69). Conclusions: In this retrospective two-center study of patients with coronary heart disease, it was determined that male patients were affected five times more frequently than female patients. The most common age groups for patients with coronary heart disease were identified as middle-aged and elderly. Early postoperative mortality following coronary artery bypass surgery on a beating heart was found to be 0.6%, with the highest rates observed in elderly (54.6%) and middle-aged (31.8%) patients. The frequency ratios demonstrated statistical significance favoring elderly patients (p = 0.03, χ² = 4.69). The frequency of early postoperative mortality was significantly higher among male patients (p = 0.0001, χ² = 40.33).

The association between the fluoxetine use and the occurrence of coronary heart disease: a nationwide retrospective cohort study

BackgroundWe explored if the administration of fluoxetine, recognized for its potential in adipocyte browning, entails a differential risk of coronary heart disease (CHD) in comparison to other SSRI medications.MethodsUsing the National Health Insurance Research Database of Taiwan from 2000 to 2013, we conducted a retrospective cohort study. The exposure cohort comprised individuals prescribed fluoxetine for over 90 days (n = 2,228). Conversely, those administered other SSRIs (excluding fluoxetine) for a duration surpassing 90 days were designated as the non-exposed cohort (n = 8,912). CHD incidence served as our primary outcome measure, and we employed Cox proportional hazards models to scrutinize the relationship between fluoxetine exposure and CHD development rates.ResultsCompared with the non-exposed cohort, the fluoxetine use had a significantly decreased 21% risk of developing CHD in the exposed cohort (adjusted hazard ratio: 0.79%, 95% confidence interval: 0.68–0.92). Noticeably, results indicated that there was an inverse association between the fluoxetine exposure and the risk of CHD, regardless of whether men, women or other age groups.ConclusionOur findings suggest that clinical use of fluoxetine was associated with a 21% reduced risk of CHD relative to other SSRI prescriptions.

Biomarkers of glucose-insulin homeostasis and incident type 2 diabetes and cardiovascular disease: results from the Vitamin D and Omega-3 trial

BackgroundDysglycemia and insulin resistance increase type 2 diabetes (T2D) and cardiovascular disease (CVD) risk, yet associations with specific glucose-insulin homeostatic biomarkers have been inconsistent. Vitamin D and marine omega-3 fatty acids (n-3 FA) may improve insulin resistance. We sought to examine the association between baseline levels of insulin, C-peptide, HbA1c, and a novel insulin resistance score (IRS) with incident cardiometabolic diseases, and whether randomized vitamin D or n-3 FA modify these associations.MethodsVITamin D and OmegA-3 TriaL (NCT01169259) was a randomized clinical trial testing vitamin D and n-3 FA for the prevention of CVD and cancer over a median of 5.3 years. Incident cases of T2D and CVD (including cardiovascular death, myocardial infarction, stroke, and coronary revascularization) were matched 1:1 on age, sex, and fasting status to controls. Conditional logistic regressions adjusted for demographic, clinical, and adiposity-related factors were used to assess the adjusted odds ratio (aOR) per-standard deviation (SD) and 95%CI of baseline insulin, C-peptide, HbA1c, and IRS (Insulin×0.0295 + C-peptide×0.00372) with risk of T2D, CVD, and coronary heart disease (CHD).ResultsWe identified 218 T2D case-control pairs and 715 CVD case-control pairs including 423 with incident CHD. Each of the four biomarkers at baseline was separately associated with incident T2D, aOR (95%CI) per SD increment: insulin 1.46 (1.03, 2.06), C-peptide 2.04 (1.35, 3.09), IRS 1.72 (1.28, 2.31) and HbA1c 7.00 (3.76, 13.02), though only HbA1c remained statistically significant with mutual adjustments. For cardiovascular diseases, we only observed significant associations of HbA1c with CVD (1.19 [1.02, 1.39]), and IRS with CHD (1.25 [1.04, 1.50]), which persisted after mutual adjustment. Randomization to vitamin D and/or n-3 FA did not modify the association of these biomarkers with the endpoints.ConclusionsEach of insulin, C-peptide, IRS, and HbA1c were associated with incident T2D with the strongest association noted for HbA1c. While HbA1c was significantly associated with CVD risk, a novel IRS appears to be associated with CHD risk. Neither vitamin D nor n-3 FA modified the associations between these biomarkers and cardiometabolic outcomes.

Protein Consumption and Risk of CVD Among U.S. Adults: The Multi-Ethnic Study of Atherosclerosis (MESA).

Although some randomized trials have reported beneficial effects of protein intake on cardiometabolic risk factors, evidence from prospective studies have not supported a strong link between protein intake and cardiovascular disease (CVD) risk. It is also unclear whether diversity in protein intake plays a role in CVD risk. We investigated prospective associations of (1) protein intake, overall and by food source and (2) diversity of protein sources with risk of CVD, coronary heart disease (CHD), and stroke. In a multi-ethnic cohort of 5879 U.S. adults (45-84 years), who were free of CVD at baseline, protein intake was assessed at baseline (2000-2002) using a validated 120-item food frequency questionnaire. Two different aspects of protein diversity were assessed including count (number of protein food consumed at least once/week) and dissimilarity (diversity of the attributes of the protein sources consumed). Relationships with incident CVD outcomes through 2019 were assessed using Cox proportional hazards models adjusting for sociodemographic, lifestyle, and comorbidity factors. During 83,430 person-years, 1045 CVD cases were identified, including 668 CHD and 332 stroke cases. In multivariable models, we found no significant associations between protein intake, overall and by food source, with incident CVD, CHD, or stroke. Protein count, but not protein dissimilarity, was weakly associated with CVD risk. We found no significant associations between diversity of consumption of animal or plant food source and CVD outcomes. Our findings suggest protein consumption may not significantly impact CVD risk in middle-aged adults.

Interplay between lifestyle factors and polygenic risk for incident coronary heart disease in a large multiethnic cohort

IntroductionThe objective of this study was to examine the interplay of polygenic risk and individual lifestyle factors (and a composite score of lifestyle) as antecedents of CHD in a large multiethnic cohort. MethodsWe used Genetic Epidemiology Resource in Adult Health and Aging (GERA) cohort participants free of CHD at baseline (n = 60,568; 67 % female; 18 % non-European). The individual and joint associations of smoking, Mediterranean diet pattern, level of physical activity and polygenic risk with incident CHD were assessed using Cox regression adjusting for genetic ancestry and non-mediating risk factors. Hazard ratios (HRs) and number needed to treat (NNT) were estimated according to these lifestyle factors and polygenic risk categories. Strengths included large sample size, long-follow-up, ethnic diversity, a clinically-validated polygenic risk score (PRS), and rich phenotype information. ResultsAfter 14 years of follow-up, there were 3159 incident CHD events. We observed no statistically significant interactions between individual lifestyle factors and polygenic risk (all p > 0.23). For individuals with a high genetic risk, moving from the worse lifestyle combination (no favorable lifestyle factors) to the best lifestyle combination (all three) is associated with 52 % lower rate of CHD. The NNT was highest in the low polygenic risk group (34), lowest in the high polygenic risk group [19] and in-between (Jin et al., 2011) [24] in the intermediate polygenic risk group. ConclusionsLifestyle and polygenic risk together influence the risk of incident CHD. Our results support consideration of polygenic risk in lifestyle interventions because those with high polygenic risk are likely to derive the most benefit.

Взаємозв’язок між хронічною хворобою нирок та серцево-судинною патологією у хворих на цукровий діабет 2-го типу різного віку

The aim – to analyze the relationship between chronic kidney disease (CKD) and cardiovascular pathology in patients with type 2 diabetes (T2D) of different ages.Materials and methods. A total of 233 patients with T2D aged 30-80 years were examined. Anthropometric indicators, blood pressure, glucose levels, glycated hemoglobin, C-peptide, total cholesterol, triglycerides, low-density and high-density lipoprotein cholesterol, creatinine, glomerular filtration rate, AST, and ALT were measured in all patients. Groups of patients were compared based on the presence of CKD and age using Student’s t-test and Pearson’s chi-squared test.Results and discussion. In patients with T2D and CKD, the incidence of coronary heart disease (CHD) (OR 1.8; 95 % CI 1.02–3.23; p=0.044), myocardial infarction (OR 2.0; 95 % CI 1.01–3.95; p=0.046), and strokes (OR 2.66; 95 % CI 1.07–6.63; p=0.036) is significantly higher compared to patients with T2D without kidney pathology. When comparing the clinical indicators of patients with T2D combined with CKD and those without it, no significant differences were found in anthropometric measurements, blood pressure, blood glucose levels, glycated hemoglobin, or C-peptide levels. The levels of total cholesterol, hemoglobin, and red blood cell count in the blood were significantly lower (р<0.05), while the levels of creatinine and glomerular filtration rate were significantly higher (р<0.001) in patients with kidney pathology.Conclusion. In patients with T2D, a relationship between CKD and cardiovascular pathology has been established. It can be assumed that the development of kidney pathology in patients with T2D is a significant risk factor for cardiovascular diseases.

Interplay between family History and polygenic risk for coronary heart disease: a cohort study among over 60 thousand individuals

Abstract Background The degree to which background genetic risk adds to self-report of family history of coronary heart disease (CHD) remains an important question. Methods We utilized data from the multiethnic Genetic Epidemiology Resource in Adult Health and Aging (GERA) cohort of 60,070 Kaiser Permanente of Northern California (KPNC) members (mean ± SD age=59 ± 9 years; 67% female; 18% non-white). We characterized the cohort at baseline in 2003-2007. Excluding those with missing self-report of family history of CHD (n=1,718) resulted in a final sample of 61,352. We stratified the cohort into not having (n=42,866; 70%) and having (n=18,486; 30%) self-reported family history of CHD and then (within stratum of family history of CHD) by three groups of CHD polygenic 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®). Incident CHD was based on ICD-9/10 codes for angina pectoris, myocardial infarction, revascularization procedures or CHD death (n=3,040) through 12/31/2022; mean follow-up was 14.5 years. Results Age-adjusted CHD incidence rates per 10,000 person years were estimated using Poisson regression (accounting for death and health plan disenrollment) by absence/presence of family history of CHD and polygenic risk groups. As shown in the Figure, polygenic risk provided additional risk stratification within categories of family history. The hazard ratio of high PRS (vs low PRS) adjusted for age, sex, 10 principal components of ancestry, smoking, body mass index, diabetes, hypertension, total cholesterol/HDL ratio and cholesterol lowering therapy was 1.62 (95% CI, 1.39-1.87; p<0.001) in those with no family history of CHD, and 1.66 (95% CI, 1.37-2.00; p<0.001) in those with family history of CHD (p-interaction PRS continuous*family history of CHD=0.93). Conclusions Our results show that polygenic risk predicts future CHD regardless of the presence of family history of CHD. Thus, it is not enough to rely of family history to fully characterize potential genetic burden. These data are therefore important for the future of precision medicine.

Sleep characteristics in relation to cardiovascular disease incidence and mortality in individuals with diabetes

Abstract Background/Introduction Evidence regarding the potential health effects of sleep characteristics among individuals with type 2 diabetes (T2D) is limited. Purpose We aimed to examine sleep characteristics in relation to subsequent risk of cardiovascular disease (CVD), including coronary heart disease (CHD), and stroke, and all-cause and cause-specific mortality among individuals with T2D. Methods We prospectively followed 21,902 men and women with T2D at baseline or diagnosed during follow-up (Nurses' Health Study: 1986-2018, Health Professionals Follow-Up Study: 1986-2018). Sleep characteristics, including sleep duration, snoring, sleep apnea, and sleep quality, were repeatedly assessed using self-reported questionnaires at baseline and follow-up. Associations of sleep characteristics with CVD risk and mortality were assessed using Cox proportional hazards models with adjustments for demographic, dietary and lifestyle factors, and medical history. Results During 170,355 and 196,458 person-years of follow-up in participants with T2D, there were 2,486 incident CVD events and 3,922 deaths, respectively. Compared with sleeping for 7-8 h/day, the multivariable-adjusted hazard ratios (HRs) of sleeping for ≤5 h/day were 1.21 (1.02, 1.45) for CVD incidence, 1.24 (1.20, 1.51) for CHD incidence, 1.40 (1.24, 1.58) for total mortality, 1.52 (1.20, 1.92) for CVD mortality, and 1.27 (1.01, 1.61) for other non-CVD and non-cancer mortality, while the HRs of ≥10 h/day were 1.42 (1.21, 1.66) for total mortality, and 1.63 (1.20, 2.10) for other non-CVD and non-cancer mortality. Furthermore, compared with participants without habitual snoring, those with habitual snoring had a 21%, 24%, 18%, and 33% higher risk for CVD incidence, CHD incidence, CVD mortality, and total mortality, respectively. Compared with participants without diagnosed sleep apnea, those with sleep apnea had a 27%-58% higher risk for CVD incidence, CVD mortality, and total mortality. In addition, lower habitual sleep quality, including sleep difficulties and restless sleep, was associated with a substantially higher risk of CVD, CHD, or CVD mortality. No associations were observed between sleep characteristics with risk of stroke and cancer mortality in individuals with T2D. Conclusions Short and long sleep durations as well as habitual snoring, sleep apnea, and lower sleep quality were independently associated with higher risks of CVD incidence and mortality, particularly CVD mortality in individuals with T2D.

Relation of apolipoprotein C3 to risk of major adverse cardiovascular events and death after acute coronary syndrome on a background of optimized statin treatment

Abstract Background Apolipoprotein C3 (ApoC3), a component of triglyceride-rich lipoproteins and some low-density lipoprotein and high-density lipoprotein particles, has been shown to predict incident coronary heart disease (CHD) and major adverse cardiovascular events (MACE). However, it is unknown whether ApoC3 predicts risk in patients with acute coronary syndrome (ACS) receiving contemporary therapies including optimized statin treatment, and if any such association is independent of apolipoprotein B (ApoB) levels. Purpose We assessed the association of ApoC3 with first MACE (CHD death, nonfatal myocardial infarction, fatal or nonfatal ischaemic stroke, or hospitalization for unstable angina) and all-cause death in patients with recent ACS treated with high-intensity or maximum-tolerated statin and blinded PCSK9 inhibitor (alirocumab, ALI) or placebo (PBO). Methods ApoC3 was measured by mass spectrometry at baseline (n=11,956) and after 4 months (M4; n=11,176) of treatment with ALI or PBO in the ODYSSEY OUTCOMES trial (which had 18,924 total participants). In continuous and spline analyses adjusted for treatment group and ApoB, we assessed the association of baseline ApoC3 with risk of MACE and death. In the ALI group we determined association of change in ApoC3 from baseline to M4 with risk of MACE and death after M4 in a model adjusted for baseline ApoC3 and ApoB, and the change in ApoB from baseline to M4. Results Median (Q1, Q3) baseline ApoC3 concentration was in a normal range [85 (65, 113) mg/L]. Continuous ApoC3 was not related to MACE (p=0.50) or death (p=0.51); spline analysis showed a slight curvilinear association of baseline ApoC3 with risk of MACE and death, but no clinically meaningful relationship (Figure). Findings were similar in the PBO group alone, and without adjustment for ApoB (data not shown). At M4, the median (Q1, Q3) change from baseline in ApoC3 was -10 (-27, -5; p<0.0001) mg/L with ALI and 2 (-14, 18; P = NS) mg/L with PBO. Overall, ALI significantly reduced the incidence of MACE (10.1% vs 12.1%; p=0.0006) and death (3.5% vs 4.2%; p=0.045) compared with PBO among those with available baseline ApoC3. However, the change in ApoC3 on treatment with ALI did not predict the risk of MACE or death after M4. Findings were qualitatively similar without adjustment for ApoB or its change. Conclusion In a cohort with recent ACS receiving optimized statin therapy and with median baseline ApoC3 in a normal range, ApoC3 did not provide clinically meaningful prediction of cardiovascular events or death. A modest reduction of ApoC3 by ALI did not associate with subsequent risk of MACE or death. It remains uncertain whether targeted therapies producing larger reductions in ApoC3 from higher baseline levels will affect cardiovascular risk.

Ultra-processed food consumption and risk of coronary heart diseases: UK Whitehall II cohort study

Abstract In recent decades, ultra-processed foods (UPFs) intake has increased drastically, sparking concerns about their potential impact on cardiometabolic diseases. However, large-scale cohort studies tracking UPF consumption at multiple time points remain limited. This study explores the prospective association between repeated measures of UPF intake and the risk of coronary heart disease (CHD), along with its secondary endpoints, within the UK Whitehall II study. The analytical sample tracked 7,138 midlife British participants without CHD from baseline. UPF consumption was measured using validated food frequency questionnaire (127 items) and classified by the NOVA system during three phases: 1991/1994 (phase 3), 1997/1999 (phase 5), and 2002/2003 (phase 7). This study assessed the onset of CHD and its secondary endpoints, including CHD and all-cause mortality, through medical exams and hospital records up to 2016 and 2021, respectively. Cox proportional hazards regression models adjusted for socio-demographics, lifestyle factors and total energy intake were used to explore the prospective association between cumulative average UPF intake (in quintiles) and CHD outcomes. During a median follow-up of 13 and 19 years, 589 cases and 1,314 deaths were documented. In multivariable adjusted cox models, the highest UPF consumption quintile versus the lowest quintile was associated with higher CHD incidence [HR:1.26; 95% Confidence Interval (CI): 1.02-1.55; p = 0.03]. Additional adjustment of total energy intake increased the CHD risk by 28% [HR:1.28; 95% CI: 1.03-1.58; p = 0.02]. No significant relationships were found between cumulative average UPF intake and CHD or all-cause mortality. In UK midlife adults, higher UPF intake is prospective associated with increased CHD risk. Although additional research is warranted, these findings emphasize the importance of public awareness and food policy interventions to reduce UPF intake for alleviating the population burden of CVD. Key messages • Our study suggests the need for increased efforts to implement population wide strategies on regulating food processing, such as taxation and front of package warning labelling of UPF. • Our study emphasizes UPF’s role in cardiovascular prevention, highlighting the need for nutrition counseling on UPF consumption for those at risk of CVD.

Phosphodiesterase 5 and its inhibitors with ischemic heart disease: a Mendelian randomization analysis and a real-world study.

Accumulating studies reported that several phosphodiesterases (PDEs) inhibitors might have cardiovascular benefits. This study aimed to explore the relationship between genetically-predicted PDEs and ischemia heart disease via drug target Mendelian randomization (MR) approach, and then examine the effect of inhibitors of identified target on the outcomes by using real-world data. In the two-sample MR study, the expression of genes encoding PDEs was used to proxy the level of PDEs and available expression quantitative trait loci (eQTLs) for each target gene were identified as the genetic instruments. The outcomes included coronary heart disease (CHD) and myocardial infarction (MI). In the real-world study, a retrospective cohort was conducted to compare the incidence of outcomes between PDE5 inhibitors and alprostadil use by linking Swedish nationwide registers. MR analyses identified two types of PDEs, PDE5 and PDE8, genetically-predicted expression in blood of the encoded genes was significantly associated with the risk of CHD (ORPDE5A=1.22,95% CI=1.06-1.40; ORPDE8A=1.26,95% CI=1.07-1.49) and MI (ORPDE5A=1.27,95% CI=1.09-1.48; ORPDE8A=1.24,95% CI=1.04-1.48). Notably, the highest expression of PDE5A was observed in artery aorta, which was also positively related to CHD (OR=1.17,95% CI=1.05-1.32) and MI (OR=1.15,95% CI=1.02-1.30). Real-world study provided supportive evidence that as compared to alprostadil use, PDE5 inhibitors use significantly reduced the incidence of CHD (adjusted HR=0.70,95% CI=0.66-0.73) and MI (adjusted HR=0.79,95% CI=0.73-0.84). This study provided observational and genetic evidence about the protective role of PDE5 inhibition against ischemic heart disease, indicating the potential of these drugs to be repurposed for ischemia heart disease prevention and treatment.

Prospective associations of genetic susceptibility to high blood pressure and muscle strength with incident cardiovascular disease outcomes.

This study explored the prospective associations of genetic susceptibility to high blood pressure (BP) and muscle strength with cardiovascular disease (CVD) mortality, incident coronary heart disease (CHD) and incident stroke. This study included 349 085 white British individuals from the UK Biobank study. Genetic risk of high BP was estimated using a weighted polygenic risk score that incorporated 136 and 135 nonoverlapping single-nucleotide polymorphisms for systolic BP and diastolic BP, respectively. Muscle strength was assessed using a hand dynamometer and expressed relative to fat-free mass. Sex- and age-specific tertiles were used to classify muscle strength into three categories. Cox regressions with age as the underlying timescale were fit for CVD mortality (n = 8275), incident CHD (n = 14 503), and stroke (n = 7518). Compared with the lowest genetic risk of high BP (bottom 20%), the highest (top 20%) had greater hazards of each outcome. Low muscle strength was associated with higher hazards of CVD mortality [hazard ratio (HR): 1.51, 95% confidence interval (CI): 1.43-1.59], incident CHD (HR: 1.16, 95% CI: 1.11-1.21), and stroke (HR: 1.20, 95% CI: 1.14-1.27), independently of confounders and genetic predisposition to high BP, compared with high muscle strength. Joint analyses revealed that the estimated 10-year absolute risks of each outcome were lower for high muscle strength combined with high genetic risk, compared with low muscle strength combined with low or medium genetic risk. Individuals who are genetically predisposed to high BP but have high muscle strength could have lower risk of major CVD events, compared with those who have low or medium genetic risk but low muscle strength.

Association between dietary inflammatory index and all-cause mortality risk in adults with coronary heart disease in the United States

Diet and inflammation are crucial in the incidence and progression of coronary heart disease (CHD). This study aimed to investigate the correlation between the Dietary inflammatory index (DII) and all-cause mortality in CHD patients. A total of 1,303 CHD patients from the National Health and Nutrition Examination Survey (NHANES) between 2003 and 2018 were included. Multivariate Cox regression was used to explore the correlation between the DII and the risk of all-cause mortality in these patients. Restricted cubic spline (RCS) analysis was also utilized to examine the relationship between the DII and all-cause mortality risk in CHD patients. Additionally, subgroup analyses were conducted to determine how the correlation between the DII and all-cause mortality varied across different demographics. During a median follow-up period of 77 months among 1,303 CHD patients, 536 died from all causes. The DII scores were significantly higher in deceased patients compared to survivors. After adjusting for confounding factors, the multivariate Cox regression analysis indicated a strong positive correlation between the DII and all-cause mortality in CHD patients. RCS analysis suggested a non-linear relationship between the DII and all-cause mortality among CHD patients. Additionally, an increase in DII was more pronounced in its impact on female patients. The DII is strongly correlated with the risk of all-cause mortality among CHD patients, particularly among females. Thus, managing dietary inflammation is vital for the prevention and treatment of CHD, especially in female patients.

6719 Sex Differences In Lipoproteins And Excess Risk Of Coronary Heart Disease In Women With Type 2 Diabetes

Abstract Disclosure: Y. Yoshida: None. D. Li: None. X. Li: None. V.A. Fonseca: None. L. Qi: None. F. Mauvais-Jarvis: None. Background: Women with type 2 diabetes (T2D) have a greater risk of coronary heart disease (CHD) than men with T2D. We compared levels of lipoproteins and their associations with CHD in women and men with new-onset T2D, pre-diabetes (PDM), and euglycemia. Method: We obtained circulating metabolomic data, including lipoprotein classes, apolipoproteins, total triglycerides (TG), and TG in very large LDL (VLDL), LDL, and HDL by nuclear magnetic resonance for 95,108 CHD-free people at baseline and incident CHD from the national health registers of the UK Biobank study. We used multivariable linear regressions to examine the association between sex and lipoprotein markers (log(x)) in groups of new-onset T2D (new T2D diagnosis or diabetes medication use within two years from the baseline), PDM (HbA1c 5.7-6.5%), and euglycemia, accounting for age, race, Townsend Deprivation Index, income, smoking, obesity, medications for hypertension, hyperlipidemia, and diabetes. We used Cox proportional hazard models to evaluate the association between lipoproteins and CHD risk in men and women separately, adjusting the same covariates. We performed sensitivity analyses using the assay-measured lipoproteins of the same participants and accounted for menopausal status. False discovery rate adjusted for multiple comparisons. Results: 1328 individuals with newly diagnosed T2D, 6204 with PDM, and 87,576 with euglycemia were included in the analysis. In adjusted linear regressions, atherogenic lipoproteins, including total cholesterol (c), non-HDL-c, remnant-c, and LDL-c were significantly higher in women than in men across glycemic status, and this sex difference was the most striking in the T2D group (β 0.5, 0.3, 0.15, and 0.23 in T2D vs. 0.44, 0.16, 0.09, and 0.12 in PDM vs. 0.37, 0.08, 0.04, and 0.08 in euglycemia). In euglycemic individuals, levels of Apo B and VLDL were higher in men than in women (β -0.01 and -0.05); however, in T2D individuals, women had higher levels of VLDL(β 0.05 and 0.05). Total TG and TG in VLDL were significantly higher in men with euglycemia (β -0.22 and -0.23) and PDM (β -0.15 and -0.16), but the sex differences were not significant in the T2D group (β -0.01 and -0.04). During the median 10-year follow-up, one SD increase in total TG (women HR 2.5, 95% 1.3-4.9 vs. men 1.07, 0.7-1.7 P-interaction=0.03), TG in VLDL (W 2.1, 1.2-3.7 vs. M 1.06 0.7-1.6 P=0.03), TG in LDL (W 3.2, 1.2-8.8 vs. M 1.3, 0.7-2.6, P=0.1), and TG in HDL (W 3.7, 1.4-9.5 vs. M 0.9, 0.5-1.7, P=0.008) was significantly associated with increased risk of CHD in women with T2D, but the associations were not significant in male patients. Results from available assay-measured markers and menopausal stratification were generally consistent with the main results. Conclusions: Women had higher levels of atherogenic lipids than men with advancing glycemic status. Women with T2D are at a higher risk of CHD associated with TG than men with T2D. Presentation: 6/3/2024

The relationship between HIV/AIDS and coronary heart disease: A bibliometric analysis.

Acquired immunodeficiency syndrome is a malignant infectious disease caused by the human immunodeficiency virus (HIV). HIV gradually destroys the body's immune system and weakens the body's ability to resist diseases. People living with HIV may have a higher incidence of coronary heart disease than people without HIV. A literature retrieval from January 1, 1993 to October 1, 2023 based on the Web of Science Core Collection database. CiteSpace6.2.R4, VOSviewer v1.6.19, and Microsoft Excel 2019 were utilized for analyzing the following terms: countries, institutions, authors, journals, references, and keywords. There were 1144 articles. The highest number of articles is in the USA, followed by Italy. University of California System, Harvard University, and Johns Hopkins University were the top 3 most productive institutions with publications in this field of research. Journal of Infectious Diseases ranked first with the highest publications (532 records), followed by Immunology (362 records), and Cardiac Cardiovascular Systems (242 records). Keyword co-occurrence analysis showed antiretroviral therapy, myocardial infarction, and protease inhibitors, etc. Keyword cluster analysis obtained 13 categories, which were roughly divided into 3 themes: (1) cardiovascular disease that has occurred or may occur; (2) HIV acquisitions that have occurred; (3) risk factors for cardiovascular disease. The article obtained the hotspots and trends and provided references for subsequent research. Based on the keyword citation burst detection analysis, we speculated that heart failure, risk, subclinical atherosclerosis, infection, and association were the research hotspots in recent years, which had a certain predictive effect on the future research direction.

Association of circulating fatty acids with cardiovascular disease risk: Analysis of individual-level data in three large prospective cohorts and updated meta-analysis.

Associations of saturated and unsaturated fatty acids (FAs) with cardiovascular disease (CVD) remain controversial. We therefore aimed to investigate the prospective associations of objectively measured FAs with CVD, including incident coronary heart disease (CHD) and stroke, as well as CVD mortality. Circulating FA concentrations expressed as the percentage of total FAs were assayed in 172,891 participants without prior vascular disease at baseline from the European Prospective Investigation into Cancer and Nutrition-CVD (EPIC-CVD) (7,343 CHD; 6,499 stroke), UK Biobank (1,825; 1,474), and INTERVAL (285; 209) cohort studies. Hazard ratio (HR) per 1-standard deviation (SD) higher FA concentrations was estimated using Cox regression models and pooled by random-effects meta-analysis. Systematic reviews with meta-analysis published by 6 May 2023 on associations between FAs and CVDs were systematically searched and updated meta-analyses using random-effects model were conducted. Evidence from randomized controlled trials (RCTs) was also summarized. Higher concentrations of total saturated FAs (SFAs) were associated with higher cardiovascular risks in the combined analysis, with differential findings noted for SFA subtypes in further analysis restricted to EPIC-CVD: positive associations for even-chain SFA [HR for CHD 1.24 (95% CI: 1.18-1.32); stroke 1.23 (1.10-1.38)] and negative associations for odd-chain [0.82 (0.76-0.87); 0.73 (0.67-0.78)] and longer-chain [0.95 (0.80-1.12); 0.84 (0.72-0.99)] SFA. In the combined analysis, total n-3 polyunsaturated FA (PUFA) [0.91 (0.85-0.97)], including docosahexaenoic acid (DHA) [0.91 (0.84-0.98)], was negatively associated with incident CHD risk. Similarly, total n-6 PUFA [0.94 (0.91-0.98)], including linoleic acid (LA) [0.89 (0.83-0.95)], was negatively associated with incident stroke risk. By contrast, more detailed analyses in EPIC-CVD revealed that several downstream n-6 PUFAs of LA were positively associated with CHD risk. Updated meta-analyses of 37 FAs including 49 non-overlapping studies, involving between 7,787 to 22,802 CHD and 6,499 to 14,221 stroke cases, showed broadly similar results as our combined empirical analysis and further suggested significant inverse associations of individual long-chain n-3 PUFAs and LA on both CHD and stroke. The findings of long-chain n-3 PUFAs were consistent with those from published RCTs on CHD despite insufficient evidence in monotherapy, while RCT evidence remained unclear for the rest of the explored FAs. Our study provides an overview of the most recent evidence on the associations between objectively measured FAs and CVD outcomes. Collectively, the data reveals notable differences in associations by SFA subtypes and calls for further studies, especially RCTs, to explore these links.