Risk Of Heart Disease Research Articles

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.

Non-fermented and fermented milk intake in relation to risk of ischemic heart disease and to circulating cardiometabolic proteins in swedish women and men: Two prospective longitudinal cohort studies with 100,775 participants

BackgroundThe effect of milk on the risk of ischemic heart disease (IHD) and acute myocardial infarction (MI) is unclear. We aimed to examine the association between non-fermented and fermented milk consumption on these endpoints and investigate the relationship between milk intake and cardiometabolic-related proteins in plasma.MethodsOur study is based on two Swedish prospective cohort studies that included 59,998 women and 40,777 men without IHD or cancer at baseline who provided repeated measures of diet and lifestyle factors and plasma proteomics data in two subcohorts. Through registry linkage, 17,896 cases with IHD were documented during up to 33 years of follow-up, including 10,714 with MI. We used time-updated multivariable Cox regression analysis to examine non-fermented or fermented milk intake with time to IHD or MI. Using high-throughput multiplex immunoassays, 276 cardiometabolic plasma proteins were measured in two subcohorts. We applied multivariable-adjusted regression models using a discovery-replication design to examine protein associations with increasing consumption of non-fermented or fermented milk.ResultsThe results for non-fermented milk differed by sex (p-value for interaction = 0.01). In women, we found a pattern of successively greater risk of IHD and MI at non-fermented milk intake levels higher than 1.5 glasses/day. Compared with an intake of 0.5 glass/day (100 mL/day), non-fermented milk intake of 2 glasses/day in women conferred a multivariable-adjusted hazard ratio (HR) of 1.05 (95% CI 1.01–1.08) for IHD, an intake of 3 glasses/day an HR of 1.12 (95% CI 1.06–1.19), and an intake of 4 glasses/day an HR of 1.21 (95% CI 1.10–1.32). Findings were similar for whole, medium-fat, and low-fat milk. We did not detect higher risks of IHD with increasing milk intakes in men. Fermented milk intake was unrelated to the risk of IHD or MI in either sex. Increasing non-fermented milk intake in women was robustly associated with a higher concentration of plasma ACE2 and a lower concentration of FGF21.ConclusionsWe show a positive association between high amounts of non-fermented milk intake and IHD in women but not men. We suggest metabolic pathways related to ACE2 and FGF21 potentially underlie the association.Graphical abstractOur analysis of two large cohort studies involving 100,775 participants and 17,896 clinically confirmed IHD events supports a dose–response positive association between non-fermented milk intake higher than 300 mL/day with higher rates of IHD (and acute MI specifically) in women, but not in men. The higher risk of IHD with high milk intake in women was evident, irrespective of the fat content of the milk. Fermented milk intake was unrelated to the risk of IHD in both women and men. Non-fermented milk intake was associated in different directions with circulating levels of ACE2 and FGF21 in women—two essential cardiometabolic proteins, also related to IHD in women in our study.

Associations Between Mosaic Loss of Sex Chromosomes and Incident Hospitalization for Atrial Fibrillation in the United Kingdom.

Mosaic loss of chromosome Y (mLOY) in leukocytes of men reflects genomic instability from aging, smoking, and environmental exposures. A similar mosaic loss of chromosome X (mLOX) occurs among women. However, the associations between mLOY, mLOX, and risk of incident heart diseases are unclear. We estimated associations between mLOY, mLOX, and risk of incident heart diseases requiring hospitalization, including atrial fibrillation, myocardial infarction, ischemic heart disease, cardiomyopathy, and heart failure. We analyzed 190 613 men and 224 853 women with genotyping data from the UK Biobank. Among these participants, there were 37 037 men with mLOY and 13 978 women with mLOX detected using the Mosaic Chromosomal Alterations caller. Multivariable Cox regression was used to estimate hazard ratios (HRs) and 95% CIs of each incident heart disease in relation to mLOY in men and mLOX in women. Additionally, Mendelian randomization was conducted to estimate causal associations. Among men, detectable mLOY was associated with elevated risk of atrial fibrillation (HR, 1.06 [95% CI, 1.03-1.11]). The associations were apparent in both never smokers (HR, 1.07 [95% CI, 1.01-1.14]) and ever smokers (HR, 1.05 [95% CI, 1.01-1.11]) as well as men aged >60 and ≤60 years. Mendelian randomization analyses supported causal associations between mLOY and atrial fibrillation (HRMR-PRESSO, 1.15 [95% CI, 1.13-1.18]). Among postmenopausal women, we found a suggestive inverse association between detectable mLOX and atrial fibrillation risk (HR, 0.90 [95% CI, 0.83-0.98]). However, associations with mLOY and mLOX were not found for other heart diseases. Our findings suggest that mLOY and mLOX reflect sex-specific biological processes or exposure profiles related to incident atrial fibrillation requiring hospitalization.

The association between alpha-1 antitrypsin and B-type natriuretic peptide blood levels in healthy African Americans

ObjectiveB-type natriuretic peptide (BNP) is a neurohormone primarily secreted from cardiac ventricles in reaction to increased volume and pressure. The plasma level of BNP is used to measure the mechanical function of the heart and the risk of developing chronic obstructive pulmonary disease (COPD). Alpha-1 antitrypsin (AAT) is a glycoprotein that acts as an inhibitor of serine proteases and plays a crucial role in protecting the lungs against potential harm. AAT deficiency also causes COPD. The data on the prevalence of BNP and AAT in African Americans (AA) are limited and inconsistent. No previous studies have investigated whether any association exists between BNP and AAT. We collected fasting blood samples from 114 AA subjects who provided informed consent. The plasma levels of the biomarkers were measured using ELISA.ResultsOur findings revealed a significant negative correlation between AAT and BNP (r=-0.266, p = 0.01) as well as between AAT and TNF-α (r=-0.242, p = 0.01). Sex hormones (estrogen and testosterone) have a significant relationship with the levels of AAT and BNP. Increasing the AAT and reducing the levels of inflammation can lower the levels of BNP, which in turn could help lower the risk of heart disease in the AA population.

Factors Associated with Heart Disease in Japan: Multivariate Analysis Based on Specific Health Checkups

The global population affected by heart failure is projected to reach 30 million. The number of deaths due to heart disease has surged, rising from 2 million in 2000 to 8.9 million in 2019. In Japan, the prevalence of heart failure is rapidly increasing, with the number expected to reach 1.3 million by 2030. Primary prevention is crucial to prevent heart disease. We explored the associations of heart disease incidence with findings from checkups performed a decade ago. A multivariate logistic regression analysis revealed that individuals who reported a history of stroke, history of chronic renal failure, or weight gain ≥ 10 kg since age 20 in the questionnaire-based health checkup are at high risk for developing heart disease. Additionally, those with biochemical test results from 10 years ago indicating the use of antihypertensive drugs, use of insulin injections or hypoglycemic medications, systolic hypertension, and abnormal creatinine levels also exhibited a significantly higher risk of heart disease. Conversely, individuals who identified as female, walked faster than people of the same age, drank alcohol daily, and felt refreshed upon awakening in the questionnaire-based health checkup were protected from heart disease.

Cardioprotective effect of tofisopam against isoprenaline-induced myocardial infarction in rats via modulation of NLRP3\\IL-1β\\caspase-1 pathway

Purpose Cardiovascular diseases (CVDs) are a leading cause of morbidity and mortality worldwide. Ischemic heart diseases, particularly acute myocardial infarction (MI), represent the most common cause of death. MI is influenced by multiple factors, including the release of inflammatory mediators. A significant percentage of individuals with CVD experience psychological effects, such as anxiety and depression, which are linked to an increased risk of coronary heart disease. Certain anti-anxiety medications have demonstrated immunomodulatory and anti-inflammatory effects. Tofisopam, a 2,3-benzodiazepine with anxiolytic properties, has been shown to exert in vitro anti-inflammatory and immunomodulatory effects. The present study investigates the potential of tofisopam as a protective adjuvant against isoprenaline-induced MI in rats and explores the possible underlying mechanisms. Methods The study included four groups: a control group, a group pretreated with tofisopam, an isoprenaline toxic group, and an isoprenaline toxic group pretreated with tofisopam. Results The findings demonstrated that isoprenaline significantly increased cardiac enzyme levels, as well as elevated oxidative and inflammatory stress parameters, along with evident apoptosis in cardiac cells. In contrast, the tofisopam-pretreated group showed a significant reversal of the cardiac damage induced by isoprenaline. Conclusions Tofisopam protects against isoprenaline-induced MI through its antioxidant, anti-inflammatory, and anti-apoptotic properties.

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.

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.

Association of age at diagnosis of type 2 diabetes mellitus with the risks of the morbidity of cardiovascular disease, cancer and all-cause mortality: Evidence from a real-world study with a large population-based cohort study.

To investigate the impact of diagnosis age of type 2 diabetes mellitus (T2DM) on subsequent adverse outcomes within the Chinese population. 549,959 eligible T2DM patients were included from Ningbo and Jinhua city in Zhejiang province, China. Standardized ratio was used to evaluate the risks of coronary heart disease (CHD), stroke, cancer and all-cause death in different T2DM diagnosis age groups. For all adverse outcomes, higher excess risks were observed in the youngest age group (30-39) than in the oldest age group (≥80) with T2DM. The standardized incidence ratios (SIR) were 5.93 (95 % CI: 3.46, 10.14) for CHD, 5.45 (95 % CI: 3.72, 7.99) for stroke and 1.85 (95 % CI: 1.38, 2.49) for cancer in the youngest age group, and were 1.32 (95 % CI: 1.08, 1.60) for CHD, 1.25 (95 % CI: 1.08, 1.44) for stroke, and 0.78 (95 % CI: 0.56, 1.09) for cancer, respectively, in the oldest age group. The standardized mortality ratios (SMR) for all-cause death were 3.15 (1.69, 5.84) vs. 1.12 (0.88,1.43). These excess risks decreased with increasing diagnosis age (all P value < 0.001). Consistent results were observed when individuals were stratified by sex or further excluded with the time from T2DM diagnosis to endpoints less than 1 or 2 years. The earlier the diagnosis of T2DM, the higher the risk for subsequent adverse outcomes. It is imperative to enhance the management and monitoring of early-onset patients during follow-up.

The research of influence factors that possibly lead to cardiovascular disease

Abstract. The emergence of cardiac disease is influenced by numerous variables. Every year a large percentage of people around the world die from heart attacks. This study was to look at how important clinical variables are connected to the chance of having CVD. The analysis used a Kaggle dataset with details from 70,000 patients and 10 different variables. The study examined how factors such as age, gender and changes in cardiac activity during exercise affect overall heart health. Multiple linear regression models were used to analyze these effects. The results show a significant correlation between these factors and an increased risk of heart disease. This emphasizes the importance of these predictors in clinical assessments. It can be concluded from this study that regular medical check-ups, early prevention and treatment should be carried out for these vulnerable groups. The general prevalence of heart disease in the nation can be decreased by implementing these strategies. According to the study, personalized health strategies have the potential to improve CVD outcomes and strengthen preventive measures. All of the experimental results suggest that continued documentation and study of these pathogenic factors in medical diagnostics and experiments could aid in drug development as well as improve medical technology and help more patients with cardiovascular disease recover.

Prediabetes and cardiovascular risk factors: the effectiveness of a guided self-determination counselling approach in primary health care, a randomized controlled trial

BackgroundIdentify individuals who are at risk of Type 2 diabetes, who also are at a greater risk of developing cardiovascular disease is important. The rapid worldwide increase in diabetes prevalence call for Primary Health Care to find feasible prevention strategies, to reduce patient risk factors and promote lifestyle changes. Aim of this randomized controlled trial was to investigate how a nurse-lead Guided Self-Determination counselling approach can assist people at risk of type 2 diabetes to lower their coronary heart disease risk.MethodsIn this randomized controlled study, 81 people at risk of developing type 2 diabetes were assigned into an intervention group (n = 39) receiving Guided Self-Determination counselling from Primary Health Care nurses over three months and a control group (n = 42) that received a diet leaflet only. Measurements included the Finnish Diabetes Risk Score questionnaire and biological measurements of Hemoglobin A1c protein, Body Mass Index, fasting blood glucose, Blood pressure, Cholesterol, High-density lipoprotein, and triglycerides, at baseline (time1), 6 (time2) and 9 months (time 3).ResultsA total of 56 participants, equal number in intervention and control groups, completed all measurements. A significant difference between the intervention and control groups, in coronary heart disease risk was not found at 6 nor 9-months. However, within-group data demonstrated that 55.4% of the participants had lower coronary heart disease risk in the next ten years at the 9-month measurement. Indicating an overall 18% relative risk reduction of coronary heart disease risk by participating in the trial, with the number needed to treat for one to lower their risk to be nine. Within the intervention group a significant difference was found between time 1 and 3 in lower body mass index (p = 0.046), hemoglobin A1c level (p = 0.018) and diastolic blood pressure (p = 0.03).ConclusionsAlthough unable to show significant group differences in change of coronary heart disease risk by this 12-weeks intervention, the process of regular measurements and the guided self-determination counselling seem to be beneficial for within-group measures and the overall reduction of coronary heart disease risk factors.Trial registrationThis study is a part of the registered study ‘Effectiveness of Nurse-coordinated Follow-Up Programme in Primary Care for People at Risk of T2DM’ at www.ClinicalTrials.gov (NCT04688359) (accessed on 30 December 2020).

Improved Heart Diseases Risk Prediction Using Optimized Super Learner Ensemble Model

Improved Heart Diseases Risk Prediction Using Optimized Super Learner Ensemble Model

Cigar-Specific Health Warnings: Attention, Recall, and Perceived Effectiveness Among Young Adult Users and Non-Users

Limited research has examined attention to these cigar-specific health warnings and their perceived effectiveness among young people. The objective of our study was to evaluate the attention to and perceptions of a set of cigar-specific health warnings among young adult tobacco users and non-users. Methods: Young adults ages 18–24 in Columbus, Ohio, were recruited into an eye-tracking experiment examining cigarillo packaging between May 2022 and February 2023. Participants (n = 124) were shown 12 unique, branded cigarillo packages featuring a rotation of four of the Food and Drug Administration’s mandated health warnings: (1) Cigar smoking can cause lung cancer and heart disease (“disease”); (2) tobacco smoke increases the risk of lung cancer and heart disease, even in nonsmokers (“nonsmokers”); (3) cigar smoking can cause cancers of the mouth and throat, even if you do not inhale (“inhale”); and (4) cigars are not a safe alternative to cigarettes (“alternative”). Software captured visual attention to each product package, including the health warning. Participants also ranked the most effective message to motivate people to quit; one week later, the participants (n = 118) self-reported unaided recall of the experiment. Results: Study participants were an average of 21.2 years old, 54.2% were female, 73.7% were White, 65.3% had some college education, and 26.3% reported tobacco use in the previous month. The health warning, “Cigar smoking can cause cancers of the mouth and throat, even if you do not inhale” was ranked the most effective cigar warning (41.5%) and drew the greatest proportion of visual attention (26.1%). More than half (52.5%) recalled details regarding the health warning messages one week following the experiment, with few recalling (17.7%) specific warning message themes. Conclusions: Understanding the best performing health warnings is a crucial strategy to share accurate information on the risks of tobacco use. Our findings suggest that the warning on cancer risk even without inhaling drew the greatest visual attention and highest rating of perceived effectiveness among this sample of young adult cigarillo users and non-users.

Using Genetics to Assess the Role of Acetate in Ischemic Heart Disease, Diabetes, and Sex-Hormone-Related Cancers: A Mendelian Randomization Study

Background: Acetate, a short-chain fatty acid, has gained attention for its contrasting roles, with evidence suggesting it may offer cardiovascular protection but also promote cancer, particularly those involving sex hormones. However, these influences have been scarcely assessed in epidemiological research. Objective: To investigate the relationship between acetate and ischemic heart disease (IHD), diabetes, and cancers related to sex hormones. Methods: Mendelian randomization (MR) was used to assess potential causal effects, selecting genetic variants without linkage disequilibrium (r2 &lt; 0.001) and with genome-wide significance for acetate (p &lt; 5 × 10−8). These variants were applied to large genome-wide association studies (GWAS) for ischemic heart disease (IHD; up to 154,373 cases), diabetes (109,731 cases), and five sex-hormone-related cancers (breast, colorectal, prostate, ovarian, and endometrial cancers, ranging from 8679 to 122,977 cases). We employed various methods for analysis, including penalized inverse variance weighting (pIVW), inverse variance weighting, weighted mode, and weighted median. Results: This study indicates that acetate may be associated with a lower risk of ischemic heart disease (IHD), with an odds ratio (OR) of 0.62 per standard deviation (SD) increase in acetate and a 95% confidence interval (CI) of 0.39 to 0.98. Additionally, acetate was linked to a higher breast cancer risk, with an OR of 1.26 and a 95% CI ranging from 1.08 to 1.46. This association remained robust across multiple sensitivity analyses. Conclusions: Acetate, along with factors that influence its activity, may serve as possible targets for breast cancer treatment and possibly IHD, offering opportunities for new drug development.

Weekend compensatory sleep is associated with reduced risk of heart disease: a prospective UK Biobank-based cohort study

Abstract Background and Aims Influenced by the demands of school or work, people often fall out of sync with their circadian rhythms, which leads to sleeping in on days off. Despite this phenomenon, there is a lack of research examining whether compensatory weekend sleep has positive effects on heart health. Methods and results Our prospective cohort study utilized data from the UK Biobank (UKB) and encompassed 90,903 participants. To evaluate the relationship between compensated weekend sleep and heart disease. The sleep data was recorded by Axivity AX3 accelerometer from UKB and grouped by quartiles. Hospitalization records and cause of death registry information were used to diagnose various cardiac diseases including IHD, HF, AF, and stroke. Then multivariate Cox proportional hazard modeling was used to examine the potential impact of compensated sleep on the risk of heart disease. At a median follow-up time of up to 13.8 years, we found that participants in the compensatory sleep group(Q4) had a lower risk of having heart disease in the fully adjusted model (HR: 0.809, 95%CI: 0.766,0.854), which was not influenced by the effect of genetic risk for IHD, HF, or AF. These relationships were even more pronounced in the subgroup with daily sleep deprivation (HR:0.801, 95%CI: 0.718,0.894). Conclusion Sufficient compensatory sleep on weekends is linked to a low risk of heart disease, including IHD, AF, HF, and stroke, which is independent of genetic risk. And the association becomes even more pronounced among individuals who regularly experience inadequate sleep on weekdays.Visual abstract

Preventing unnecessary echocardiograms in de novo patients referred to the cardiology outpatient clinic using electrocardiogram-based deep learning

Abstract Introduction The growing demand on European echocardiography labs, driven by the rise in structural heart disease (SHD), is further complicated by a shortage of skilled sonographers, necessitating resource optimisation strategies. Electrocardiogram (ECG)-based deep learning models may assist in streamlining the echocardiography workflow. Purpose This study sought to develop a deep learning model capable of identifying patients at very low risk of SHD in a population of de novo patients referred to the cardiology outpatient clinic. Methods We identified all adult patients who underwent a 12-lead ECG and echocardiogram at a Dutch academic teaching hospital between 2011 and August 2023. Echocardiogram outcomes were extracted from reports, including left ventricular systolic dysfunction (LVSD), left ventricular dilatation (LVD), aortic stenosis (AS), aortic regurgitation (AR), mitral regurgitation (MR), and tricuspid regurgitation (TR), from which a composite outcome label was derived. A cohort of patients newly referred to our cardiology outpatient clinic with a primary complaint of chest pain, dyspnea, palpitations, dizziness, a murmur, or an abnormal ECG was held out as a test set, while the remaining dataset was split patient-wise into training (90%) and validation (10%) sets. A convolutional neural network was trained using only the ECG tracing as input and the composite label as outcome. Results We included 92,210 ECG-echo pairs from 44,785 patients (19,717 female) with 25,543 (27.7%) abnormal ECG-echo pairs. Among 2724 newly referred patients in the test set, 210/1389 males (15.1%) and 201/1335 females (15.1%) were diagnosed with SHD. In the test set, the model for predicting composite outcome demonstrated an area-under-the-curve, negative predictive value, and specificity of 0.74 (95% confidence interval [CI] 0.71-0.79), 0.94 (95% CI 0.92-0.95), and 0.47 (95% CI 0.45-0.49), respectively. Conclusion This study demonstrates the feasibility of employing deep learning models based solely on electrocardiogram (ECG) data to identify patients at very low risk of structural heart disease (SHD). Further validation and prospective studies are warranted to confirm the generalizability and clinical utility of our findings in diverse patient populations and healthcare settings.

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&amp;lt;0.001) in those with no family history of CHD, and 1.66 (95% CI, 1.37-2.00; p&amp;lt;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.

Relationship between lipoprotein(a) and endogenous fibrinolytic status in patients with STEMI

Abstract Background The risk of myocardial infarction is at least doubled in individuals with lipoprotein(a) (Lp[a]) levels &amp;gt;90th percentile.[1] Lp(a) may exert pro-thrombotic effects by impairing fibrinolysis. Lp(a) has a high degree of homology to plasminogen and can competitively inhibit tissue plasminogen activator (tPA)-mediated plasminogen activation and tPA-mediated clot lysis.[2] Furthermore, Lp(a) stimulates the activity of plasminogen activator inhibitor-1, the major inhibitor of the fibrinolytic system. In patients with ST-segment elevation myocardial infarction (STEMI), impaired endogenous fibrinolysis is a strong, independent risk factor for recurrent cardiovascular events,[3] but the drivers of this are not fully understood. Whether impaired endogenous fibrinolysis is related to increased Lp(a) levels in patients with STEMI, is not known. Purpose We aimed to assess the relationship between Lp(a) and endogenous fibrinolysis in patients with STEMI. Methods In a prospective, observational study, venous blood samples were drawn from patients presenting with STEMI immediately before revascularisation, after dual antiplatelet therapy but before heparin administration. Endogenous fibrinolysis was measured immediately in non-anticoagulated whole blood using the point-of-care Global Thrombosis Test, which measures the time for occlusive thrombus formation under high shear (occlusion time) and the time for spontaneous lysis of the thrombus (lysis time).[3] Assessment of Lp(a) levels, measured by particle enhanced immunoturbidimetric assay, was performed with paired plasma samples, standardized against the International Federation of Clinical Chemistry reference material SRM2B for nmol/L. Lp(a) &amp;gt;32 nmol/L is associated with increased risk of ischaemic heart disease. Results A total of 80 patients were included (age 64±14y, 25% females and 86% Caucasian). There was a positive correlation between Lp(a) level and lysis time (r = 0.330, P = 0.003) (Figure 1). Lysis time was significantly longer in patients with Lp(a) &amp;gt;32 nmol/L (2782 [1626-3683] vs. 1725 [1259-2955] s, P = 0.044). Using a cut-point of lysis time ≥2500 s previously associated with a significantly increased cardiovascular risk in patients with STEMI, we showed that Lp(a) was significantly higher in patients with lysis time ≥2500 s (40 (22-111) vs. 18 (7-73) nmol/L, P = 0.045). Table 1 shows the relationship between clinical characteristics and Lp(a) and lysis time. Lp(a) level was higher in non-Caucasian patients. There was no correlation between Lp(a) and occlusion time (r = 0.156, P = 0.168). Conclusion In patients with STEMI, longer endogenous fibrinolysis time is related to higher Lp(a) level. Raised Lp(a) levels may, in part, contribute to impaired endogenous fibrinolysis. Future studies are required to assess whether reduction in Lp(a) with novel therapies currently in phase 3 trials can favourably modulate fibrinolysis and improve clinical outcomes.Figure 1

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.

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

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