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Introduction: The 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. Methods: We 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. Results: After 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. Conclusions: Lifestyle 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.

Introduction: The 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., Methods: We 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., Results: After 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., Conclusions: Lifestyle 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., Competing Interests: Carlos Iribarren received a research grant from GENinCode, Plc, for this study. Meng Lu has no disclosures. Martha Gulati serves on the advisory Board for Esperion, Novartis and Boehringer Ingelheim. Nathan Wong receives research support through his institution from Novartis, Novo Nordisk, and Regeneron and is a consultant for Novartis and Ionis. Roberto Elosua is a member of the scientific advisory board of GENinCode, Plc, and inventor in a patent application based on the CARDIOinCODE-Score® CHD PRS whose applicant is GENinCode, Plc. Jamal S. Rana has no disclosures., (© 2024 The Authors. Published by Elsevier B.V.)

Sleep is an important modulator of cardiovascular function and is recognized to play an important role in the pathogenesis and progression of cardiovascular disease. However, results of the studies investigating the relationship between sleep complaints and cardiovascular outcomes are still controversial. This study aimed to investigate the associations of sleep duration and sleep quality with Framingham 10-year hard coronary heart disease (CHD) risk score in Turkish adults. We included a total of 362 participants (mean age: 48.5 ± 9.0 years, 50.6% males) and measured sleep quality and sleep duration using Pittsburgh Sleep Quality Index (PSQI). Framingham risk scoring system was utilized to calculate the 10-year hard CHD risk of participants. Binary logistic regression analysis was performed to determine the association between sleep quality, sleep duration, and CHD risk. Both short sleep duration (<6 hours) (OR = 3.858, 95% CI: 1.245–11.956) and long sleep duration (≥8 hours) (OR = 2.944, 95% CI: 1.087–7.967) were identified as the predictors of 10-year hard CHD risk. However, sleep quality was not associated with 10-year CHD risk even as a categorical or continuous variable (OR = 0.864, 95% CI: 0.418–1.787 and OR = 0.985, 95% CI: 0.868–1.117, respectively). Our findings highlighted previous studies demonstrating the U-shaped relationship, with both short and long sleep durations to be associated with a higher CHD risk. Evaluation of habitual sleeping patterns may provide additional information in clinical cardiovascular risk assessment. Future research should investigate whether interventions to optimize sleep duration may help to prevent coronary events in large population-based cohorts. [ABSTRACT FROM AUTHOR]

Background Excess adiposity, which affects 69% of US adults, increases coronary heart disease (CHD) risk in an association that manifests below conventional obesity cut points. The population‐level impact on CHD risk that is attainable through modest adiposity reductions in populations is not well characterized. We estimated the effect of hypothetical reductions in both body mass index (BMI) and waist circumference (WC) on CHD incidence. Methods and Results The study population included 13 610 ARIC (Atherosclerosis Risk in Communities) participants. Our hypothetical reduction in BMI or WC was applied relative to the temporal trend, with no hypothetical reduction among those with BMI >24 or WC >88 cm, respectively. This threshold for hypothetical reduction is near the clinical guidelines for excess adiposity. CHD risk differences compared the hypothetical reduction with no reduction. Sensitivity analysis was conducted to estimate the effect of applying the hypothetical BMI reduction at the established overweight cut point of 25. Cumulative 12‐year CHD incidence with no intervention was 6.3% (95% CI, 5.9–6.8%). Risk differences following the hypothetical BMI and WC reductions were −0.6% (95% CI, −1.0% to −0.1%) and −1.0% (95% CI, −1.4% to −0.5%), respectively. These results were robust for the sensitivity analyses. Consequently, we estimated that this hypothetical reduction of 5% in BMI and WC, respectively, could have prevented 9% and 16%, respectively, of the CHD events occurring in this study population over 12 years, after adjustment for established CHD risk factors. Conclusions Meaningful CHD risk reductions could derive from modest reductions in adiposity attainable through lifestyle modification.

Background: Cardiovascular risk is becoming a growing concern in patients receiving psychotropic medications. An increased Framingham risk score (FRS) and 10-year coronary artery disease risk has been reported in patients suffering from mental diseases. Aim: This study aims to evaluate the cardiometabolic risk profile in patients suffering from psychiatric disorders being treated with antipsychotics and antidepressants. Materials and Methods: This cross-sectional study was conducted on 68 patients diagnosed with psychiatric disorders according to International Statistical Classification of Diseases-10 at a tertiary health-care center. Patient's demographic details, family history, level of education, duration of disease, use of alcohol and or nicotine, use of concomitant medications, psychotropic drug history, history of treatment of diabetes, dyslipidemia, hypertension, or any other medical conditions were also recorded. Waist circumference, blood pressure, fasting blood sugar, triglyceride, and high-density lipoprotein values were estimated by taking fasting venous samples under aseptic measures. Metabolic syndrome was diagnosed using the International Diabetes Federation Criteria. Ten-year cardiovascular risk was assessed using the FRS. Statistical evaluation was done using appropriate parametric and nonparametric statistical methods. Results: A total of 49 patients were being treated with antipsychotic drugs and 19 were receiving antidepressants. The mean age of patient receiving antipsychotics were 37.51, and those receiving antidepressant were 34.15. The metabolic syndrome was 36.76% in patients taking antipsychotics as compared to 11.76% in patients on antidepressant. The mean FRS score in antipsychotic group was 7.48, and those receiving antidepressants were 4.7. The 10-year coronary heart disease (CHD) risk score was significantly higher in patients receiving antipsychotics as compared to patients on antidepressants. Conclusion: Treatment with antipsychotics is associated with significantly higher 10-year CHD risk scores as compared to treatment with antidepressants.

In the 1980s debate intensified over whether there was a protective effect of high-density lipoprotein cholesterol (HDL-C) or an adverse effect of triglycerides on coronary heart disease (CHD) risk. In a 1991 paper reprinted in the IJE we suggested that the high degree of correlation between the two, together with plausible levels of measurement error, made it unlikely that conventional epidemiological approaches could contribute to causal understanding. The consensus that HDL-C was protective, popularly reified in the notion of 'good cholesterol', strengthened over subsequent years. Reviewing the biostatistical and epidemiological literature from before and after 1991 we suggest that within the observational epidemiology pantheon only Mendelian randomization studies-that began to appear at the same time as the initial negative randomized controlled trials-made a meaningful contribution. It is sobering to realize that many issues that appear suitable targets for epidemiological investigation are simply refractory to conventional approaches. The discipline should surely revisit this and other high-profile cases of consequential epidemiological failure-such as that with respect to vitamin E supplementation and CHD risk-rather than pass them over in silence. [ABSTRACT FROM AUTHOR]

Background: Data are sparse on the safety and efficacy of commercially available energy-restricted meal plans in obese subjects with type 2 diabetes mellitus (T2DM). This study examined the safety and efficacy of a commercially available low-energy diet in insulin-treated obese men with type 2 diabetes. Methods: Eighteen men ≥ 35 years old who had class III obesity, had received insulin treatment for ≥ 1 year for type 2 diabetes, and had glycated hemoglobin (Hb) ≥ 6.5% were randomized to receive either a low-energy diet (N = 9) or standard medical nutrition intervention (N = 9) for 6 months. Results: Compared with 1.5% (± 3.55) in the control group, the mean percentage weight loss in the intervention group at 6 months was 9.6% (±4.91) (p < 0.01). Complete and partial diabetes remission occurred in one subject each in the intervention group and no subjects in the control group. Mean glycated Hb levels were 8.9% (± 2.76) and 9.1% (± 1.53) (p = NS) at baseline and 6.5% (± 0.64) and 7.4% (± 1.12) (p = 0.0606) at 6 months for the intervention and control groups, respectively. Compared with 0.85 mmol/L at baseline, the mean high-density lipoprotein cholesterol (HDL-C) level in the intervention group at 6 months increased to 0.96 mmol/L (p < 0.01) while it remained unchanged in the control group. Conclusions: Among obese men with insulin-treated type 2 diabetes, compared with standard medical nutrition, 6 months of a low-energy diet resulted in complete diabetes remission in one subject and partial remission in another while improving diabetes control and decreasing the median daily dose of insulin in the remainder. [ABSTRACT FROM AUTHOR]

Background: Use of smokeless tobacco (SLT) products has been linked to multiple adverse effects, especially precancer and cancer of oral cavity. However, the association of SLT use with risk of coronary heart disease (CHD) is shrouded with controversy due to conflicting results in the literature. The present meta-analysis aimed to evaluate the risk of CHD among adult ever-users of SLT products along with sub-group analysis.Methods: The analysis included studies retrieved from a systematic literature search for published articles assessing risk of CHD with SLT use. Two authors independently extracted risk estimates and study characteristics of the included studies. Summary relative risks were estimated using the random-effect model.Results: Twenty studies from four WHO regions were included in the analysis. The summary risk of CHD in SLT users was not significantly positive (1.05, 95% CI = 0.96 to 1.15) although a higher risk of fatal CHD was seen (1.10, 95% CI = 1.00 to 1.20). The risk was significant for users in European Region (1.30, 95% CI = 1.14 to 1.47). The results remained unchanged even after strict adjustment for smoking. Product-wise analysis revealed a significant positive association of fatal CHD with snus/snuff use (1.37, 95% CI = 1.14 to 1.61). The SLT-attributable fraction of fatal CHD was calculated to be 0.3%, highest being for European region (5%).Conclusion: A significant positive association was detected between SLT use and risk of fatal CHD, especially for European users and those consuming snus/snuff. In view of the positive association even after strict adjustment for smoking, these results underscore the need for inclusion of cessation efforts for smokeless tobacco in addition to smoking for control of fatal cardiovascular diseases.Implications: The present meta-analysis demonstrates a global perspective of association between coronary heart disease (CHD) and use of smokeless tobacco (SLT), especially for fatal cardiac events, even with strict adjustment for smoking. There appears to be some difference in this effect based on the type of SLT product used. These results highlight the independent deleterious effect of SLT products on the outcome of CHD and might help to resolve the long-standing controversy regarding the association of SLT with the risk of CHD. Hence, we propose that in addition to smoking, cessation efforts should be directed towards SLT products as well, for control of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

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Background: Cardiovascular risk is becoming a growing concern in patients receiving psychotropic medications. An increased Framingham risk score (FRS) and 10-year coronary artery disease risk has been reported in patients suffering from mental diseases. Aim: This study aims to evaluate the cardiometabolic risk profile in patients suffering from psychiatric disorders being treated with antipsychotics and antidepressants. Materials and Methods: This cross-sectional study was conducted on 68 patients diagnosed with psychiatric disorders according to International Statistical Classification of Diseases-10 at a tertiary health-care center. Patient's demographic details, family history, level of education, duration of disease, use of alcohol and or nicotine, use of concomitant medications, psychotropic drug history, history of treatment of diabetes, dyslipidemia, hypertension, or any other medical conditions were also recorded. Waist circumference, blood pressure, fasting blood sugar, triglyceride, and high-density lipoprotein values were estimated by taking fasting venous samples under aseptic measures. Metabolic syndrome was diagnosed using the International Diabetes Federation Criteria. Ten-year cardiovascular risk was assessed using the FRS. Statistical evaluation was done using appropriate parametric and nonparametric statistical methods. Results: A total of 49 patients were being treated with antipsychotic drugs and 19 were receiving antidepressants. The mean age of patient receiving antipsychotics were 37.51, and those receiving antidepressant were 34.15. The metabolic syndrome was 36.76% in patients taking antipsychotics as compared to 11.76% in patients on antidepressant. The mean FRS score in antipsychotic group was 7.48, and those receiving antidepressants were 4.7. The 10-year coronary heart disease (CHD) risk score was significantly higher in patients receiving antipsychotics as compared to patients on antidepressants. Conclusion: Treatment with antipsychotics is associated with significantly higher 10-year CHD risk scores as compared to treatment with antidepressants. [ABSTRACT FROM AUTHOR]

Background Apolipoprotein B-100 (ApoB) is a well-researched lipoprotein marker used in assessing the risk of coronary heart disease (CHD) development. Despite its continued use at the bedside, ApoB methodologies have not been thoroughly compared and may differentially discriminate CHD risk, resulting in patient misclassification. Objective This study compared 3 ApoB immunoassays and their associations with incident CHD risk over a 12-year follow-up period in the Multi-Ethnic Study of Atherosclerosis. Methods Plasma ApoB concentrations were measured in 4679 participants of Multi-Ethnic Study of Atherosclerosis at baseline, using 3 immunoturbidimetric methods. Roche and Kamiya reagent-based methods were analyzed on a Roche modular P analyzer, and the Diazyme reagent-based method was analyzed on a Siemens Dimension analyzer. Cox proportional analysis estimated ApoB-related risk of incident CHD over a median follow-up period of 12.5 years with adjustments for nonlipid CHD risk factors. ApoB concentrations were examined as continuous variables but were also dichotomized based on clinical designations of borderline (100 mg/dL), high (120 mg/dL), and very high ApoB levels (140 mg/dL). Results Moderate to strong correlations among ApoB methods were observed (r = 0.79–0.98). ApoB concentrations (per standard deviation) were similarly associated with CHD risk and hazard ratio (95% confidence interval): Roche: 1.16 (1.03–1.30); Kamiya: 1.14 (1.02–1.28); and Diazyme: 1.14 (1.02–1.28). Conclusion Although all 3 ApoB were similarly associated with risk of incident CHD over the study period regardless of the reagent type, the bias between methods suggests that these reagents are not fungible, and assay harmonization may be warranted. [ABSTRACT FROM AUTHOR]

BackgroundCirculating microRNAs (miRNAs/miRs) are regulated in patients with coronary artery disease. The impact of transient coronary ischemia on circulating miRNA levels is unknown. We aimed to investigate circulating miRNA kinetics in response to cardiac stress in patients with or without significant coronary stenosis. Methods and ResultsEighty of 105 screened patients with stable coronary artery disease underwent dobutamine stress echocardiography before coronary angiography. Nine circulating vascular miRNAs (miRNA‐21, miRNA‐26, miRNA‐27a, miRNA‐92a, miRNA‐126‐3p, miRNA‐133a, miRNA‐222, miRNA‐223, and miRNA‐199‐5p) were quantified in plasma by reverse transcription polymerase chain reaction before, immediately after, and 4 and 24 hours after dobutamine stress echocardiography. Quantitative polymerase chain reaction revealed increased miRNA‐21, miRNA‐126‐3p, and miRNA‐222 levels at 24 hours after dobutamine stress echocardiography in all patients. On coronary angiography, significant coronary artery stenoses (>80% diameter stenosis) were found in 41 patients. Stratifying patients according to the prevalence of significant stenoses, patients with stenosis showed an increase of circulating miRNA‐21, miRNA‐126‐3p, and miRNA‐222 in response to cardiac stress. In patients without significant stenoses (