Odds Of Coronary Heart Disease Research Articles

Physical activity and odds of coronary heart disease among Lebanese women.

It is known that physical activity (PA) is protective against cardiovascular morbidity and mortality. However, few studies have examined the association between PA, sedentary lifestyle and coronary heart disease (CHD) in women. This case-control study investigates the relationship between PA and sedentary behavior on CHD odds in Lebanese women over forty. One thousand five hundred selected Lebanese women (300 cases and 1200 controls) were included between 2018-2019. Cases were hospitalized women newly diagnosed with CHD, whereas the control groups were free of any heart diseases. Data on socio-demographic, lifestyle, cardiovascular factors, PA and sedentary lifestyle were collected. Multivariate logistic regressions, adjusted for covariates, were performed to investigate the association of PA domains and sedentary behavior with CHD. A sedentary lifestyle combined with low activity levels increased the odds of CHD. Among cases, 46.7% participated in moderate or vigorous PA against almost 60.3% of controls. 36.3% of coronary patients had more than 10h/day of sedentary time, with a positive correlation with CHD (adjusted OR: 1.533, 95%CI: 1.046-2.247). Conversely, moderate and high levels (respectively 600-3000 and ≥ 3000 metabolic equivalents [MET]-minutes/week) of domestic/garden PA revealed lower CHD odds (OR: 0.566, 95%CI: 0.396-0.808 and 0.193, 0.065-0.578 respectively). The detrimental influence of sedentary lifestyle appeared to be significantly reversed by weekly moderate PA, especially as weekly sedentary time was less (OR: 0.616, 95%CI: 0.427-0.888/ 6 to10h of sedentary time and OR: 0.537, 95% CI: 0.37-0.779/ ≤ 6h), and except sedentary time exceeding 10h daily. Two PA patterns revealed lower CHD odds: transport-related and domestic/garden PA, as early as low amount, even after adjustment for possible confounders. The current study highlights the importance of combating sedentary behaviors and engaging in regular, easily accessible PA to reduce the odds of coronary disease among aging women. Therefore, better information regarding the benefits of physical activities such as transportation-related activities or gardening would be helpful in enhancing the prevention of CHD in aging women.

The Relationship Between Allergic Rhinitis, Asthma, and Cardiovascular Disease in the National Health Interview Surveys (NHIS), 1999–2018

BackgroundAtopic disease has been associated with immune dysregulation and chronic inflammation, but current practice guideline recommendations do not include the evaluation of inflammatory outcomes among patients with asthma and allergic rhinitis. ObjectiveThis study investigates the relationship between asthma, allergic rhinitis and cardiovascular disease (CVD) using data from the US National Health Interview Survey (NHIS) between 1999-2018. MethodsWe used data from adults in the NHIS (n = 603,140, representing a population of 225,483,286). Exposures were physician-diagnosed asthma (lifetime/past-year) and allergic rhinitis (past-year). Outcomes were physician-diagnosed heart disease: coronary heart disease (CHD), angina, heart-attack, and non-specific “heart-condition” (all lifetime). We used survey-weighted descriptive analysis and logistic regression adjusting for demographic and socioeconomic factors. Results11.44% reported at least one heart condition, with CHD the most prevalent (4.27%) across 20 years of pooled data. Asthma and rhinitis were associated with higher CVD in all bivariate analyses. Specifically, lifetime asthma was associated with increased odds of CHD, OR=1.36 (1.29, 1.42), with stronger effects observed for a past-year asthma-attack, OR= 1.66 (1.55, 1.80). The strongest effect of all was observed in those with a past-year asthma attack having increased odds of angina, OR=2.42 (2.24, 2.63). Allergic rhinitis was independently associated with increased odds of CHD (OR=1.25, 1.18-1.28). ConclusionsAsthma and allergic rhinitis are risk factors for all types of CVD in this nationally representative study covering a two-decade period in the US. Clinicians should consider screening patients with severe and/or uncontrolled asthma and allergic rhinitis early for CVD, particularly angina and CHD. Future studies are warranted to explore the immunological milieu in these patients and identify therapeutic targets.

Workplace Harassment and Health: A Long Term Follow up.

We examine relationships between workplace harassment (WH) and onset of health conditions over a 23-year period. Participants were surveyed at seven points between 1997-2006 and again in 2020. Regression analyses (n = 921) assessed effects of chronic WH exposure on onset or recent health conditions by 2020. Growth mixture modeling revealed infrequent and chronic classes of generalized workplace harassment (GWH; 33.39% chronic) and sexual harassment (SH; 32.32% chronic). Prevalence of health conditions ranged from 3.71% for myocardial infarction to 43.06% for hypertension. Analysis via propensity score matching showed chronic WH class membership increased odds of coronary heart disease (GWH, odds ratio [OR] = 3.42, P < 0.05), arthritic/rheumatic conditions (SH, OR = 1.56, P < 0.05), and recent migraine (SH, OR = 1.68, P < 0.05). Workplace harassment is associated with coronary heart disease, arthritic/rheumatic conditions, and migraine. Worker health can be protected through strengthening and enforcing organizational and social antiharassment policies and laws.

A linear weighted combination of polygenic scores for a broad range of traits improves prediction of coronary heart disease

Polygenic scores (PGS) for coronary heart disease (CHD) are constructed using GWAS summary statistics for CHD. However, pleiotropy is pervasive in biology and disease-associated variants often share etiologic pathways with multiple traits. Therefore, incorporating GWAS summary statistics of additional traits could improve the performance of PGS for CHD. Using lasso regression models, we developed two multi-PGS for CHD: 1) multiPGSCHD, utilizing GWAS summary statistics for CHD, its risk factors, and other ASCVD as training data and the UK Biobank for tuning, and 2) extendedPGSCHD, using existing PGS for a broader range of traits in the PGS Catalog as training data and the Atherosclerosis Risk in Communities Study (ARIC) cohort for tuning. We evaluated the performance of multiPGSCHD and extendedPGSCHD in the Mayo Clinic Biobank, an independent cohort of 43,578 adults of European ancestry which included 4,479 CHD cases and 39,099 controls. In the Mayo Clinic Biobank, a 1 SD increase in multiPGSCHD and extendedPGSCHD was associated with a 1.66-fold (95% CI: 1.60–1.71) and 1.70-fold (95% CI: 1.64–1.76) increased odds of CHD, respectively, in models that included age, sex, and 10 PCs, whereas an already published PGS for CHD (CHD_PRSCS) increased the odds by 1.50 (95% CI: 1.45–1.56). In the highest deciles of extendedPGSCHD, multiPGSCHD, and CHD_PRSCS, 18.4%, 17.5%, and 16.3% of patients had CHD, respectively.

Associations of polyunsaturated fatty acids with cardiovascular disease and mortality: a study of NHANES database in 2003–2018

BackgroundThis study was to explore the association between dietary polyunsaturated fatty acids (PUFAs) consumption and cardiovascular diseases (CVDs), all-cause mortality, and CVD-specific mortality.MethodsThis retrospective cohort study extracted demographic and clinical data of 38,838 adult participants from the National Health and Nutrition Examination Survey (NHANES) database in 2003–2018. We explored the association between octadecadienoic acid (ODA), octadecatrienoic acid (ALA), octadecatetraenoic acid (ODTA), eicosatetraenoic acid (AA), eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA) and different CVDs using weighted univariate and multivariate logistic regression analyses with odds ratio (OR) and 95% confidence interval (CI). The PUFAs were divided into four levels according to the quartiles (≤ Q1, Q1 to Q2, Q1 to Q2, > Q3). Weighted univariate and multivariate COX regression analyses with hazard ratio (HR) and 95% CI were used for exploring the association between PUFAs and all-cause mortality, CVD-specific mortality and other cause-specific mortality.ResultsDuring the follow-up, a total of 4,908 (9.12%) eligible participants died. The results showed that after adjusting for covariates, ODTA intake was related to low odds of coronary heart disease (CHD) [OR = 0.75, 95%CI: (0.64–0.88)]. Q1-Q2 quartile of ALA [OR = 0.81, 95%CI: (0.66–0.99)] and Q2-Q3 quartile of DPA [OR = 0.78, 95%CI: (0.62–0.99)] intakes were linked to low odds of heart attack, and > Q3 quartile of ODA intake was associated with low odds of congestive heart failure (CHF) [OR = 0.66, 95%CI: (0.49–0.90)] and stroke [OR = 0.65, 95%CI: (0.47–0.90)]. Q2-Q3 quartile of DPA intake was linked to low odds of angina [OR = 0.76, 95%CI: (0.58–0.99)]. Higher ALA intake was associated with a lower risk of all-cause mortality [Q2-Q3: HR = 0.86, 95%CI: (0.74–0.99); > Q3: HR = 0.76, 95%CI: (0.63–0.91)]. Additionally, Q2-Q3 quartile of ALA, Q1-Q2 quartile of AA and DPA intakes were respectively related to a low risk of CVD-specific mortality, while that > Q3 quartile of ALA related to that of mortality by other causes.ConclusionOur study found that PUFAs were associated with different CVDs, and higher ALA intake was related to lower risk of all-cause mortality. Ensuring adequate intake of PUFAs was beneficial to the health and may decrease the risk of mortality.

Prediction of Coronary Heart Disease Events in Blood or Marrow Transplantation Recipients.

The long-term risk of coronary heart disease (CHD) and clinical models that predict this risk remain understudied in blood or marrow transplantation (BMT) recipients. This study sought to examine the risk of CHD after BMT and identify the associated risk factors. Participants included patients transplanted between 1974 and 2014 at City of Hope, University of Minnesota, or University of Alabama at Birmingham and those who survived≥2 years after BMT. Multivariable logistic regression models assessed CHD risk in BMT survivors compared with a sibling cohort. A self-reported questionnaire and medical records provided information regarding sociodemographics, comorbidities, and therapeutic exposures, which were used to develop a CHD risk prediction nomogram. Overall, 6,677 BMT recipients participated; the mean age at BMT was 43.9 ± 17.7 years, 58.3% were male, and 73.3% were non-Hispanic Whites. The median length of follow-up was 6.9 years (range: 2-46.2 years) from BMT. CHD was reported in 249 participants, with a 20-year cumulative incidence of 5.45% ± 0.39%. BMT survivors had a 1.6-fold greater odds of CHD compared with a sibling cohort (95% CI: 1.09-2.40). A nomogram was then developed to predict the risk of CHD at 10 and 20 years after BMT including age at BMT (HR: 1.06/y; 95% CI: 1.04-1.08), male sex (HR: 1.89; 95% CI: 1.15-3.11), a history of smoking (HR: 1.61; 95% CI: 1.01-2.58), diabetes (HR: 2.45; 95% CI: 1.23-4.89), hypertension (HR: 2.02; 95% CI: 1.15-3.54), arrhythmia (HR: 1.90; 95% CI: 0.89-4.06), and pre-BMT chest radiation (yes vs no: HR: 2.83; 95% CI: 1.20-6.67; unknown vs no: HR: 0.88; 95% CI: 0.34-2.28). The C-statistic was 0.77 in the test set (95% CI: 0.70-0.83). This study identified BMT recipients at high risk for CHD, informing targeted screening for early detection and aggressive control of risk factors.

Systemic immune-inflammation index is associated with coronary heart disease: a cross-sectional study of NHANES 2009-2018.

Inflammation has been linked to the development of coronary heart disease (CHD). The systemic immune inflammation index (SII) is a useful biomarker of systemic inflammation. Our study aimed to explore the correlation between SII and CHD. We conducted a multivariate logistic regression analysis, smoothing curve fitting, and segmented model comparison on 15,905 participants with a CHD prevalence of 3.31% and a mean age of 46.97 years. Adjusting for gender, age, and race, we found a negative association between SII and CHD [odds ratio (OR) 0.66; 95% confidence interval (CI) 0.48, 0.90]. There was an inverse trend where increasing SII was associated with decreasing odds of CHD (p for trend = 0.0017). After further adjustment, the association was strengthened, with a similar trend (p for trend = 0.0639). Smoothing curve fitting demonstrated a gender-specific association between SII and CHD. Our findings suggest that higher SII values may be associated with a higher incidence of CHD, which varies by gender. SII may be a cost-effective and convenient method to detect CHD. Further studies are needed to confirm the causality of these findings in a larger prospective cohort.

Triglyceride-rich lipoprotein remnants, low-density lipoproteins, and risk of coronary heart disease: a UK Biobank study.

The strength of the relationship of triglyceride-rich lipoproteins (TRL) with risk of coronary heart disease (CHD) compared with low-density lipoprotein (LDL) is yet to be resolved. Single-nucleotide polymorphisms (SNPs) associated with TRL/remnant cholesterol (TRL/remnant-C) and LDL cholesterol (LDL-C) were identified in the UK Biobank population. In a multivariable Mendelian randomization analysis, TRL/remnant-C was strongly and independently associated with CHD in a model adjusted for apolipoprotein B (apoB). Likewise, in a multivariable model, TRL/remnant-C and LDL-C also exhibited independent associations with CHD with odds ratios per 1 mmol/L higher cholesterol of 2.59 [95% confidence interval (CI): 1.99-3.36] and 1.37 [95% CI: 1.27-1.48], respectively. To examine the per-particle atherogenicity of TRL/remnants and LDL, SNPs were categorized into two clusters with differing effects on TRL/remnant-C and LDL-C. Cluster 1 contained SNPs in genes related to receptor-mediated lipoprotein removal that affected LDL-C more than TRL/remnant-C, whereas cluster 2 contained SNPs in genes related to lipolysis that had a much greater effect on TRL/remnant-C. The CHD odds ratio per standard deviation (Sd) higher apoB for cluster 2 (with the higher TRL/remnant to LDL ratio) was 1.76 (95% CI: 1.58-1.96), which was significantly greater than the CHD odds ratio per Sd higher apoB in cluster 1 [1.33 (95% CI: 1.26-1.40)]. A concordant result was obtained by using polygenic scores for each cluster to relate apoB to CHD risk. Distinct SNP clusters appear to impact differentially on remnant particles and LDL. Our findings are consistent with TRL/remnants having a substantially greater atherogenicity per particle than LDL.

Chronic disease outcomes among South Asian cancer survivors.

e24098 Background: Although racial and ethnic disparities in cancer survivorship are widely known, the understanding of cancer survivorship among South Asian patients is limited, especially in the United States. Previous studies identified significant health-related disparities within the wider Asian diaspora, however, less is known among Asian subgroups. Thus, we conducted a study examining the differences in chronic disease outcomes between South Asian cancer survivors compared to other races/ethnicities. Methods: We used a name list algorithm to identify South Asian patients among cancer survivors treated at Northwestern Medicine between 2005-2020. After patients were identified, we conducted chi-square tests and logistic regression (adjusting for age and gender) to evaluate variation in prevalence of chronic diseases including diabetes mellitus, hypertension, coronary heart disease, and more. Racial and ethnic comparisons were done using the self-reported race fields within the Northwestern Medicine database. Results: The algorithm identified 1,217/102,579 (1.2%) South Asian patients. We found that 49% self-identified as Asian, 18% as White or Caucasian, 17% as Other, and 9.7% as ‘Declined or Unable to Answer’. The self-reported racial comparison groups used were Asian (not South Asian) (n = 2,631, 2.6%), Black (n = 9,350, 9.4%), and White (n = 75,252, 75%). We found that South Asian patients had a higher frequency of leukemia, lymphoma, kidney, and multiple myeloma cancers and a lower frequency of lung, colorectal, liver, cervical, and thyroid cancers compared to Asian (not South Asian) patients (p &lt; .05). We also found the average baseline BMI is greater in South Asians (mean = 26.2, SD = 4.7) compared with Asians (mean = 24.7, SD = 4.4) (p &lt; .05). From the logistic regression models, South Asian cancer survivors had higher odds of diabetes compared with White cancer survivors (OR 1.93 [95% CI 1.50-2.49]). In contrast, the odds of coronary heart disease, hypertension, and heart failure were lower among South Asian compared to Black cancer survivors (0.69 [95% CI 0.53-0.92]; 0.57 [95% CI 0.48-0.68]; 0.49 [95% CI 0.37-0.65], respectively). The odds of atrial fibrillation were lower among South Asian compared to Asian (not South Asian), White, and Black patients (0.59 [95% CI 0.41-0.86]; 0.46 [95% CI 0.34-0.64], 0.58 [95% CI 0.42-0.80], respectively). We did not identify statistically significant associations for these chronic diseases with the other racial groups. Conclusions: These results show there are differences for cancer survivors who were identified as South Asian compared with other groups, even other Asian patients. Analysis of racial and ethnic differences in chronic disease risk among cancer survivors is necessary for understanding the full scope of cancer survivorship. Further understanding the health disparities that exists among the Asian subgroups is important to advancing cancer care for patients from every demographic.

Familial Hypercholesterolemia in the Electronic Medical Records and Genomics Network: Prevalence, Penetrance, Cardiovascular Risk, and Outcomes After Return of Results.

The implications of secondary findings detected in large-scale sequencing projects remain uncertain. We assessed prevalence and penetrance of pathogenic familial hypercholesterolemia (FH) variants, their association with coronary heart disease (CHD), and 1-year outcomes following return of results in phase III of the electronic medical records and genomics network. Adult participants (n=18 544) at 7 sites were enrolled in a prospective cohort study to assess the clinical impact of returning results from targeted sequencing of 68 actionable genes, including LDLR, APOB, and PCSK9. FH variant prevalence and penetrance (defined as low-density lipoprotein cholesterol >155 mg/dL) were estimated after excluding participants enrolled on the basis of hypercholesterolemia. Multivariable logistic regression was used to estimate the odds of CHD compared to age- and sex-matched controls without FH-associated variants. Process (eg, referral to a specialist or ordering new tests), intermediate (eg, new diagnosis of FH), and clinical (eg, treatment modification) outcomes within 1 year after return of results were ascertained by electronic health record review. The prevalence of FH-associated pathogenic variants was 1 in 188 (69 of 13,019 unselected participants). Penetrance was 87.5%. The presence of an FH variant was associated with CHD (odds ratio, 3.02 [2.00-4.53]) and premature CHD (odds ratio, 3.68 [2.34-5.78]). At least 1 outcome occurred in 92% of participants; 44% received a new diagnosis of FH and 26% had treatment modified following return of results. In a multisite cohort of electronic health record-linked biobanks, monogenic FH was prevalent, penetrant, and associated with presence of CHD. Nearly half of participants with an FH-associated variant received a new diagnosis of FH and a quarter had treatment modified after return of results. These results highlight the potential utility of sequencing electronic health record-linked biobanks to detect FH.

Abstract 10360: Polygenic Risk Score, Rare Monogenic Variants, and Family History Have Independent and Additive Effects on the Risk of Coronary Heart Disease

Introduction. We assessed the effects of a polygenic risk score (PRS), monogenic variants (Mono + ), and family history (FamHx) on the risk of coronary heart disease (CHD) and whether incorporating a PRS into the Pooled Cohort Equations (PCE) improves risk prediction. Method. In 199,997 UK Biobank participants, we calculated a PRS CHD (metaGRS, based on ~1.6 million single nucleotide variants), identified individuals with monogenic etiology (presence of a pathogenic variant in LDLR , APOB , or PCSK9 ), and ascertained family history of CHD (CHD in a first-degree relative). Odds of CHD (myocardial infarction/ coronary revascularization/ cardiovascular death) associated with PRS CHD , Mono + , and FamHx at age 55 were computed using logistic regression analyses adjusted for age, sex, and first 4 principal components of ancestry. We combined PRS CHD and PCE into an integrated score (IS) and assessed net reclassification using an actionable risk threshold of 7.5%. Results. The odds ratio (OR) for CHD in the top 5 th percentile of PRS CHD (PRS P95 ), Mono + , and FamHx were 3.37 (2.98 - 3.81), 2.68 (1.67 - 4.07), and 1.61 (1.47 - 1.76), respectively (all p&lt;0.001). These effects were independent and similar in different subgroups. ( Figure 1-A ) Compared to PRS Q2-4 Mono - (3 middle quintiles of PRS CHD and no monogenic variants), the OR for CHD ranged from 1.73 (0.28 - 5.48, p = 0.446) in PRS Q1 Mono + to 5.10 (2.14 - 10.24, p &lt;0.001) in PRS Q5 Mono + . A similar pattern was seen for other combinations, indicating additive effects ( Figure 1-B ). Incorporating PRS CHD into PCE resulted in a net reclassification improvement of 4.56%. Compared to those with high PCE and low IS, the hazard ratio for CHD in those with low PCE and high IS was 1.48 (1.34 - 1.64, p &lt;0.001). Conclusion. The CHD risk associated with PRS CHD , monogenic variants, and family history is independent and additive. Combining PRS CHD and PCE improved risk prediction, that could improve further by adding monogenic variants and family history.

Level of education is associated with coronary heart disease and chronic kidney disease in individuals with type 2 diabetes: a population-based study

IntroductionTo study the relationship between education level and vascular complications in individuals with type 2 diabetes in Norway.Research design and methodsMultiregional population-based cross-sectional study of individuals with type 2 diabetes...

Serum Orotidine: A Novel Biomarker of Increased CVD Risk in Type 2 Diabetes Discovered Through Metabolomics Studies.

To identify novel biomarkers of cardiovascular disease (CVD) risk in type 2 diabetes (T2D) via a hypothesis-free global metabolomics study, while taking into account renal function, an important confounder often overlooked in previous metabolomics studies of CVD. We conducted a global serum metabolomics analysis using the Metabolon platform in a discovery set from the Joslin Kidney Study having a nested case-control design comprising 409 individuals with T2D. Logistic regression was applied to evaluate the association between incident CVD events and each of the 671 metabolites detected by the Metabolon platform, before and after adjustment for renal function and other CVD risk factors. Significant metabolites were followed up with absolute quantification assays in a validation set from the Joslin Heart Study including 599 individuals with T2D with and without clinical evidence of significant coronary heart disease (CHD). In the discovery set, serum orotidine and 2-piperidinone were significantly associated with increased odds of incident CVD after adjustment for glomerular filtration rate (GFR) (odds ratio [OR] per SD increment 1.94 [95% CI 1.39-2.72], P = 0.0001, and 1.62 [1.26-2.08], P = 0.0001, respectively). Orotidine was also associated with increased odds of CHD in the validation set (OR 1.39 [1.11-1.75]), while 2-piperidinone did not replicate. Furthermore, orotidine, being inversely associated with GFR, mediated 60% of the effects of declining renal function on CVD risk. Addition of orotidine to established clinical predictors improved (P < 0.05) C statistics and discrimination indices for CVD risk (ΔAUC 0.053, rIDI 0.48, NRI 0.42) compared with the clinical predictors alone. Through a robust metabolomics approach, with independent validation, we have discovered serum orotidine as a novel biomarker of increased odds of CVD in T2D, independent of renal function. Additionally, orotidine may be a biological mediator of the increased CVD risk associated with poor kidney function and may help improve CVD risk prediction in T2D.

Association Between Gestational Diabetes Mellitus and the Risks of Type-Specific Cardiovascular Diseases

ObjectiveGestational diabetes mellitus (GDM) has been linked to subsequent overall cardiovascular diseases. However, evidence on the associations of GDM with type-specific cardiovascular diseases is lacking, and findings on the potential impact of type 2 diabetes on the associations are not consistent. This study aimed to explore the associations between GDM and the risks of type-specific cardiovascular diseases.MethodsData were from 12,025 women (≥20 years) who had delivered at least one live birth in the National Health and Nutrition Examination Survey, 2007–2018. GDM history and type-specific cardiovascular diseases including coronary heart disease (CHD), heart failure and stroke were defined by self-report. We also combined our results with those from previously related publications on the associations between GDM and risks of type-specific cardiovascular diseases with a random-effect model.ResultsCompared with women without GDM, the multivariable-adjusted odds ratios (95% confidence intervals) were 1.82 (1.21–2.72) for CHD, 1.43 (0.80–2.53) for heart failure, and 1.19 (0.76–1.86) for stroke among women with a history of GDM. Type 2 diabetes was associated with 43.90, 67.44, and 63.16% of the excess odds of CHD, heart failure and stroke associated with GDM, respectively. Combining results from this study with those from previously related studies yielded odds ratios (95% confidence intervals) of 1.81 (1.60–2.05) for CHD (12 studies, 7,615,322 participants, I2= 72.6%), 1.66 (1.25–2.21) for heart failure (5 studies, 4,491,665 participants, I2= 88.6%), and 1.25 (1.07–1.46) for cerebrovascular disease (9 studies, 6,090,848 participants, I2= 77.8%).ConclusionsGDM showed stronger associations with coronary heart diseases and heart failure than cerebrovascular disease, and the excess risks are attributable, in part, to type 2 diabetes.

Taller height and risk of coronary heart disease and cancer: A within-sibship Mendelian randomization study.

Taller people have a lower risk of coronary heart disease but a higher risk of many cancers. Mendelian randomization (MR) studies in unrelated individuals (population MR) have suggested that these relationships are potentially causal. However, population MR studies are sensitive to demography (population stratification, assortative mating) and familial (indirect genetic) effects. In this study, we performed within-sibship MR analyses using 78,988 siblings, a design robust against demography and indirect genetic effects of parents. For comparison, we also applied population MR and estimated associations with measured height. Within-sibship MR estimated that 1 SD taller height lowers the odds of coronary heart disease by 14% (95% CI: 3-23%) but increases the odds of cancer by 18% (95% CI: 3-34%), highly consistent with population MR and height-disease association estimates. There was some evidence that taller height reduces systolic blood pressure and low-density lipoprotein cholesterol, which may mediate some of the protective effects of taller height on coronary heart disease risk. For the first time, we have demonstrated that the purported effects of height on adulthood disease risk are unlikely to be explained by demographic or familial factors, and so likely reflect an individual-level causal effect. Disentangling the mechanisms via which height affects disease risk may improve the understanding of the etiologies of atherosclerosis and carcinogenesis. This project was conducted by researchers at the MRC Integrative Epidemiology Unit (MC_UU_00011/1) and also supported by a Norwegian Research Council Grant number 295989.

Antioxidant potential of diet – Association between dietary antioxidant index and odds of coronary heart disease: A case-control study

BACKGROUND: Oxidative stress and chronic inflammation are among the leading causes of coronary heart disease (CHD). Studies investigated the relationship between dietary antioxidants and the risk/odds of CHD, and contradictory results have been reported. Dietary antioxidant index (DAI) is a novel and reliable nutritional tool that examines the diet’s overall antioxidant capacity. Its validity was examined using serum total antioxidant capacity and malondialdehyde. OBJECTIVE: This study aimed to investigate the relationship between DAI score and odds of CHD. METHODS: In this incidence case-control study, 320 individuals with a definitive diagnosis of CHD and 320 participants without CHD or related risk factors attending the same hospitals/polyclinics were selected as the case and control groups. We estimated the DAI by summing up six standardized intakes of major dietary antioxidants, including manganese, vitamin E, A, C, selenium, and zinc. RESULTS: Modeling DAI categorized according to the median (–0.38), in multi-adjusted model showed a significant protective association with the odd of CHD (OR = 0.72; 95%CI:0.51–0.99, p-value = 0.05). Also, modeling DAI as a continuous variable in multi-adjusted models (OR = 0.94;95%CI:0.90–0.95; p-value = 0.01) showed significant results. CONCLUSION: Using the DAI to investigate the relationship between dietary antioxidants and CHD can show more realistic results than a single study of antioxidants.

Abstract EP59: Duration Of Cannabis Exposure Is Associated With Coronary Heart Disease

Background: Cannabis is the most widely used illicit substance in the U.S. Observational studies have shown an increased risk of coronary heart disease (CHD). However, little evidence is available describing how duration of cumulative exposure influences CHD risk. We hypothesized that longer cumulative cannabis exposure is associated with CHD. Methods: This study included 12,493 participants (age 38.8 ± 11.6 years, 50.3% male, 37.9% White) from the National Health and Nutrition Examination Survey years 2011-2018. Cannabis use was self-reported. CHD was defined as history of physician-diagnosis of myocardial infarction, angina, or coronary artery disease. Duration of exposure was defined as time since first-reported cannabis use. Multivariable logistic regression was used to examine the association between duration of exposure and CHD. Subgroup analyses were performed based on various demographic and comorbid stratifications. Results: About 14.2% (n=1779) of participants were current cannabis users, and 2.3% (n=287) had CHD. In multivariable models, current users with &lt;10 years of cumulative exposure did not have increased odds of CHD compared to never users (p=0.55). However, those with ≥10 years of cumulative exposure had nearly three-fold increased odds of CHD (p&lt;0.001). A similar pattern of results was obtained when 20 years was used as a cut-point for duration of exposure (Table). This association was stronger among those with hypertension versus those without (interaction p-value=0.003), those with diabetes versus those without (interaction p-value&lt;0.001), and those of non-white race versus those of white race (interaction p-value=0.006). Conclusions: Longer duration of cannabis exposure was associated with increased odds of CHD, and the association was stronger among those with hypertension, diabetes, and non-white race. These findings underscore the importance of understanding the long-term consequences of cannabis exposure and the need for a personalized risk assessment for certain groups

Physical activity and odds of coronary heart disease among Lebanese women.

Background and Aims: Physical activity (PA) is an independent and a protective risk factor (RF) against cardiovascular morbidity and mortality. Few studies have examined the association between PA and coronary heart disease (CHD) in women. This study investigates the relationship between reported PA and CHD among Lebanese women aged 40 years and above.

Chromosome Xq23 is associated with lower atherogenic lipid concentrations and favorable cardiometabolic indices

Autosomal genetic analyses of blood lipids have yielded key insights for coronary heart disease (CHD). However, X chromosome genetic variation is understudied for blood lipids in large sample sizes. We now analyze genetic and blood lipid data in a high-coverage whole X chromosome sequencing study of 65,322 multi-ancestry participants and perform replication among 456,893 European participants. Common alleles on chromosome Xq23 are strongly associated with reduced total cholesterol, LDL cholesterol, and triglycerides (min P = 8.5 × 10−72), with similar effects for males and females. Chromosome Xq23 lipid-lowering alleles are associated with reduced odds for CHD among 42,545 cases and 591,247 controls (P = 1.7 × 10−4), and reduced odds for diabetes mellitus type 2 among 54,095 cases and 573,885 controls (P = 1.4 × 10−5). Although we observe an association with increased BMI, waist-to-hip ratio adjusted for BMI is reduced, bioimpedance analyses indicate increased gluteofemoral fat, and abdominal MRI analyses indicate reduced visceral adiposity. Co-localization analyses strongly correlate increased CHRDL1 gene expression, particularly in adipose tissue, with reduced concentrations of blood lipids.

Microvascular and macrovascular complications in type 2 diabetes in a multi-ethnic population based in Amsterdam. The HELIUS study

ObjectiveTo assess ethnic differences in diabetes-related microvascular and macrovascular complication rates in a multi-ethnic population in the Netherlands. Study, design and settingData from the HELIUS study comprising of 165 Dutch, 591 South-Asian Surinamese, 494 African Surinamese, 272 Ghanaian, 368 Turkish, and 444 Moroccan participants with diabetes were analyzed. Logistic regression was used to assess ethnic differences in microvascular (nephropathy) and macrovascular (coronary heart disease (CHD), peripheral artery disease (PAD) and stroke) complications, with adjustments for age, sex, education, and the conventional risk factors. ResultsIn an age-sex adjusted model, ethnic minorities had higher odds of nephropathy than Dutch except for Ghanaians and African Surinamese. The difference remained statistically significant in South-Asian Surinamese (odds ratio: 2.29; 95% CI, 1.09–4.80), but not in the Turkish (1.01; 0.43–2.38) and Moroccan (1.56; 0.68–3.53) participants. The odds of CHD was higher in all ethnic minorities than in Dutch, with the odds ratios ranging from 2.73 (1.09–6.84) in Ghanaians to 6.65 (2.77–15.90) in Turkish in the fully-adjusted model. There were no ethnic differences in the odds of PAD and stroke. ConclusionsThe findings suggest ethnic inequalities in macrovascular and microvascular complications in diabetes, with nephropathy and CHD being the most common complications affecting ethnic minorities.