Odds Ratio For Coronary Heart Disease Research Articles

Questionable Effects of Electronic Cigarette Use on Cardiovascular Diseases From the National Health Interview Survey (NHIS, 2014-2021).

Electronic cigarettes (e-cigarettes) and cardiovascular health risks have gained attention among tobacco researchers. While the cardiovascular risks from e-cigarettes are still unclear, a recent paper by Alzahrani in Cureus claimed that current usage of e-cigarettes increases the risks of cardiovascular diseases, such as myocardial infarction and stroke, in subjects who were never cigarette smokers. The National Health Interview Survey (NHIS) data from 2014 to 2021 and logistic regression models were used to replicate and extend Alzahrani's analysis. Only 12 never smokers who were current e-cigarette users had a myocardial infarction in all eight years. The crude odds ratio (OR) for e-cigarette use was 0.42 (95%CI: 0.24, 0.75). After adjusting for age and other confounding factors and health conditions, the OR of e-cigarette use increased to 2.48 (95%CI: 1.35, 4.55). The omission of age while adjusting for all other risk factors resulted in an OR of 0.80 (95%CI: 0.45, 1.43). In addition, the adjusted ORs for coronary heart disease and stroke were 1.12 (95%CI: 0.58, 2.17) and 1.13 (95%CI: 0.55, 2.29), respectively. The findings indicate that Alzahrani's study is scientifically unreliable. The association between e-cigarette use and heart attack reported by Alzahrani was substantially driven by age, and the very small number of exposed cases makes the association very unstable. Given the nature of cross-sectional NHIS data, it is impossible to establish a robust association or causal claim that e-cigarette use "increases" the risks of any disease.

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.

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<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 <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 <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.

Prevalence of cardiovascular disease risk factors in Chinese patients with type 2 diabetes mellitus, 2013–2018

Objective Coronary heart disease (CHD) is the most common cause of death in patients with type 2 diabetes (T2DM). We aim to estimate the prevalence of CHD and cardiovascular risk factors in Chinese patients with T2DM. Methods A total of 66,536 inpatients with diabetes treated from 2013 to 2018 were investigated, and demographic and clinical data were collected from 30,693 patients with T2DM. Age-standardized prevalence of CHD was calculated on the basis of data from the Chinese population census in 2010. Logistic regression analysis was used to analyze the risk factors. Results The crude prevalence of CHD was estimated to be 23.5% and a standardized prevalence was 13.9% (16.0% in men and 11.9% in women). More than half of patients with CHD have four or more of the five traditional risk factors, much higher than the 38.96% of patients without CHD (p < .01). Multivariate regression analysis showed that diabetes duration, hypertension, smoking, underweight, overweight, obesity and hypoglycaemia were significantly associated with increased risk of CHD (all p < .05). The odds ratio of CHD in patients with three, four or five defined CHD risk factors (i.e. diabetes, hypertension, dyslipidaemia, overweight or obese, and smoking) were 2.35 (95% CI 1.81–3.04), 2.96 (95% CI 2.28–3.85) or 5.29 (95% CI 4.04–6.93), compared with diabetes patients without any other risk factors. Conclusions The prevalence of CHD was rather high in Chinese T2DM inpatients, and the aggregation of CHD risk factors was severe. Thus, hierarchical CHD prevention strategies based on risk factors are necessary.

Association of cardiovascular disease with 30-day hospital readmission in Chinese patients receiving maintenance dialysis.

BackgroundPrevious studies have shown cardiovascular disease (CVD) to be a risk factor in the prediction of 30-day hospital readmission among patients receiving dialysis. However, studies of Asian populations are limited. In the present study, we examined the association between CVD and 30-day hospital readmission in Chinese patients receiving maintenance dialysis.MethodsPatients receiving maintenance dialysis were identified by searching a national claims database, the China Health Insurance Research Association (CHIRA) database, using the International Classification of Diseases revision 10 (ICD-10) and items of medical service claims. Patients aged ≥18 years who were discharged after index hospitalization between January 2015 and December 2015 were included in our retrospective analysis. CVD-related diagnoses were divided into three categories: coronary heart disease (CHD), heart failure (HF), and stroke. Thirty-day hospital readmission was defined as any hospital readmission within the 30 days following discharge. Logistic regression models adjusted for logit of propensity scores (PS) were used to assess the association of CVD with 30-day hospital readmission.ResultsOf 4,700 patients receiving dialysis, the 30-day hospital readmission rate was 10.4%. Compared with patients without CVD, there was an increased risk of 30-day hospital readmission among maintenance dialysis patients with total CVD [odds ratio (OR): 1.33, 95% confidence interval (CI): 1.06–1.66]. Patients with HF (OR: 1.77, CI: 1.27–2.47) and stroke (OR: 2.14, 95% CI: 1.53–2.98) had a greater risk of 30-day hospital readmission. The fully adjusted OR of CHD for the risk of 30-day hospital readmission was 1.22 (95% CI: 0.97–1.55).ConclusionsCVDs, especially stroke and HF, are independent predictors of 30-day hospital readmission in Chinese patients receiving dialysis, and could help to guide interventions to improve the quality of care for these patients.

Levels of Prebeta-1 High-Density Lipoprotein Are a Strong Independent Positive Risk Factor for Coronary Heart Disease and Myocardial Infarction: A Meta-Analysis.

BackgroundWe previously showed that levels of prebeta‐1 high‐density lipoprotein (HDL), the principal acceptor of cholesterol effluxed from cells, including artery wall macrophages, are positively associated with coronary heart disease (CHD) and myocardial infarction (MI) risk.Methods and ResultsIn a multiethnic follow‐up cohort of 1249 individuals from University of California–San Francisco clinics, we determined the degree to which prebeta‐1 HDL levels, both absolute and percentage of apolipoprotein AI, are associated with CHD and history of MI. Independent, strong, positive associations were found. Meta‐analysis revealed for the absolute prebeta‐1 HDL for the top tertile versus the lowest, unadjusted odds ratios of 1.90 (95% CI, 1.40–2.58) for CHD and 1.79 (95% CI, 1.35–2.36) for MI. For CHD, adjusting for established risk factors, the top versus bottom tertiles, quintiles, and deciles yielded sizable odds ratios of 2.37 (95% CI, 1.74–3.25, P<0.001), 3.20 (95% CI, 2.07–4.94, P<0.001), and 4.00 (95% CI, 2.11–7.58, P<0.001), respectively. Men and women were analyzed separately in a combined data set of 2507 individuals. The odds ratios for CHD and MI risk were similar. Higher levels of prebeta‐1 HDL were associated with all 5 metabolic syndrome features. Addition of prebeta‐1 HDL to these 5 features resulted in significant improvements in risk‐prediction models.ConclusionsAnalysis of 2507 subjects showed conclusively that levels of prebeta‐1 HDL are strongly associated with a history of CHD or MI, independently of traditional risk factors. Addition of prebeta‐1 HDL can significantly improve clinical assessment of risk of CHD and MI.

Evaluating the relationship between alcohol consumption, tobacco use, and cardiovascular disease: A multivariable Mendelian randomization study.

BackgroundAlcohol consumption and smoking, 2 major risk factors for cardiovascular disease (CVD), often occur together. The objective of this study is to use a wide range of CVD risk factors and outcomes to evaluate potential total and direct causal roles of alcohol and tobacco use on CVD risk factors and events.Methods and findingsUsing large publicly available genome-wide association studies (GWASs) (results from more than 1.2 million combined study participants) of predominantly European ancestry, we conducted 2-sample single-variable Mendelian randomization (SVMR) and multivariable Mendelian randomization (MVMR) to simultaneously assess the independent impact of alcohol consumption and smoking on a wide range of CVD risk factors and outcomes. Multiple sensitivity analyses, including complementary Mendelian randomization (MR) methods, and secondary alcohol consumption and smoking datasets were used. SVMR showed genetic predisposition for alcohol consumption to be associated with CVD risk factors, including high-density lipoprotein cholesterol (HDL-C) (beta 0.40, 95% confidence interval (CI), 0.04–0.47, P value = 1.72 × 10−28), triglycerides (TRG) (beta −0.23, 95% CI, −0.30, −0.15, P value = 4.69 × 10−10), automated systolic blood pressure (BP) measurement (beta 0.11, 95% CI, 0.03–0.18, P value = 4.72 × 10−3), and automated diastolic BP measurement (beta 0.09, 95% CI, 0.03–0.16, P value = 5.24 × 10−3). Conversely, genetically predicted smoking was associated with increased TRG (beta 0.097, 95% CI, 0.014–0.027, P value = 6.59 × 10−12). Alcohol consumption was also associated with increased myocardial infarction (MI) and coronary heart disease (CHD) risks (MI odds ratio (OR) = 1.24, 95% CI, 1.03–1.50, P value = 0.02; CHD OR = 1.21, 95% CI, 1.01–1.45, P value = 0.04); however, its impact was attenuated in MVMR adjusting for smoking. Conversely, alcohol maintained an association with coronary atherosclerosis (OR 1.02, 95% CI, 1.01–1.03, P value = 5.56 × 10−4). In comparison, after adjusting for alcohol consumption, smoking retained its association with several CVD outcomes including MI (OR = 1.84, 95% CI, 1.43, 2.37, P value = 2.0 × 10−6), CHD (OR = 1.64, 95% CI, 1.28–2.09, P value = 8.07 × 10−5), heart failure (HF) (OR = 1.61, 95% CI, 1.32–1.95, P value = 1.9 × 10−6), and large artery atherosclerosis (OR = 2.4, 95% CI, 1.41–4.07, P value = 0.003). Notably, using the FinnGen cohort data, we were able to replicate the association between smoking and several CVD outcomes including MI (OR = 1.77, 95% CI, 1.10–2.84, P value = 0.02), HF (OR = 1.67, 95% CI, 1.14–2.46, P value = 0.008), and peripheral artery disease (PAD) (OR = 2.35, 95% CI, 1.38–4.01, P value = 0.002). The main limitations of this study include possible bias from unmeasured confounders, inability of summary-level MR to investigate a potentially nonlinear relationship between alcohol consumption and CVD risk, and the generalizability of the UK Biobank (UKB) to other populations.ConclusionsEvaluating the widest range of CVD risk factors and outcomes of any alcohol consumption or smoking MR study to date, we failed to find a cardioprotective impact of genetically predicted alcohol consumption on CVD outcomes. However, alcohol was associated with and increased HDL-C, decreased TRG, and increased BP, which may indicate pathways through impact CVD risk, warranting further study. We found smoking to be a risk factor for many CVDs even after adjusting for alcohol. While future studies incorporating alcohol consumption patterns are necessary, our data suggest causal inference between alcohol, smoking, and CVD risk, further supporting that lifestyle modifications might be able to reduce overall CVD risk.

Overall dietary variety and adherence to the Mediterranean diet show additive protective effects against coronary heart disease

Background and aimAlong with the increasing evidence of the cardioprotective effects of the Mediterranean Diet (MD), the scientific interest and advocacy of dietary variety as a potentially healthy eating habit gradually faded, until its complete oblivion in the latest European cardiovascular prevention guidelines. Our study aims to investigate whether dietary variety adds to the “Mediterranean-ness” of the diet in protecting against coronary heart disease (CHD). Methods and resultsIn this case–control Italian study, data on eating habits were collected from 178 patients with CHD and 155 healthy controls, primarily males, frequency matched for age and gender, using the Food Frequency Questionnaire (FFQ) of the European Prospective Investigation into Cancer and Nutrition. Adherence to MD was estimated from FFQ by the Mediterranean Diet Score (MDS), an index developed by Trichopoulou (2003) ranging from 0 to 9, with higher scores indicating a stricter adherence. Overall dietary variety was computed from FFQ as a count of single food items consumed at least once a month. Associations between MDS or overall dietary variety and coronary status were evaluated by logistic regression models adjusted for BMI, physical activity, smoking, education, and caloric intake; the Odds Ratio (OR) for CHD for each 1.5-point increase in MDS was 0.76 [IC 95% 0.59; 0.98], whereas the OR for CHD for each 15-item increase in dietary variety was 0.62 [IC 95% 0.46; 0.84]. Remarkably, adherence to MD and overall dietary variety were independently associated with a significantly reduced chance of CHD. ConclusionDietary Mediterranean-ness and overall dietary variety exhibit additive cardioprotective effects.

Associations between high levels of hostility and coronary heart disease in an open urban population among 25-64-year-old men

To establish the associations of the prevalence of coronary heart disease (CHD) with high levels of hostility in the open population of 25-64-year-old men in an average urbanized Siberian town. A cross-sectional epidemiological survey was conducted in a representative sample of the electorate of a Tyumen administrative district among 1000 males, with 250 being in each of 4 life decades (25-34, 35-44, 45-54, and 55-64 years). There were 850 (85%) responses. Different forms of CHD were identified by standard methods (the WHO exertional angina questionnaire, resting EEG, and Minnesota coding) used in epidemiological surveys. Definite CHD (DCHD) and possible CHD were identified. A continuous survey method was used by self-filling out the WHO MONICA-psychosocial questionnaire to estimate the levels of hostility. In an average urbanized Siberian town, the prevalence of high levels of hostility among 25-64-year-old men was 46.4% (age-adjusted rate). The high levels of hostility increased with age, peaking in the 55-64-year-old group. In the Tyumen male population aged 25-64-year-old, the odds ratio (OR) for coronary heart disease and high levels of hostility was 2.71; 95% confidence interval (CI), 1.63-4.52 (p<0.05); that for DCHD was almost twice higher (OR, 4.65; 95% CI, 2.14-10.12 (p<0.05). In the older men aged 55-64 years, OR for coronary heart disease and high levels of hostility was 5.42; 95% CI, 2.32-12.66 (p<0.05); that for DCHD was 25.85; 95% CI, 3.30-202.60 (p<0.05). Consequently, the epidemiological criteria for psychosocial risk factors, including hostility, which are detected by the standardized survey methods, should be used in prophylactic examinations of a male population and in the selection of able-bodied people with cardiovascular disease to be comprehensively examined and followed up.

Abstract 9793: Pcsk9 Loss-of-function Variants, Low-density Lipoprotein Cholesterol, and Risk of Coronary Heart Disease and Stroke: Data From the REGARDS Study and CHARGE Consortium

Introduction: PCSK9 loss-of-function variants are associated with reduced low-density lipoprotein cholesterol (LDL-C) concentrations. Genetic association studies of PCSK9 loss-of-function variants allow for the examination of the effects of lifetime low LDL-C on cardiovascular outcomes. Hypothesis: PCSK9 loss-of-function variants are associated with lower concentrations of LDL-C and reduced risk of coronary heart disease (CHD) and stroke. Methods: We studied the association of PCSK9 loss-of-function Y142X and C679X nonsense variants (n=366; 2.1%) in 17,459 African Americans (AAs) and R46L missense variants (n=962; 3.1%) in 31,469 whites with LDL-C, CHD and stroke in the US-based REasons for Geographic And Racial Difference in Stroke (REGARDS) study and 8 cohorts in the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. We combined multivariable adjusted differences in LDL-C between participants with and without PCSK9 variants across studies using inverse-variance weighted fixed-effects models. We calculated unadjusted odds ratios (ORs) for associations between PCSK9 variants and incident CHD (851 events in AAs and 2,662 events in whites) and stroke (523 events in AAs and 1,660 events in whites) using pooled Mantel-Haenszel estimates with continuity correction factors. Results: In the pooled cohorts, PCSK9 variants were associated with 36 mg/dL (95% confidence interval [CI]: 31, 40) lower LDL-C in AAs and 13 mg/dL (95% CI: 11, 16) lower LDL-C in whites. PCSK9 variants were associated with a pooled OR for CHD of 0.51 (95% CI: 0.28, 0.92) in AAs and 0.82 (95% CI: 0.63, 1.06) in whites. PCSK9 variants were not associated with incident stroke (OR=0.84 [95% CI: 0.48, 1.47] in AAs and OR=1.06 [95% CI: 0.80, 1.41] in whites). Conclusions: These results provide evidence that PCSK9 variants are associated with lifelong reduction in LDL-C and may lead to lower CHD risk, but no effect on stroke risk.

Serum total bilirubin levels and coronary heart disease — Causal association or epiphenomenon?

Observational epidemiological evidence supports a linear inverse and independent association between serum total bilirubin levels and coronary heart disease (CHD) risk, but whether this association is causal remains to be ascertained. A Mendelian randomization approach was employed to test whether serum total bilirubin is causally linked to CHD. The genetic variant rs6742078 – well known to specifically modify levels of serum total bilirubin and accounting for up to 20% of the variance in circulating serum total bilirubin levels – was used as an instrumental variable. In pooled analysis of estimates reported from published genome-wide association studies, every copy of the T allele of rs6742078 was associated with 0.42 standard deviation (SD) higher levels of serum total bilirubin (95% confidence interval, 0.40 to 0.43). Based on combined data from the Coronary Artery Disease Genome wide Replication and Meta-analyses and the Coronary Artery Disease (C4D) Genetics Consortium involving a total of 36,763 CHD cases and 76,997 controls, the odds ratio for CHD per copy of the T allele was 1.01 (95% confidence interval, 0.99 to 1.04). The odds ratio of CHD for a 1 SD genetically elevated serum total bilirubin level was 1.03 (95% confidence interval, 0.98 to 1.09). The current findings casts doubt on a strong causal association of serum total bilirubin levels with CHD. The inverse associations demonstrated in observational studies may be driven by biases such as unmeasured confounding and/or reverse causation. However, further research in large-scale consortia is needed.

Serum CD121a (Interleukin 1 Receptor, Type I): A Potential Novel Inflammatory Marker for Coronary Heart Disease.

Inflammation is now believed to be responsible for coronary heart disease (CHD). This belief has stimulated the evaluation of various inflammatory markers for predicting CHD. This study was designed to investigate the association between four inflammatory cytokines (CD121a, interleukin [IL]-1β, IL-8, and IL-11) and CHD. Here, we evaluated 443 patients with CHD and 160 CHD-free controls who underwent coronary angiography. Cytokines were evaluated using flow cytometry, and statistical analyses were performed to investigate the association between cytokine levels and the risk of CHD. Patients with CHD had significantly higher levels of CD121a. The odds ratios for CHD according to increasing CD121a quartiles were 1.00, 1.47 [95% confidence interval (CI): 0.79–2.72], 2.67 (95% CI: 1.47–4.84), and 4.71 (95% CI: 2.65–8.37) in an age- and sex-adjusted model, compared to 1.00, 1.48 (95% CI: 0.70–3.14), 2.25 (95% CI: 1.10–4.62), and 4.39 (95% CI: 2.19–8.79) in a model that was adjusted for multiple covariates. A comparison of the stable angina, unstable angina, and acute myocardial infarction (AMI) subgroups revealed that patients with AMI had the highest CD121a levels, although IL-1β levels were similar across all groups. IL-8 levels were also increased in AMI patients, and IL-11 levels were higher in CHD patients than in non-CHD patients. Correlation analysis revealed a positive association between CD121a, IL-8, and the Gensini score. Together, the significant increase in CD121a levels among CHD patients suggests that it may be a novel inflammatory marker for predicting CHD.

Novel Genetic Approach to Investigate the Role of Plasma Secretory Phospholipase A2 (sPLA 2 )-V Isoenzyme in Coronary Heart Disease

Background— Secretory phospholipase A 2 (sPLA 2 ) enzymes are considered to play a role in atherosclerosis. sPLA 2 activity encompasses several sPLA 2 isoenzymes, including sPLA 2 -V. Although observational studies show a strong association between elevated sPLA 2 activity and CHD, no assay to measure sPLA 2 -V levels exists, and the only evidence linking the sPLA 2 -V isoform to atherosclerosis progression comes from animal studies. In the absence of an assay that directly quantifies sPLA 2 -V levels, we used PLA2G5 mRNA levels in a novel, modified Mendelian randomization approach to investigate the hypothesized causal role of sPLA 2 -V in coronary heart disease (CHD) pathogenesis. Methods and Results— Using data from the Advanced Study of Aortic Pathology, we identified the single-nucleotide polymorphism in PLA2G5 showing the strongest association with PLA2G5 mRNA expression levels as a proxy for sPLA 2 -V levels. We tested the association of this SNP with sPLA 2 activity and CHD events in 4 prospective and 14 case–control studies with 27 230 events and 70 500 controls. rs525380C&gt;A showed the strongest association with PLA2G5 mRNA expression ( P =5.1×10 −6 ). There was no association of rs525380C&gt;A with plasma sPLA 2 activity (difference in geometric mean of sPLA 2 activity per rs525380 A-allele 0.4% (95% confidence intervals [−0.9%, 1.6%]; P =0.56). In meta-analyses, the odds ratio for CHD per A-allele was 1.02 (95% confidence intervals [0.99, 1.04]; P =0.20). Conclusions— This novel approach for single-nucleotide polymorphism selection for this modified Mendelian randomization analysis showed no association between rs525380 (the lead single-nucleotide polymorphism for PLA2G5 expression, a surrogate for sPLA 2 -V levels) and CHD events. The evidence does not support a causal role for sPLA 2 -V in CHD.

GW24-e0526 The Relationship Between MPO-463 G/A, MPO-129 G/A Gene Polymorphism and Coronary Heart Disease:a Meta-Analysis

ObjectivesCoronary heart disease (CHD) susceptibility may be modulated partly through polymorphyisms in oxidative enzymes, one of wich is myeloperoxidase (MPO). Previous studies have evaluated the association between MPO-463 G/A, MPO-129...

The Risk for Coronary Heart Disease According to Insulin Resistance with and without Type 2 Diabetes

Objective. To examine the role of insulin resistance versus hyperglycemia in the risk for coronary heart disease (CHD) and to explore the interaction of insulin resistance with hyperglycemia. Methods. This is a cross-sectional study based on the National Health and Nutrition Examination Survey III (NHANES). 4,825 subjects were selected from 9,737 adults aged 340 years excluding those with fasting <8 hours, type 1 diabetes, pregnancy, or missing data. Insulin resistance was calculated using the HOMA II and then log-transformed (log IR). Odds ratios (OR) of CHD was obtained with multiple logistic regression with reference to non-diabetics with log IR > 1. Results. CHD and type 2 diabetes were present in 9.1 % and 10.5%. Elevated insulin resistance was common; diabetics and non-diabetics with log IR > 1 constituted 6.3% and 12.1% of the population, respectively. ORs for CHD increased as insulin resistance increased in both non-diabetic and diabetics. When log IR > 1, the risk for CHD was not different between diabetics and non-diabetics (OR 1.12, 95% CI; 0.76–1.65). Furthermore, the risk for CHD was higher in non-diabetics with log IR > 1 than in diabetics with log IR1 (OR 0.55, 95% CI; 0.36–0.85). Conclusions. Insulin resistance was a greater risk for CHD than type 2 diabetes. Non-diabetics can have a higher risk for CHD than diabetics when insulin resistance is elevated. More research is warranted to develop strategies to identify and treat insulin resistance.

The effect of PPARG gene polymorphisms on the risk of coronary heart disease: a meta-analysis

The peroxisome proliferator-activated receptor-γ (PPARG) is a member of the nuclear hormone receptor superfamily that has attracted considerable attention as a candidate gene for coronary heart disease (CHD) based on its function as a key factor involved in the regulation of lipid and glucose metabolism. In the past decade, a number of case-control studies have been carried out to investigate the relationship between the PPARG polymorphisms and CHD. However, these studies have yielded contradictory results. To derive a more precise estimation of the relationship, a meta-analysis of 33 studies including a total of 12,340 cases and 17,471 controls on 3 PPARG polymorphisms (Pro12Ala, C161T and C1431T) was performed. In a combined analysis, the summary per-allele odds ratio for CHD was 1.02 (95% CI: 0.93-1.13), 0.86 (95% CI: 0.72-1.02), and 0.92 (95% CI: 0.74-1.16) for PPARG 12Ala, 161T and 1431T alleles, respectively. No significant results were observed under dominant or recessive genetic models for these polymorphisms in almost all comparisons. In the stratified analyses according to ethnicity, sample size, CHD endpoints and HWE status, no evidence of any gene-disease association was obtained. Our results suggest that the Pro12Ala, C161T and C1431T polymorphisms of PPARG gene are not associated with CHD susceptibility.

Synergistic Association of Serum Albumin and Globulin with Coronary Heart Disease

Serum albumin and globulin have important roles in atherosclerosis development; however, separate studies exploring the relationship between albumin or globulin and coronary heart disease (CHD) have been conducted. We explored whether there was a synergistic effect of albumin and globulin on the presence of CHD. A total of 395 patients aged 50-74 years with angiographically documented CHD were recruited, and 596 age- and sex-matched controls without CHD were randomly selected from the general population. The association of albumin and globulin with CHD was analyzed using conditional logistic regression after adjusting for traditional CHD risk factors. Mean values of serum albumin and globulin were significantly lower in cases than in controls (p<0.001). In the fully adjusted model, compared with participants whose albumin (≥47.3 g/L) and globulin (≥25.6 g/L) levels were both higher than the median levels in these participants, the odds ratio for CHD was 1.59 (p= 0.048) for participants with higher albumin (≥47.3 g/L) but lower globulin (<25.6 g/L), 2.79 (p<0.001) for participants with lower albumin (<47.3 g/L) but higher globulin (≥25.6 g/L), and 16.03 (p<0.001) for participants with lower levels of both albumin (<47.3 g/L) and globulin (<25.6 g/L). Low serum albumin and globulin are independently associated with CHD. The synergistic association of both low albumin and low globulin with CHD is greater than either one alone. The synergistic effect deserves further investigation.

Is Bitter Better? The Benefits of Chocolate for the Cardiovascular System

Background and Aims: Cocoa, particularly dark chocolate, is rich in flavonoids, and recent studies have demonstrated blood pressure lowering effects of dark chocolate. Because limited data are available on the association of chocolate consumption and the risk of coronary heart disease (CHD), the investigators examined the association between chocolate consumption and prevalence of CHD. Methods: Using a cross-sectional design, 4,970 participants 25to 93years ofage were studiedintheNationalHeart, Lung, and Blood Institute (NHLBI) Family Heart Study. Chocolate intakewasassessedthroughasemiquantitativefoodfrequency questionnaire. The workers generalized estimating equations to assess adjusted odds ratios. Results: Compared with subjects who did not report any chocolate intake at all, the odds ratios for CHD were 1.01 (95% CI, 0.76–1.37), 0.74 (95% CI, 0.56–0.98), and 0.43 (95% CI, 0.28–0.67) in subjects consuming chocolate 1–3 times per month, 1–4 times per week, or 5+ times per week, respectively (P for trend <0.0001), adjusting for age, sex, family CHD risk group, and a large number of other confounders. Interestingly, subjects who consumed nonchocolate candy 5+ times per week had a 49% higher prevalence of CHD than those with no such consumption (OR, 1.49; 95% CI, 0.96–2.32). Discussion: The authors suggest that consumption of chocolate is inversely related with prevalent CHD in a general United States population.

Paraoxonase 1 polymorphisms as the risk factor of coronary heart disease in a Thai population

Objective — Two common polymorphisms of the paraoxonase (PON1) gene, L55M and Q192R, were proven to mitigate atherosclerosis pathogenesis by protecting lipoproteins against peroxidation. This study was to evaluate the associations between both PON1 gene polymorphisms in Thai hyperlipidaemia with and without coronary heart disease (CHD).Methods — Both PON1 genotypes were determined using PCR-RFLP in 103 healthy control subjects, 103 primary hyperlipidaemia without history of such diseases and 106 angiographically documented CHD patients.Results — The frequencies of PON1 192R allele and 192RR genotype were significantly higher in CHD patients than in normal control subjects (P = 0.009 and 0.037, respectively). The significantly higher frequencies of 55M allele and 55LM genotype were also observed in CHD patients (P = 0.037 and P = 0.034, respectively). The frequencies of both PON1 polymorphisms were not different in primary hyperlipidaemia as compared to the normal control subjects.The odds ratio (OR) of 192RR genotype and 192R allele for CHD were 2.84 (1.17-6.99, P = 0.011) and 1.70 (1.11-2.61, P = 0.009), respectively. The age-adjusted OR for CHD was 2.72 (1.25-5.94, P = 0.012). These frequencies of both PON1 alleles were similar to those seen in other Asian populations.Conclusions — The association between PON1 polymorphisms and CHD risk was demonstrated in a Thai population.These new data underscore the essence of ethnic variations in the interpretation of CHD associated with PON1 polymorphism.

Impact of the metabolic syndrome and its individual components on risk and severity of coronary heart disease

The clinical use of criteria for metabolic syndrome (MetS) and its individual components with respect to risk prediction of coronary heart disease (CHD) remains uncertain. In this study, we investigated whether and to what extent MetS and its individual components were related to risk for CHD. A total of 1,028 subjects, who had undergone coronary angiography or were diagnosed as acute myocardial infarction, were selected according to inclusion criteria. MetS was diagnosed with National Cholesterol Education Program Adult Treatment Panel III (NCEP ATPIII) criteria. CHD was diagnosed with clinical data and confirmed by coronary angiography. The severity of coronary atherosclerosis was estimated by CHD Gensini cumulative index. All the patients were aged 33-87 years. The results showed that the age- and sex-adjusted odds ratios (ORs) for CHD in different individual components of MetS were as follows: low-high density lipoprotein (low-HDL), 3.15 (1.94-5.12); high-fasting plasma glucose (high-FPG), 2.26 (1.63-3.69); high-blood pressure (high-BP), 2.13 (1.38-3.29); high-triglycerides (high-TG), 1.55 (1.13-2.11); all P < 0.05, whereas high-body mass index (high-BMI), 0.75 (0.55-1.03) and high-waist circumference, 0.75 (0.51-1.10), both P > 0.05. Among all the components, the triad of low-HDL, high-FPG, and high-BP had the highest OR for CHD: 4.28 (3.12-5.87) (P < 0.001). MetS subjects had significant increases in number of disease vessel and CHD Gensini index (P < 0.001). When individual components of MetS were considered separately, groups with low-HDL, or high-FPG, or high-BP had significant increases in number of disease vessel and Gensini index (all P < 0.001). In conclusion, our present results demonstrated that individual components of MetS and their various combinations may have different contributions to CHD and the severity of coronary artery stenosis. Clinical focus should remain on establishing optimum-risk algorithms for CHD.