Abstract P190: Triggering of Coronary Heart Disease by Infection Type: The Atherosclerosis Risk in Communities Study

Introduction: Acute infections are known triggers of coronary heart disease (CHD). It is unclear how the strength of the association varies by infection type. Hypothesis: We hypothesized that all acute infections increase CHD risk but the level of increased risk varies by infection type. Methods: Incident CHD (myocardial infarction and fatal CHD) cases were identified and adjudicated in the ARIC cohort. ARIC participants were linked to Medicare claims data. We used ICD-9 codes to identify 4 infection types based on infection frequency: cellulitis, pneumonia, urinary tract infections (UTI), and bloodstream infections. We used a case-crossover design and conditional logistic regression to compare infections among CHD cases 90 days before the event with two corresponding control periods 1 year and 2 years prior. The Wald test was used to assess differences between infection types. Results: A total of 1,312 CHD cases were identified. Among cases, 43 had cellulitis, 102 had pneumonia, 116 had a UTI, and 28 had a bloodstream infection within 90 days of the CHD event. All infection types were associated with higher CHD risk within 90 days of the infection; (odds ratios and 95% Cis) (cellulitis = 1.41 (0.93, 2.15), pneumonia = 5.60 (3.72, 8.43), UTI = 2.62 (1.92, 3.57), bloodstream infections = 4.77 (2.34, 9.71)) although cellulitis was not statistically significant (Figure). The association between infection and CHD was significantly stronger for pneumonia, UTI, and bloodstream infections compared to cellulitis (p<0.05). Pneumonia and bloodstream infections were stronger CHD triggers compared to UTI but only pneumonia reached statistical significance (p<0.05). Conclusions: Patients with pneumonia or bloodstream infections may be at particularly elevated CHD risk. Clinical trials of CHD preventive therapies during and immediately following infection to reduce the otherwise elevated CHD risk are needed. Healthcare providers should consider CHD risk during and immediately after infection and optimize preventive therapies.

Download Full-text

Abstract P150: Association of Cholesterol Measures With Coronary Heart Disease Risk in Blacks and Whites in the Reasons for Geographic and Racial Differences in Stroke Study (regards)

Circulation ◽

10.1161/circ.141.suppl_1.p150 ◽

2020 ◽

Vol 141 (Suppl_1) ◽

Author(s):

Neil Zakai ◽

Jessica Minnier ◽

Monika M Safford ◽

Lisandro Colantonio ◽

Marguerite M Irvin ◽

...

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Total Cholesterol ◽

Racial Differences ◽

Cox Regression ◽

Disease Risk ◽

Point Estimate ◽

Chd Risk ◽

Increased Risk ◽

Blacks And Whites

Introduction: Abnormal plasma lipid levels associate with coronary heart disease (CHD) risk. Race interaction for these associations are not established. Hypothesis: We hypothesized that the association of HDL, LDL, and triglyceride with CHD is stronger in whites versus blacks. Methods: The REasons for Geographic and Racial Differences in Stroke (REGARDS) cohort recruited 30,283 black and white individuals aged 45+ from the contiguous U.S. from 2003-7. Participants were followed until December 31, 2016 for CHD events (i.e., myocardial infarction or CHD death), participants with history of CHD at baseline were excluded. Cox regression models were used to assess the association between baseline lipids and incident CHD events adjusting for traditional cardiovascular risk factors. Results: With 23,894 participants (57.8% white and 58.4% female, mean age 64.11± 9.32), over a median 9.9 years of follow-up, 1,487 CHD events occurred (615 among blacks). Overall, higher total Cholesterol, LDL cholesterol, and triglycerides were associated with increased risk of CHD in both blacks and whites with no evidence of a race interaction (Table 1). For HDL, the point estimate was more protective in whites (HR 0.90) than in blacks (HR 0.98), but the interaction was non-significant (p=0.15). However, when HDL was stratified into clinical categories (<40, 40-59, and ≥60), the reduction in point estimates was maintained among whites (HR 1.00, 0.88, and 0.74) but not among blacks (HR 1.00, 1.31, and 1.19) for HDL <40, 40-59, and ≥60 respectively, p-interaction 0.01. Conclusion: Total cholesterol, LDL, and triglycerides predict CHD risk equally in blacks and whites in the REGARDS study, however there is heterogeneity in the protective effect by race, especially when traditional clinical categories are used. In whites, higher HDL is associated with reduced risk, whereas in blacks the association is not maintained. These findings suggest that HDL levels are a more viable metric for white than blacks to predict CHD risk.

Download Full-text

Assessment of coronary heart disease risk in testicular cancer survivors

Journal of Clinical Oncology ◽

10.1200/jco.2006.24.18_suppl.4592 ◽

2006 ◽

Vol 24 (18_suppl) ◽

pp. 4592-4592 ◽

Cited By ~ 1

Author(s):

S. C. Palmer ◽

J. Carver ◽

L. Jacobs ◽

K. H. Schmitz ◽

C. Fung ◽

...

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Testicular Cancer ◽

Cancer Survivors ◽

Disease Risk ◽

Objective Measures ◽

Chd Risk ◽

Increased Risk ◽

Hs Crp ◽

Testicular Cancer Survivors

4592 Background: Testicular cancer survivors (TCS) who receive cisplatin-based chemotherapy (CBCT) are reported to have an increased risk of coronary heart disease (CHD) compared to chemo-naive TCS (J Clin Oncol 21:1513–1523, 2003). We hypothesized that TCS treated with CBCT would demonstrate abnormal objective measures of future CHD risk compared to chemo-naive TCS. Methods: TCS ≥ 2 years from diagnosis underwent evaluation using established objective measures predictive of future CHD risk: body mass index (BMI), Framingham relative risk (RR), flow-mediated endothelium-dependent vasodilation of the brachial artery (FMD), carotid artery intima-media thickness (IMT), serum intercellular adhesion molecule-1 (ICAM-1), and high sensitivity C-reactive protein (hs-CRP). Data were analyzed using parametric and non-parametric statistics as appropriate. Results: 30 TCS who received CBCT and 20 chemo-naive TCS were recruited. The mean age and time from diagnosis were similar between the 2 groups. Both groups demonstrated elevated BMI, increased Framingham RR, and impaired FMD, consistent with an increased risk of CHD. However, there were no statistically significant differences in these measures between the two groups. Carotid IMT, ICAM-1, and hs-CRP were not significantly abnormal and these measures also did not differ between the two groups. Conclusions: TCS demonstrate abnormal objective measures of CHD risk in both CBCT-treated and chemo-naive groups. These data suggest that behavioral interventions to modify CHD risk should target all TCS independent of chemotherapy status. All values reported are mean ± standard deviation [Table: see text] No significant financial relationships to disclose.

Download Full-text

Abstract 19: Dietary Lipophilic Load and Dietary Lipophilic Index with Risk of Coronary Heart Disease in Middle-Aged Women: Beyond Conventional Fat Classifications

Circulation ◽

10.1161/circ.131.suppl_1.19 ◽

2015 ◽

Vol 131 (suppl_1) ◽

Author(s):

Eric L Ding ◽

Katerina M De Vito ◽

Hongyu Wu ◽

Qi Sun ◽

An Pan ◽

...

Keyword(s):

Risk Factors ◽

Coronary Heart Disease ◽

Heart Disease ◽

Dietary Fat ◽

Hdl Cholesterol ◽

Health Study ◽

Chd Risk ◽

Increased Risk ◽

Total Fat ◽

Traditional Risk Factors

Introduction: Studies indicate dietary types of fats are associated with risk of coronary heart disease (CHD). Traditional broad classifications may incompletely capture the diversity of fatty acids on CHD. The novel lipid index Dietary Lipophilic Load (DLL) reflects a unique combination of fatty acid fluidity, intermolecular attraction, plus relative fat quantity, while Dietary Lipophilic Index (DLI) is a measure of average fat fluidity, regardless of fat quantity. Thus, we evaluated the association, DLL and DLI, with risk of incident CHD. METHODS: Participants included 30,932 women in the Women’s Health Study (WHS), who were free of major chronic diseases at baseline. DLL was calculated by weighted summation of the multiplicative product of each fatty acid’s intakes (g/day) and its melting points (Celcius); DLI was calculated by dividing DLL by total fat intake (g/day). Hazard ratios (HRs) were adjusted for established risk factors, with updated dietary data, and potential mediators. We also investigated hypothesized interactions with C-Reactive Protein (CRP). RESULTS: There were 1137 cases of incident CHD in 525,828 person-years over 19 years follow-up. At baseline in over 27,000 women with blood samples, DLL and DLI were not correlated with serum cholesterol, triglyceride, HbA1c, ICAM-1, or CRP biomarkers (r<0.02 for all). In overall multivariate analysis, DLL was associated with higher risk of CHD (extreme quintile HR=1.40, 95%CI: 1.11-1.76, P trend=0.0002), while DLI was not (HR=0.83, 95%CI: 0.67-1.03, P trend=0.75). DLL results were independent beyond adjustment for dietary trans, saturated, monounsaturated, and polyunsaturated fats, nor their aggregate adjustment or the P:S ratio. DLL effects persisted even adjusting for CRP (HR=1.29, P-trend=1 mg/dL for DLL (extreme quintile HR=1.38, 1.02-1.88), than among individuals with low CRP <1 mg/dl for DLL (HR=1.08, 0.68-1.72), with P-interaction<0.0001. Furthermore, CRP also modified DLI, where effects again diverged among higher CRP (HR=0.98, 0.73-1.31) versus low CRP (HR=0.45, 0.27-0.74), with P-interaction<0.0001. Moreover, adjustment of triglycerides, HbA1c, ICAM-1, LDL or HDL cholesterol also did not materially affect overall results. CONCLUSION: Results indicate that DLL is associated with increased risk of incident CHD, independent of traditional risk factors, conventional dietary fat classifications, and major CHD biomarkers. Effects of DLL and DLI appear to be modified by levels of CRP. DLL appears to be an important novel dietary fat index that captures additional CHD risk information beyond biomarkers and traditional dietary fat categories. Further studies are warranted.

Download Full-text

Abstract P186: Circulating Desphospho-uncarboxylated Matrix Gla Protein and the Risk of Coronary Heart Disease and Stroke

Circulation ◽

10.1161/circ.129.suppl_1.p186 ◽

2014 ◽

Vol 129 (suppl_1) ◽

Author(s):

Geertje W Dalmeijer ◽

Yvonne T van der Schouw ◽

Elke J Magdeleyns ◽

Cees Vermeer ◽

W. Monique M Verschuren ◽

...

Keyword(s):

Coronary Heart Disease ◽

Cohort Study ◽

Heart Disease ◽

General Population ◽

Vitamin K ◽

Stroke Risk ◽

Matrix Gla Protein ◽

Chd Risk ◽

Increased Risk ◽

Incident Cases

Background: Matrix Gla protein (MGP) is a vitamin K dependent protein and a potent inhibitor of vascular calcification. Desphospho-uncarboxylated MGP (dp-ucMGP) is a marker for vitamin K status with high dp-ucMGP concentration reflecting a low vitamin K status. High dp-ucMGP concentrations are thought to be associated with an increased risk of cardiovascular disease, but this has never been investigated in the general population. Objective: This study aimed to investigate the association of dp-ucMGP with incident coronary heart disease (CHD) or stroke in the general population. Design and Methods: A prospective case-cohort study with a representative baseline sample of 1406 participants and 1154 and 380 incident cases of CHD and stroke, respectively, was nested within the EPIC-NL study. Dp-ucMGP concentrations were measured by ELISA technique in baseline plasma samples. The incidence of fatal and non-fatal CHD and stroke was obtained by linkage to national registers. Cox proportional hazard models adapted for the case-cohort design were used to calculate hazard ratios (HRs) per standard deviation (SD) and per quartile of circulating dp-ucMGP levels, adjusted for cardiovascular risk factors. Results: This case-cohort study had an average follow-up of 11.5 years. Circulating dp-ucMGP levels were not associated with CHD risk with a HR per SD of 1.00 (95% CI: 0.93-1.07) and a HR Q4 vs Q1 of 0.94 (95% CI: 0.79-1.13) after multivariate adjustment. Circulating dp-ucMGP was not associated with stroke risk with a HR per SD of 0.98 (95% CI: 0.90-1.08) and a HR Q4 vs Q1 of 1.09 (95% CI: 0.78-1.51). Conclusion: This study does not support the hypothesis that high dp-ucMGP levels, reflecting a poor vitamin K status, are associated with increased CHD or stroke risk.

Download Full-text

High Density Lipoprotein pathway as a therapeutic target for coronary heart disease: individual participant meta-analysis in 28,597 individuals with 4197 coronary events

10.1101/2020.03.02.19010173 ◽

2020 ◽

Author(s):

Amy R Mulick ◽

David Prieto-Merino ◽

Therese Tillin ◽

Aki Havulinna ◽

Martin Shipley ◽

...

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

High Density Lipoprotein ◽

Longitudinal Studies ◽

Meta Analysis ◽

Density Lipoprotein ◽

High Density ◽

Resonance Spectroscopy ◽

Chd Risk ◽

Increased Risk

AbstractImportanceCholesterol content in high-density lipoprotein particles (HDL-C) is associated inversely with coronary heart disease (CHD), but findings from Mendelian randomization studies and randomized trials of HDL-C raising drugs have questioned whether this link is causal. However, these analyses do not exclude a causal role for specific HDL sub-fractions of different density, mobility, size and composition.ObjectiveTo determine whether sub-components of the HDL pathway exhibit differing relationships with CHD risk.DesignIn seven longitudinal studies, we used factor analysis to reduce 21 measures of HDL particle size and lipid content to a smaller number of factors representing different components of the HDL pathway. We constructed factor scores and modelled their associations on CHD risk in adjusted Cox regression analyses. We pooled results using random-effects meta-analysis.SettingSeven population-, individual-, occupational- or community-based longitudinal studies in the UK and Finland.Participants28,597 participants (49% female, mean age 59.6 years) contributed to the analysis.ExposuresSub-components of the HDL pathway, characterized by 21 measures of HDL size and lipid content based on nuclear magnetic resonance spectroscopy.Main OutcomesIncident fatal or non-fatal CHD.ResultsWe identified 4 HDL components with highly replicable across studies; 3 were indices of particle size/composition (extra-large (XL), large (L) and medium/small (MS)), and the other an index of triglycerides (TG) carried in HDL of all sizes. After up to 17 years of follow-up, 4179 incident CHD cases occurred. After adjusting for age, sex, ethnicity, smoking, systolic blood pressure, body mass index, diabetes and LDL-C, higher levels of the XL and MS factors were linked to a reduced risk of CHD (hazard ratio per 1 standard deviation (SD) increase 0.88 [95% CI 0.85, 0.92] and 0.91 [0.87, 0.94]). In contrast, a SD increase in the level of the TG factor was associated with increased risk of CHD (1.10 [1.07, 1.14]).Conclusions and RelevanceWe found qualitative differences between sub-components of the HDL pathway and the risk of developing CHD. Discovery of the biological determinants of these components, possibly through genetic analysis, will facilitate selection of drug targets and inform trial design.Key PointsQuestionCan investigation of sub-components of the high-density lipoprotein (HDL) pathway, measured through nuclear magnetic resonance spectroscopy, point to specific therapeutic targets for prevention of coronary heart disease (CHD)?FindingsUsing individual-level data from seven longitudinal studies including 28,597 participants and 4197 CHD events, we identified two components of the HDL pathway that were associated with reduced, and one that was associated with increased, risk of CHD.MeaningThese sub-components of the HDL pathway, if causally related to atherogenesis, offer a route to more precise therapeutic targets for prevention of CHD.

Download Full-text

Analysis for interaction between interleukin-35 gene polymorphisms and risk factors on susceptibility to coronary heart disease in the Chinese Han population

10.21203/rs.3.rs-31682/v1 ◽

2020 ◽

Author(s):

Hu LI ◽

Ying-Xue LIU ◽

Jin-Yan Huang ◽

Yu- Feng Zhu ◽

Kui Wang

Keyword(s):

Coronary Heart Disease ◽

Logistic Regression ◽

Heart Disease ◽

Cross Validation ◽

Sign Test ◽

Control Group ◽

Environment Interaction ◽

Current Smoking ◽

Chd Risk ◽

Increased Risk

Abstract Objective To explore the effect of single nucleotide polymorphisms (SNPs) of interleukin-35 (IL-35) gene and its relationship with environment on the risk of coronary heart disease (CHD). Methods Prior to the analysis, we performed hardy Weinberg equilibrium test on the control group. The relationship between the four SNPs of IL-35 gene and the risk of coronary heart disease was studied by multivariate logistic regression. The best interaction was identified with generalized multifactor dimensionality reduction (GMDR). Logistic regression was used for investigation on association between four SNPs and CHD risk. Results Logistic regression analysis showed that the C allele of rs428253 and the G allele of rs2243115 were independently correlated with increased risk of CHD, and adjusted ORs (95%CI) were 1.91 (1.28–2.64) and 1.80 (1.30–2.23), respectively. However, there was no significant association between CHD and rs4740 or rs568408. GMDR model, indicated the best model for CHD risk consisted of rs428253 and current smoking, which scored 10/10 for both the sign test and cross-validation consistency (P = 0.010). Therefore, this overall multi-dimensional model had the highest cross-validation consistency, regardless of how the data were divided. This provided an evidence of gene-environment interaction effects. We also found that current smokers with rs428253 - GC/ CC genotype have the highest CHD risk, compared to subjects with never smokers with rs428253 - GG genotype, OR (95%CI) = 3.04 (1.71–4.41), after adjustment for age, gender, hypertension, T2DM and alcohol consumption status. Conclusions In this study, the C allele of rs428253 and the G allele of rs2243115, and the interaction rs428253 and current smoking were correlated with increased risk of CHD.

Download Full-text

L162v Polymorphism of Par-Α Gene, A603g Polymorphism of Tissue Factor Gene and Risk of Coronary Heart Disease in Russian Population

Journal of Bioinformatics and Diabetes ◽

10.14302/issn.2374-9431.jbd-19-2788 ◽

2019 ◽

Vol 1 (4) ◽

pp. 1-11

Author(s):

E.G. Sergeeva ◽

O.A. Berkovich ◽

Z.I. Ionova ◽

M.I. Zaraisky ◽

...

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Tissue Factor ◽

Restriction Analysis ◽

Russian Population ◽

Control Group ◽

Factor Gene ◽

Chd Risk ◽

Increased Risk ◽

Increase Risk

Purpose The goal of this study is to determine the association of L162V polymorphism of PPAR-alpha gene, A603G polymorphism of tissue factor gene and the risk of coronary heart disease development in Russian population. Materials and Methods A clinical and genetic study of 414 patients with CHD and 220 people of comparable age without CHD which amounted to a control group was performed. L162L and L162V genotypes of L162V polymorphism of PPAR-α gene, A603A, A603G and G603G genotypes of A603G polymorphism of tissue factor gene were determined by polymerase chain reaction followed by restriction analysis. Results A carriage of L162V genotype and V allele of PPAR-α gene was associated with an increase risk of CHD in 2,13 times (L162V genotype) and in 2,21 times (V allele), with an increase in risk of CHD before the age of 45 years in 4,68 times (L162V genotype) and in 3,88 times (V allele). Significantly higher in patients with CHD compared with the general population and in patients with a carriage of G603G genotype and G allele of tissue factor gene was associated with the increase of CHD risk in 2,68 times (G603G genotype) and in 4,37 times (G allele), occurred more frequently in patients with debut of disease at age of 45 years and younger. The level of tissue factor was significantly higher in patients with CHD – carriers G603G genotype compared with carriers A603A genotype (217,9±15,2 pg/ml and 152,6±30,4 pg/ml, respectively, p=0,04). A carriage of the combination of L162V and G603G genotypes was associated with an increased risk of CHD in 3,04 times. Conclusion A carriage of V allele of L162V polymorphism of PPAR-α gene and G allele of A603G polymorphism of tissue factor gene, as well as their pair combination are associated with an increased CHD risk, especially at age 45 years or less.

Download Full-text

Trajectories of body mass index and risk for coronary heart disease: A 38-year follow-up study

PLoS ONE ◽

10.1371/journal.pone.0258395 ◽

2021 ◽

Vol 16 (10) ◽

pp. e0258395

Author(s):

Susanna Calling ◽

Sven-Erik Johansson ◽

Veronica Milos Nymberg ◽

Jan Sundquist ◽

Kristina Sundquist

Keyword(s):

Body Mass Index ◽

Coronary Heart Disease ◽

Heart Disease ◽

Life Course ◽

Body Mass ◽

Normal Weight ◽

World Health ◽

Chd Risk ◽

Increased Risk ◽

Overweight Or Obesity

Objective Obesity is a well-known risk factor for coronary heart disease (CHD), but there is little evidence on the effect of long-term trajectories of body mass index (BMI) over the life course. By using repeated assessments, the aim was to study the risk of CHD in adults during 38 years in different trajectories of BMI. Methods A sample of 2129 men and women, aged 20–59 years at baseline, took part in four repeated interviews between 1980 and 2005. Data on BMI, medical history, lifestyle and socioeconomy were collected. Based on the World Health Organization categories of BMI, life course trajectories of stable normal weight, stable overweight, stable obesity, increasing BMI and fluctuating BMI were created. The individuals were followed through national registers for first hospitalization of CHD (389 events) until the end of 2017, and Hazard Ratios (HRs) were calculated, adjusted for age, sex, socioeconomic factors, lifestyle factors and metabolic comorbidities. Results Stable normal weight in all assessments was the reference group. Those who had an increase in BMI from normal weight in the first assessment to overweight or obesity in later assessments had no increased risk of CHD, HR 1.04 (95% CI: 0.70–1.53). The HR for individuals with fluctuating BMI was 1.25 (0.97–1.61), for stable overweight 1.43 (1.03–1.98), for stable obesity 1.50 (0.92–2.55), and for stable overweight or obesity 1.45 (1.07–1.97), after full adjustments. Conclusion Having a stable overweight or obesity throughout adult life was associated with increased CHD risk but changing from normal weight at baseline to overweight or obesity was not associated with increased CHD risk. Prevention of obesity early in life may be particularly important to reduce CHD risk.

Download Full-text

Abstract P064: Dietary Glycemic Index and Glycemic Load and Risk of Coronary Heart Disease in a Prospective Study Among US Male Health Professionals

Circulation ◽

10.1161/circ.125.suppl_10.ap064 ◽

2012 ◽

Vol 125 (suppl_10) ◽

Author(s):

Shanshan Li ◽

Frank B Hu ◽

John P Forman ◽

Eric B Rimm

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Glycemic Index ◽

Glycemic Load ◽

Effect Modification ◽

Fiber Intake ◽

Chd Risk ◽

Increased Risk ◽

Dietary Glycemic Index

Introduction: The associations between dietary glycemic index (GI) and glycemic load (GL) with subsequent risk of coronary heart disease (CHD) are inconclusive among men. The association is further complicated by the potential biological interactions between the carbohydrate quality of the diet and factors that may influence underlying insulin resistance. Hypothesis: We hypothesized that long-term exposure to a diet with high GI and GL would be associated with increased CHD risk in a cohort of US men, and the association would be further modified by fiber intake, alcohol consumption and BMI. Methods: We included 37,736 men aged 40–75 years from the Health Professional Follow-up Study, with no previous diagnosis of CHD, cancer, or type 2 diabetes. We confirmed 3,121 total incident CHD cases during 22 years of follow-up. Cox proportional hazard models were used to adjust for covariates. Results: After adjusting for lifestyle and dietary covariates, the hazard ratio (RR) and 95% confidence intervals comparing men in the highest vs. the lowest quintile was 1.16 (1.04, 1.31; p for trend=0.03) for dietary GI, and 1.09 (0.94, 1.27; p for trend =0.16) for GL. We found a significant effect modification by fiber intake (p=0.02); The associations between GL and CHD risk were strongest among participants in the lowest tertile of fiber intake (RR= 1.00, 1.00, 0.93, 1.11 and 1.16 with increasing quintiles of GL; RR=1.00, 0.68, 0.79, 0.73 and 0.76 for participants in the highest tertile of fiber intake). The association between GL and CHD was stronger among men with body mass index (BMI) greater than 25 kg/m2 than normal weight men, even though the test for interaction was only marginally significant (RR=1.00, 1.03, 1.05, 1.10, and 1.16 for increasing quintles of GL among men with BMI≥25 kg/m2 and RR= 1.00, 0.92, 0.96, 1.09 and 1.04 for men with BMI<25 kg/m2, p for interaction=0.09). Alcohol intake did not modify the association of GL with CHD (p for interaction=0.44). Conclusion: We observed a significantly increased risk of CHD with high GI diet and a modestly elevated association between GL and CHD among men with low fiber intakes or who were overweight or obese. No effect modification by alcohol was observed, but we did find that the association between GL and CHD was more pronounced among those with lower fiber intake or higher BMI.

Download Full-text

Lipoprotein-associated Phospholipase A2 and Coronary Heart Disease

Current Pharmaceutical Design ◽

10.2174/1381612824666180111110550 ◽

2018 ◽

Vol 24 (3) ◽

pp. 291-296 ◽

Cited By ~ 5

Author(s):

Areti Sofogianni ◽

Stelina Alkagiet ◽

Konstantinos Tziomalos

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Phospholipase A2 ◽

Therapeutic Target ◽

Association Studies ◽

Genetic Association Studies ◽

Markers Of Inflammation ◽

Chd Risk ◽

Increased Risk

In the last decades, the role of inflammation in the pathogenesis of atherosclerosis has been the topic of intense research. Several markers of inflammation have shown predictive value for first and recurrent coronary events in patients without and with established Coronary Heart Disease (CHD). Among these markers, lipoprotein- associated phospholipase A2 (Lp-PLA2) has recently received considerable attention. In the present review, the potential role of Lp-PLA2 as a marker of CHD risk and as a therapeutic target is discussed. Elevated Lp- PLA2 mass and activity appears to be associated with increased risk for CHD, both in the general population and in patients with established CHD. However, it is unclear whether the measurement of Lp-PLA2 improves risk discrimination when incorporated in models that include traditional cardiovascular risk factors. Moreover, the lack of effect on CHD events of darapladib, a potent, selective Lp-PLA2 inhibitor, in two large, randomized, placebo-controlled trials and the mostly negative findings of genetic association studies suggest that Lp-PLA2 is unlikely to represent a causal factor in atherogenesis. Therefore, it is doubtful whether Lp-PLA2 will constitute a therapeutic target for the prevention of CHD.

Download Full-text