More knocks to the oxidation hypothesis for vascular disease?

The oxidation hypothesis for CHD (coronary heart disease) is attractive; however, the almost universal failure of antioxidant vitamin supplementation as a CVD (cardiovascular disease) risk modifier challenges the oxidation hypothesis, at least as a concept that easily ‘translates’ into clinical benefit for the population. At the same time, quality prospective data on lipid or protein oxidation markers as predictors of vascular events are sparse. In the present issue of Clinical Science, Woodward and co-workers provide much needed prospective data examining the relationship between markers of oxidative damage and CHD outcome in a general population. Despite noting the expected associations between several established CHD risk factors and CHD events, no significant link was observed between measured oxidation markers and CHD risk, a finding which further challenges the oxidation hypothesis for CHD.

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The Reversion of DNA Methylation at Coronary Heart Disease Risk Loci in Response to Prevention Therapy

Processes ◽

10.3390/pr9040699 ◽

2021 ◽

Vol 9 (4) ◽

pp. 699

Author(s):

Willem Philibert ◽

Allan M. Andersen ◽

Eric A. Hoffman ◽

Robert Philibert ◽

Meeshanthini Dogan

Keyword(s):

Risk Factors ◽

Coronary Heart Disease ◽

Heart Disease ◽

Disease Risk ◽

Methylation Status ◽

Digital Pcr ◽

Response To Treatment ◽

Chd Risk ◽

Chd Risk Factors ◽

The Relationship

Coronary heart disease (CHD) is preventable, but the methods for assessing risk and monitoring response rely on imprecise lipid-based assessments. Recently, we have shown that an integrated genetic–epigenetic test that includes three methylation-sensitive digital PCR assays predicts 3-year risk for incident CHD better than lipid-based methods. However, whether methylation sites change in response to therapies that alter CHD risk is not known. Therefore, we assessed methylation at these three incident CHD-related sites in DNA from 39 subjects before and after three months of biochemically verified smoking cessation, then analyzed the relationship between change in methylation at each of the sites to the change in smoking intensity as assessed by cg05575921 methylation. We found that, in those who quit smoking, methylation change at one CHD risk marker (cg00300879) was significantly associated with change in cg05575921 methylation (p < 0.04). We conclude that changes in incident CHD-related methylation occur within three months of cessation of smoking, a major risk factor for CHD. This suggests that the effectiveness of treatment of other CHD risk factors, such as high cholesterol, may be similarly quantifiable using epigenetic approaches. Further studies to determine the relationship of changes of methylation status in response to treatment of other CHD risk factors are indicated.

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Habitual sleep quality, plasma metabolites and risk of coronary heart disease in post-menopausal women

International Journal of Epidemiology ◽

10.1093/ije/dyy234 ◽

2018 ◽

Vol 48 (4) ◽

pp. 1262-1274 ◽

Cited By ~ 6

Author(s):

Tianyi Huang ◽

Oana A Zeleznik ◽

Elizabeth M Poole ◽

Clary B Clish ◽

Amy A Deik ◽

...

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Sleep Quality ◽

Disease Risk ◽

Cardiovascular Disease Risk ◽

Health Study ◽

Plasma Metabolites ◽

Cardiometabolic Health ◽

Chd Risk ◽

Chd Risk Factors

Abstract Background Epidemiologic studies suggest a strong link between poor habitual sleep quality and increased cardiovascular disease risk. However, the underlying mechanisms are not entirely clear. Metabolomic profiling may elucidate systemic differences associated with sleep quality that influence cardiometabolic health. Methods We explored cross-sectional associations between sleep quality and plasma metabolites in a nested case–control study of coronary heart disease (CHD) in the Women’s Health Initiative (WHI; n = 1956) and attempted to replicate the results in an independent sample from the Nurses’ Health Study II (NHSII; n = 209). A sleep-quality score (SQS) was derived from self-reported sleep problems asked in both populations. Plasma metabolomics were assayed using LC–MS with 347 known metabolites. General linear regression was used to identify individual metabolites associated with continuous SQS (false-discovery rate <0.05). Using least absolute shrinkage and selection operator (LASSO) algorithms, a metabolite score was created from replicated metabolites and evaluated with CHD risk in the WHI. Results After adjusting for age, race/ethnicity, body mass index (BMI) and smoking, we identified 69 metabolites associated with SQS in the WHI (59 were lipids). Of these, 16 were replicated in NHSII (15 were lipids), including 6 triglycerides (TAGs), 4 phosphatidylethanolamines (PEs), 3 phosphatidylcholines (PCs), 1 diglyceride (DAG), 1 lysophosphatidylcholine and N6-acetyl-L-lysine (a product of histone acetylation). These metabolites were consistently higher among women with poorer sleep quality. The LASSO selection resulted in a nine-metabolite score (TAGs 45: 1, 48: 1, 50: 4; DAG 32: 1; PEs 36: 4, 38: 5; PCs 30: 1, 40: 6; N6-acetyl-L-lysine), which was positively associated with CHD risk (odds ratio per SD increase in the score: 1.16; 95% confidence interval: 1.05, 1.28; p = 0.0003) in the WHI after adjustment for matching factors and conventional CHD risk factors. Conclusions Differences in lipid metabolites may be an important pathogenic pathway linking poor habitual sleep quality and CHD risk.

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The Relationship between Immigration Status and Cardiovascular Disease Risk Factors in United States Adults with Diabetes—A 14-Year Study

Diabetes ◽

10.2337/db18-1491-p ◽

2018 ◽

Vol 67 (Supplement 1) ◽

pp. 1491-P

Author(s):

APRILL DAWSON ◽

EMMA GARACCI ◽

MUKOSO N. OZIEH ◽

REBEKAH J. WALKER ◽

LEONARD E. EGEDE

Keyword(s):

United States ◽

Risk Factors ◽

Cardiovascular Disease ◽

Disease Risk ◽

Cardiovascular Disease Risk ◽

Cardiovascular Disease Risk Factors ◽

Immigration Status ◽

The Relationship

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Relationship between Depressive Symptoms and Cardiovascular Disease Risk Factors in African American Individuals

Depression Research and Treatment ◽

10.1155/2011/836542 ◽

2011 ◽

Vol 2011 ◽

pp. 1-6 ◽

Cited By ~ 1

Author(s):

Ali A. Weinstein ◽

Preetha Abraham ◽

Guoqing Diao ◽

Stacey A. Zeno ◽

Patricia A. Deuster

Keyword(s):

Risk Factors ◽

Cardiovascular Disease ◽

African American ◽

Depressive Symptoms ◽

Disease Risk ◽

Cardiovascular Disease Risk ◽

Regression Analyses ◽

Cvd Risk Factors ◽

Cvd Risk ◽

The Relationship

Objective. To examine the relationship between depressive symptoms and cardiovascular disease (CVD) risk factors in a group of African American individuals.Design. A nonrandom sample of 253 (age 43.7 ± 11.6 years; 37% male) African American individuals was recruited by advertisements. Data were obtained by validated questionnaires, anthropometric, blood pressure, and blood sample measurements.Results. Regression analyses were performed to assess the relationship between depressive symptoms and CVD risk factors controlling for socioeconomic status indicators. These analyses demonstrated that those with higher levels of depressive symptoms had larger waist-to-hip ratios, higher percent body fat, higher triglycerides, and were more likely to be smokers.Conclusions. It has been well documented that higher levels of depressive symptoms are associated with higher CVD risk. However, this evidence is derived primarily from samples of predominantly Caucasian individuals. The present investigation demonstrates that depressive symptoms are related to CVD risk factors in African American individuals.

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Circulating Proangiogenic Cell Activity Is Associated with Cardiovascular Disease Risk

CrossRef Listing of Deleted DOIs ◽

10.1177/1087057112454919 ◽

2012 ◽

Vol 17 (9) ◽

pp. 1163-1170 ◽

Cited By ~ 8

Author(s):

Kreton Mavromatis ◽

Konstantinos Aznaouridis ◽

Ibhar Al Mheid ◽

Emir Veledar ◽

Saurabh Dhawan ◽

...

Keyword(s):

Risk Factors ◽

Cardiovascular Disease ◽

Bone Marrow ◽

Disease Risk ◽

Cardiovascular Disease Risk ◽

Cell Activity ◽

Atherosclerotic Cardiovascular Disease ◽

Cvd Risk ◽

The Relationship

Vascular injury mobilizes bone marrow–derived proangiogenic cells into the circulation, where these cells can facilitate vascular repair and new vessel formation. We sought to determine the relationship between a new biomarker of circulating bone marrow–derived proangiogenic cell activity, the presence of atherosclerotic cardiovascular disease (CVD) and its risk factors, and clinical outcomes. Circulating proangiogenic cell activity was estimated using a reproducible angiogenic colony-forming unit (CFU-A) assay in 532 clinically stable subjects aged 20 to 90 years and ranging in the CVD risk spectrum from those who are healthy without risk factors to those with active CVD. CFU-A counts increased with the burden of CVD risk factors ( p < 0.001). CFU-A counts were higher in subjects with symptomatic CVD than in those without ( p < 0.001). During follow-up of 232 subjects with CVD, CFU-A counts were higher in those with death, myocardial infarction, or stroke than in those without (110 [70–173] vs 84 [51–136], p = 0.01). Therefore, we conclude that circulating proangiogenic cell activity, as estimated by CFU-A counts, increases with CVD risk factor burden and in the presence of established CVD. Furthermore, higher circulating proangiogenic cell activity is associated with worse clinical outcome in those with CVD.

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The relationship between cardiovascular disease risk factors and gender

Health ◽

10.4236/health.2012.46051 ◽

2012 ◽

Vol 04 (06) ◽

pp. 309-315 ◽

Cited By ~ 5

Author(s):

Chung-Min Cho ◽

Young-Mi Lee

Keyword(s):

Risk Factors ◽

Cardiovascular Disease ◽

Disease Risk ◽

Cardiovascular Disease Risk ◽

Cardiovascular Disease Risk Factors ◽

And Gender ◽

The Relationship

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Relationship between sRAGE and hsCRP as Markers of Cardiovascular Disease Risk Factors in Diabetic and Non-Diabetic Men with Central Obesity

Molecular and Cellular Biomedical Sciences ◽

10.21705/mcbs.v1i2.14 ◽

2017 ◽

Vol 1 (2) ◽

pp. 70 ◽

Cited By ~ 1

Author(s):

Rambu Beppy Hamuaty ◽

Indriyanti Rafi Sukmawati ◽

Ferry Sandra

Keyword(s):

Central Obesity ◽

Disease Risk ◽

Inflammatory Marker ◽

Cardiovascular Disease Risk ◽

Fasting Blood Glucose ◽

High Sensitivity ◽

Strong Positive Correlation ◽

Protective Function ◽

Soluble Rage ◽

The Relationship

Background: Interaction between advanced glycation end product (AGE) and receptor for AGE (RAGE) triggers the escalation of inflammatory cytokine expressions. High-sensitivity C-reactive protein (hsCRP), an important inflammatory marker, has been reported to be modulated by soluble RAGE (sRAGE). However, the relationship between hsCRP and sRAGE in diabetes was not clearly described. Therefore present study was conducted to determine the relationship between sRAGE with hsCRP in men with central obese diabetic and non-diabetic. Materials and Methods: Adult men aged 25-60 years with central obese diabetes and non-diabetes, were recruited. Patient’s profiles were collected before the physical and blood examination. Physical examinations were conducted by measuring waist/abdomen, blood pressure, height, and weight. The routine blood test was performed to obtain concentrations of fasting blood glucose, HbA1c, hsCRP and sRAGE level.Results: Fifty-seven subjects with central obese and waist size ≥90 cm were selected. It was found that hsCRP values were significantly different (p=0.000) in HbA1c <6.5% dan HbA1c ≥6.5% groups. There was an inverse relationship between hsCRP and sRAGE levels for both in HbA1c <6.5% (r=-0.073) and HbA1c≥6.5% (r=-0.022) groups. In HbA1c ≥6.5% group, sRAGE showed strong positive correlation with 1 mg/dL ≤ hsCRP <3 mg/dL group (r>0.5).Conclusions: In the early stages of diabetes with hsCRP <1 mg/dL, the protective function was demonstrated with greater sRAGE levels. However, in further phase with 3 ≤ hsCRP < 10 mg/dL, the level of sRAGE was low, which is assumed to be associated with complications. Hence, sRAGE could be suggested as a complementary marker for hsCRP to evaluate diabetic men with central obesity.Keywords: sRAGE, hsCRP, diabetes, HbA1c, central obesity

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