scholarly journals Effect of Vitamin D3 on the Postprandial Lipid Profile in Obese Patients: A Non-Targeted Lipidomics Study

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1194 ◽  
Author(s):  
Salvador Fernández-Arroyo ◽  
Anna Hernández-Aguilera ◽  
Marijke A. de Vries ◽  
Benjamin Burggraaf ◽  
Ellen van der Zwan ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Lipid Profile ◽  
Vitamin D3 ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Low Grade ◽  
Lipid Species ◽  
Increased Risk ◽  
Wide Range ◽  
Postprandial Lipid

Postprandial lipemia can lead to an accumulation of atherogenic lipoproteins in the circulation associated with systemic low-grade inflammation and an increased risk of cardiovascular disease. Lifestyle and pharmacological treatments are usually prescribed for prevention. Vitamin D3 (cholecalciferol), as an anti-atherogenic agent, is being taken into consideration due to its potential beneficial effects in lipid metabolism and its anti-inflammatory potency. To assess the effects of vitamin D3 in the postprandial lipid profile in obese, vitamin D-deficient women, a non-targeted lipidomics approach using liquid chromatography coupled to a quadrupole time-of flight mass spectrometer was used to identify and quantitate a wide-range of circulating lipid species, including diglycerides, lysophosphatidylcholines, phosphatidylcholines, phosphatidylethanolamines, sphingomyelins and triglycerides. The most important changes were found in plasmatic sphingomyelin levels, which experience a decrease after vitamin D3 intake. Our results suggest a turnover of sphingomyelins, probably due to an increased activity of neutral sphingomyelinases, and, therefore, with implications in the clearance of chylomicrons, LDL and VLDL, decreasing postprandial inflammation and macrophage adherence to endothelia, potentially improving cardiovascular disease risk.

Cardiovascular disease risk in survivors of 20 adult cancers.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 11571-11571
Author(s):  
Helen Strongman ◽  
Sarah Gadd ◽  
Anthony Matthews ◽  
Kathryn Mansfield ◽  
Susannah Jane Stanway ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cancer Survivors ◽  
Cox Regression ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Cancer Site ◽  
Cvd Risk ◽  
Increased Risk ◽  
Wide Range

11571 Background: There are concerns about long-term cardiovascular disease (CVD) risk in cancer survivors, but few studies have quantified the risks for a wide range of cancers and specific CVD outcomes. Methods: Using UK electronic health records, we identified cohorts of adults alive one year after a cancer diagnosis at 20 different sites. Risks of a range of CVD outcomes were compared to age, sex and general practice matched cancer free controls using Cox regression; crude and adjusted models were compared to investigate the role of shared cancer/CVD risk factors (e.g. smoking and diabetes). Results: 126 120 cancer survivors and 603 144 controls were followed over a median (IQR) 4.6 (2.5-8.1) and 5.6 (3.2-9.2) years. Crude and adjusted hazard ratios (HRs) were similar. In adjusted models, there was strong evidence (p<0.01) of increased risk of CVDs among cancer survivors compared with controls: venous thromboembolism (VTE, 18 cancers), heart failure/cardiomyopathy (7 cancers), arrhythmia (4 cancers), and stroke (3 cancers). In stratified analyses HRs were higher in younger people and continued beyond 5 years post diagnosis. Conclusions: We found increased long term CVD risk among survivors of several cancers compared to the general population, which varied by cancer site and specific CVD outcome.[Table: see text]

scholarly journals Plasma Dehydroepiandrosterone Sulfate and Cardiovascular Disease Risk in Older Men and Women

2020 ◽  
Vol 105 (12) ◽  
pp. e4304-e4327 ◽  
Author(s):  
Xiaoming Jia ◽  
Caroline Sun ◽  
Olive Tang ◽  
Ivan Gorlov ◽  
Vijay Nambi ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Dehydroepiandrosterone Sulfate ◽  
Mortality Data ◽  
Atherosclerosis Risk In Communities ◽  
Percentage Decrease ◽  
Increased Risk ◽  
Study Population

Abstract Context Lower dehydroepiandrosterone-sulfate (DHEA-S) levels have been inconsistently associated with coronary heart disease (CHD) and mortality. Data are limited for heart failure (HF) and association between DHEA-S change and events. Objective Assess associations between low DHEA-S/DHEA-S change and incident HF hospitalization, CHD, and mortality in older adults. Design DHEA-S was measured in stored plasma from visits 4 (1996-1998) and 5 (2011-2013) of the Atherosclerosis Risk in Communities study. Follow-up for incident events: 18 years for DHEA-S level; 5.5 years for DHEA-S change. Setting General community. Participants Individuals without prevalent cardiovascular disease (n = 8143, mean age 63 years). Main Outcome Measure Associations between DHEA-S and incident HF hospitalization, CHD, or mortality; associations between 15-year change in DHEA-S (n = 3706) and cardiovascular events. Results DHEA-S below the 15th sex-specific percentile of the study population (men: 55.4 µg/dL; women: 27.4 µg/dL) was associated with increased HF hospitalization (men: hazard ratio [HR] 1.30, 95% confidence interval [CI], 1.07-1.58; women: HR 1.42, 95% CI, 1.13-1.79); DHEA-S below the 25th sex-specific percentile (men: 70.0 µg/dL; women: 37.1 µg/dL) was associated with increased death (men: HR 1.12, 95% CI, 1.01-1.25; women: HR 1.19, 95% CI, 1.03-1.37). In men, but not women, greater percentage decrease in DHEA-S was associated with increased HF hospitalization (HR 1.94, 95% CI, 1.11-3.39). Low DHEA-S and change in DHEA-S were not associated with incident CHD. Conclusions Low DHEA-S is associated with increased risk for HF and mortality but not CHD. Further investigation is warranted to evaluate mechanisms underlying these associations.

scholarly journals Lipid profile of nutrition students and its association with cardiovascular disease risk factors

2001 ◽  
Vol 76 (2) ◽  
Author(s):  
Regina Mara Fisberg ◽  
Roberta Horschutz Stella ◽  
Juliana Masami Morimoto ◽  
Luciana Sicca Pasquali ◽  
Sonia Tucunduva Philippi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Lipid Profile ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Cardiovascular Disease Risk Factors

scholarly journals Effects of Bilberry Supplementation on Metabolic and Cardiovascular Disease Risk

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1653
Author(s):  
Sze Wa Chan ◽  
Brian Tomlinson
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Vision Loss ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Cardiovascular Complications ◽  
Increased Risk ◽  
Potential Benefits

Metabolic syndrome is a cluster of interrelated conditions that is associated with an increased risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). Oxidative stress may impair normal physiological functions, leading to various illnesses. T2DM is considered to be associated with increased oxidative stress, inflammation, and dyslipidemia, which may play a significant role in the development of cardiovascular complications, cancer and vision loss through cataracts and retinopathy. While conventional therapies are a cornerstone for the management of the major risk factors of metabolic syndrome, increasing antioxidant defense by increasing intake of antioxidant-rich foods may improve long term prospects in CVD, obesity and T2DM. Bilberry (Vaccinium myrtillus L.) is one of the richest natural sources of anthocyanins which give berries their red/purple/blue coloration. Anthocyanins are powerful antioxidants and are reported to play an important role in the prevention of metabolic disease and CVD as well as cancer and other conditions. This review focuses on the potential effects of bilberry supplementation on metabolic and cardiovascular risk factors. Although there is evidence to support the use of bilberry supplementation as part of a healthy diet, the potential benefits from the use of bilberry supplementation in patients with T2DM or CVD needs to be clarified in large clinical trials.

scholarly journals Novel Cardiovascular Biomarkers Associated with Increased Cardiovascular Risk in Women With Prior Preeclampsia/HELLP Syndrome: A Narrative Review

2021 ◽  
Vol 16 ◽  
Author(s):  
Esmee ME Bovee ◽  
Martha Gulati ◽  
Angela HEM Maas
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Hellp Syndrome ◽  
Troponin I ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Narrative Review ◽  
Elevated Liver Enzymes ◽  
Increased Risk ◽  
Cardiovascular Biomarkers

Evidence has shown that women with a history of preeclampsia or haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome have an increased risk of cardiovascular disease later in life. Recommendations for screening, prevention and management after such pregnancies are not yet defined. The identification of promising non-traditional cardiovascular biomarkers might be useful to predict which women are at greatest risk. Many studies are inconsistent and an overview of the most promising biomarkers is currently lacking. This narrative review provides an update of the current literature on circulating cardiovascular biomarkers that may be associated with an increased cardiovascular disease risk in women after previous preeclampsia/HELLP syndrome. Fifty-six studies on 53 biomarkers were included. From the summary of evidence, soluble fms-like tyrosine kinase-1, placental growth factor, interleukin (IL)-6, IL-6/IL-10 ratio, high-sensitivity cardiac troponin I, activin A, soluble human leukocyte antigen G, pregnancy-associated plasma protein A and norepinephrine show potential and are interesting candidate biomarkers to further explore. These biomarkers might be potentially eligible for cardiovascular risk stratification after preeclampsia/HELLP syndrome and may contribute to the development of adequate strategies for prevention of hypertension and adverse events in this population.

Should we Consider Lipoprotein (a) in Cardiovascular Disease Risk Assessment in Patients with Familial Hypercholesterolaemia?

2019 ◽  
Vol 24 (31) ◽  
pp. 3665-3671 ◽  
Author(s):  
Panagiotis Anagnostis ◽  
Pavlos Siolos ◽  
Dimitrios Krikidis ◽  
Dimitrios G. Goulis ◽  
John C. Stevenson
Keyword(s):  
Cardiovascular Disease ◽  
Familial Hypercholesterolaemia ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Pcsk9 Inhibitors ◽  
Cvd Risk ◽  
Lipoprotein A ◽  
Increased Risk

Background: Familial hypercholesterolaemia (FH) is a genetically determined lipid disorder, affecting 1 per 200-500 individuals in the general population. It is significantly and independently associated with an increased risk of Cardiovascular Disease (CVD), although it remains still an underrecognized and undertreated disease. Lipoprotein (a) [Lp(a)] is a low-density-lipoprotein (LDL)-like molecule, containing an additional protein, apolipoprotein (a). Objective: This review aims to present and discuss available data on the role of Lp(a) in patients with FH, in terms of its potential augmentation of CVD risk. Methods: A comprehensive search of the literature was performed to identify studies evaluating the CV effects of Lp(a) in patients with FH. Results: Lp(a) has been recognised as an independent risk factor for CVD, mainly coronary artery disease (CAD). Most, but not all, studies show increased Lp(a) concentrations in adults and children with FH. There is also evidence of an independent association between Lp(a) and CVD (mainly CAD) risk in these patients. Conclusion: Some therapeutic modalities, such as niacin, oestrogens, tibolone and proprotein convertase subtilisin/ kexin type 9 (PCSK9) inhibitors may effectively reduce Lp(a) concentrations by 25-30%, although their clinical benefit of this effect remains to be established.

scholarly journals Cohort study on the effects of depression on atherosclerotic cardiovascular disease risk in Korea

BMJ Open ◽  
2019 ◽  
Vol 9 (6) ◽  
pp. e026913 ◽  
Author(s):  
Yon Ho Jee ◽  
Hyoungyoon Chang ◽  
Keum Ji Jung ◽  
Sun Ha Jee
Keyword(s):  
Cardiovascular Disease ◽  
Cohort Study ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Population Based ◽  
Western World ◽  
Atherosclerotic Cardiovascular Disease ◽  
Cvd Risk ◽  
National Health Insurance System ◽  
Increased Risk

ObjectivesDepression has been reported to be a risk factor of cardiovascular disease in the western world, but the association has not yet been studied among Asian populations. The aim of this study was to investigate whether depression increases the risk of developing atherosclerotic cardiovascular disease (ASCVD) in a large Korean cohort study.DesignPopulation based cohort study.SettingDatabase of National Health Insurance System, Republic of Korea.Participants481 355 Koreans (260 695 men and 220 660 women) aged 40–80 years who had a biennial health check-up between 2002 and 2005.Main outcome measureThe main outcome in this study was the first ASCVD event (hospital admission or death).ResultsDepression increased the risk of developing ASCVD by 41% for men and 48% for women. In men, 3–4 outpatient visits for depression increased the risk of angina pectoris by 2.12 times (95% CI 1.55 to 2.90) and acute myocardial infarction by 2.29 times (95% CI 1.33 to 3.95). Depression was also associated with stroke in men (HR 1.29, 95% CI 1.19 to 1.39) and in women (HR 1.37, 95% CI 1.29 to 1.46). However, no increased risk of ASCVD was found for men who received 10 or more depressive treatments, compared with those without any outpatient visit for depression.ConclusionsIn this cohort, depressed people were at increased risk of ASCVD incidence. Therefore, individuals with depression may need routine monitoring of heart health that may prevent their future CVD risk.

scholarly journals Association of the Novel Inflammatory Marker GlycA and Incident Heart Failure and Its Subtypes of Preserved and Reduced Ejection Fraction

2020 ◽  
Vol 13 (8) ◽  
Author(s):  
Sunyoung Jang ◽  
Oluseye Ogunmoroti ◽  
Chiadi E. Ndumele ◽  
Di Zhao ◽  
Vishal N. Rao ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Ejection Fraction ◽  
Disease Risk ◽  
Inflammatory Marker ◽  
Cardiovascular Disease Risk ◽  
Unique Identifier ◽  
Acute Phase Reactants ◽  
Reduced Ejection Fraction ◽  
Increased Risk

Background: GlycA, a nuclear magnetic resonance composite marker of systemic inflammation, reflects serum concentration and glycosylation state of main acute phase reactants. Prior studies have shown plasma GlycA levels were associated with cardiovascular disease even after adjusting for other inflammatory markers. However, little is known about the association of GlycA with the heart failure (HF) subtypes: heart failure with preserved ejection fraction (HFpEF) or heart failure with reduced ejection fraction. We examined the association of GlycA with incident HF and its subtypes in a multiethnic cohort. Methods: We studied 6507 Multi-Ethnic Study of Atherosclerosis participants aged 45 to 84 without baseline cardiovascular disease or HF who had data on GlycA and incident hospitalized HF. We used multivariable-adjusted Cox hazards models to evaluate the association of GlycA with incident total HF, HFpEF, and heart failure with reduced ejection fraction. Models were adjusted for sociodemographics, cardiovascular disease risk factors, and inflammatory biomarkers. Results: The mean (SD) for age was 62 (10) years and for GlycA was 375 (82) μmol/L; 53% women. Over a median follow-up of 14.0 years, participants in the highest quartile of GlycA, compared with the lowest, experienced increased risk of developing any HF (hazard ratio, 1.48 [95% CI, 1.01–2.18]) in fully adjusted models. However, this increased risk was only seen for HFpEF (2.18 [1.15–4.13]) and not heart failure with reduced ejection fraction [1.06 (0.63–1.79)]. There was no significant interaction by sex, age, or race/ethnicity. Conclusions: GlycA was associated with an increased risk of any HF, and in particular, HFpEF. Future studies should examine mechanisms that might explain differential association of GlycA with HF subtypes, and whether therapeutic lowering of GlycA can prevent HFpEF development. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00005487.

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