Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women

Bansal, Sandeep; Buring, Julie E.; Rifai, Nader; Mora, Samia; Sacks, Frank M.; Ridker, Paul M.

doi:10.1001/jama.298.3.309

Cited by 1,401 publications

(1,096 citation statements)

References 43 publications

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“…Historically, some studies have suggested that this association is attenuated by the inclusion of other potentially causal factors such as HDL‐C, thus raising the question of whether RLPs may represent a surrogate for other causative factors in atherosclerotic disease 12, 13. Recent Mendelian randomization studies have served as the strongest evidence that RLPs are etiologic for atherosclerosis 6, 14, 15, 16.…”

Section: Introductionmentioning

confidence: 99%

Remnant Lipoprotein Cholesterol and Incident Coronary Heart Disease: The Jackson Heart and Framingham Offspring Cohort Studies

Joshi

Khokhar

Massaro

et al. 2016

JAHA

141

102

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BackgroundRemnant lipoproteins (RLPs), the triglyceride‐enriched precursors to low‐density lipoprotein, are an emerging risk factor for coronary heart disease (CHD). We sought to determine the association of RLP cholesterol (RLP‐C) levels with incident CHD in 2 diverse, prospective, longitudinal observational US cohorts.Methods and ResultsWe analyzed cholesterol levels from serum lipoprotein samples separated via density gradient ultracentrifugation in 4114 US black participants (mean age 53.8 years, 64% women) from the Jackson Heart Study and a random sample of 818 predominantly white participants (mean age 57.3 years, 52% women) from the Framingham Offspring Cohort Study. Multivariable‐adjusted hazard ratios (HRs) for RLP‐C (the sum of very low‐density lipoprotein3 cholesterol and intermediate‐density lipoprotein cholesterol) were derived to estimate associations with incident CHD events consisting of myocardial infarction, CHD death, and revascularizations for each cohort separately and as a combined population. There were 146 CHD events in the combined population. After adjustments for age, sex, body mass index, smoking, blood pressure, diabetes, and lipid‐lowering therapy for the combined population, RLP‐C (HR 1.23 per 1‐SD increase, 95% CI 1.06–1.42, P<0.01) and intermediate‐density lipoprotein cholesterol (HR 1.26 per 1‐SD increase, 95% CI 1.08–1.47, P<0.01) predicted CHD during an 8‐year follow‐up. Associations were attenuated by high‐density lipoprotein cholesterol and ultimately lost significance with inclusion of real low‐density lipoprotein cholesterol, which excludes Lp(a) and IDL cholesterol fractions. Similar associations were seen in multivariable analyses within each cohort.Conclusion RLP‐C levels are predictive of incident CHD in this diverse group of primary prevention subjects. Interventions aimed at reducing RLP‐C to prevent CHD warrant further intensive investigation.Clinical Trial Registration URL: http://www.ClinicalTrials.gov. Unique identifier: NCT00415415.

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Section: Introductionmentioning

confidence: 99%

Remnant Lipoprotein Cholesterol and Incident Coronary Heart Disease: The Jackson Heart and Framingham Offspring Cohort Studies

Joshi

Khokhar

Massaro

et al. 2016

JAHA

141

102

View full text Add to dashboard Cite

show abstract

“…The extent and duration of the postprandial TAG response is recognised to be an important determinant of CHD risk (86)(87)(88)(89) , with ever-increasing population incidence, given its strong association with excess body weight. The impact of an exaggerated postprandial lipaemic response appears to be more evident in women relative to men.…”

Section: Nutrigenetics and Postprandial Lipaemiamentioning

confidence: 99%

Nutrigenetics and personalised nutrition: how far have we progressed and are we likely to get there?

Rimbach

Minihane

2009

Proc. Nutr. Soc.

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Nutrigenetics and personalised nutrition are components of the concept that in the future genotyping will be used as a means of defining dietary recommendations to suit the individual. Over the last two decades there has been an explosion of research in this area, with often conflicting findings reported in the literature. Reviews of the literature in the area of apoE genotype and cardiovascular health, apoA5 genotype and postprandial lipaemia and perilipin and adiposity are used to demonstrate the complexities of genotype-phenotype associations and the aetiology of apparent between-study inconsistencies in the significance and size of effects. Furthermore, genetic research currently often takes a very reductionist approach, examining the interactions between individual genotypes and individual disease biomarkers and how they are modified by isolated dietary components or foods. Each individual possesses potentially hundreds of 'atrisk' gene variants and consumes a highly-complex diet. In order for nutrigenetics to become a useful public health tool, there is a great need to use mathematical and bioinformatic tools to develop strategies to examine the combined impact of multiple gene variants on a range of health outcomes and establish how these associations can be modified using combined dietary strategies.

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“…Low HDL is a risk factor for CVD in addition to the more commonly known lipid risk factor -increased lowdensity lipoprotein (LDL). Although there is more controversy regarding the cardiovascular risk associated with high triglycerides, there are now several large trials suggesting that they are a risk factor for CVD, particularly in women [15,16]. The increase in triglycerides appears to be at least in part due to an increase in fatty acid (FA) turnover and delivery to the liver resulting in an increase in very low-density lipoprotein (VLDL) production [17].…”

Section: Obesity and Dyslipidemiamentioning

confidence: 99%

Cardiovascular consequences of obesity and targets for treatment

Mittendorfer

Peterson

2008

Drug Discovery Today: Therapeutic Strategies

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Obesity is a risk factor for cardiovascular disease, including coronary artery disease and heart failure, but the mechanisms by which it may cause them are not completely clear. Currently, therapies aimed at obesity-related cardiovascular disease include weight loss strategies and reduction of the other risk factors that are associated with obesity and cardiovascular disease. Other pathways with for potential drug development for obesity-related CVD are also discussed. Keywordsobesity; myocardium; metabolism; systolic function; diastolic function; coronary artery disease Cardiovascular disease (CVD) is still the leading cause of death in developed countries, despite a recent decline in coronary artery disease-related deaths. In the United States approximately 35% of all deaths are due to CVD [1]. Obesity (defined as a body mass index [BMI] of ≥ 30 kg/m 2 ) is a risk factor for CVD, especially coronary heart disease and heart failure. It is estimated that the relative risk of coronary heart disease in obesity is approximately 1.5 even after adjusting for all other traditional coronary heart disease risk factors that often co-migrate with obesity (e.g. hyperlipidemia, hypertension) [2]. Obesity also is associated with an increased risk of heart failure, with ~11 -14% of all heart failure thought to be attributable to obesity [3]. Given that excess body weight now affects more than 300 million persons worldwide, prevention and treatment of obesity should be considered one of the cornerstones for the prevention of CVD (http://www.who.int/dietphysicalactivity/publications/facts/obesity/en/). This review will focus on the impact of obesity on CVD, particularly atherosclerotic coronary artery disease and heart failure and treatment of obesity-related heart disease.

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Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women

Cited by 1,401 publications

References 43 publications

Remnant Lipoprotein Cholesterol and Incident Coronary Heart Disease: The Jackson Heart and Framingham Offspring Cohort Studies

Remnant Lipoprotein Cholesterol and Incident Coronary Heart Disease: The Jackson Heart and Framingham Offspring Cohort Studies

Nutrigenetics and personalised nutrition: how far have we progressed and are we likely to get there?

Cardiovascular consequences of obesity and targets for treatment

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