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Plasma triglyceride and coronary heart disease
Open accessAbstract
Although the literature on epidemiological associations between plasma triglyceride and CHD is not completely consistent, trends do emerge from the studies described here. First, the majority of observational studies demonstrate a significant univariate relation, although the results of case-control and cross-sectional studies are more uniform than those from prospective study designs. In many but not all studies, triglyceride remains a significant predictor of CHD in multivariate statistical analyses after controlling for TC or LDL-C. Perhaps the least consistent result is that the triglyceride association does not persist in some analyses controlling for HDL-C, while in other studies, the association remains significant. Although most studies have been conducted in men, the studies providing data on women, normocholesterolemic subjects, and diabetic subjects have generally found triglyceride to be, at the very least, a univariate risk factor. The results of intervention trials differ considerably, but no such study to date has been specifically designed to evaluate triglyceride-lowering effects on primary prevention of CHD. Important statistical properties must be taken into consideration in evaluating triglyceride as a risk factor for CHD. The large variability of triglyceride measurements and the correlation of triglyceride values with other lipid measures appears to result in the underestimation of the association between triglyceride and disease in multivariate analyses. Finally, individual genetic susceptibility may play an important role in the relation between plasma triglyceride levels and CHD. For example, risk of CHD clearly varies among the well-established familial forms of hypertriglyceridemia. A predominance of small, dense, LDL particles (LDL subclass pattern B) also appears to be a genetic trait associated with both increased risk of MI and increases in plasma triglyceride levels.
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“Recent advances in human genetics, together with a large body of epidemiologic, preclinical, and clinical trial results, provide strong support for a causal association between triglycerides (TG), TG-rich lipoproteins (TRL), and TRL remnants, and increased risk of myocardial infarction, ischaemic stroke, and aortic valve stenosis.”
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“Over the past three decades, epidemiologic and genetic evidence has accumulated to support the concept that elevated levels of plasma TG, TRL, and TRL remnants are causally related to an increased risk of ASCVD-related events—myocardial infarction (MI), stroke, and aortic valve stenosis—and all-cause mortality.1,2,17,19,20,24–28”
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“23.31.32 This work has clearly shown that it is much more difficult to establish a statistical association between hypertriglyceridemia and CAD than it is for total LDL and HDL cholesterol.”
InfluentialPathophysiology of Atherosclerosis
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“…explained by increased triglyceride (TG)-rich lipoprotein remnants 5) , a high prevalence of small dense low-density lipoprotein (sdLDL) particles 6) , and low levels of high-density lipoprotein (HDL)- indicate TG excess due to an increase in VLDL containing more TG than the average VLDL.…”
What should we do about Hypertriglyceridemia in Coronary Artery Disease Patients?
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“Studies have shown that elevated HDL appears to offer a protective effect in lowering the risk of CHD.(25,63,64) Conversely, low HDL cholesterol”
BackgroundRecent developments in the treatment of hypertriglyceridemia
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Alcohol's influence on plasma lipoproteins: A nonhuman primate model
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“Elevated plasma triglycerides increase the risk for car27 diovascular disease directly [1–3], or indirectly by decreas28 ing plasma high-density lipoprotein (HDL) cholesterol con29 centrations[4,5], increasing the levels of smaller, denser 30 low-density lipoprotein (LDL) particles in plasma [6,7], or 31 affecting oth…”
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“Moreover, the putative role of hypertriacylglycerolaemia as an independent risk factor in the development of heart disease (Castelli, 1986; Austin, 1991) may also involve an interaction between cholesterol and dietary fat intake.”
BackgroundLipoprotein disorder in brain infarction and hemorrhage
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Metadata
- Authors
- Austin, M. A.
- Affiliations
- University of Washington (US)
- Corresponding author
- Austin, M A
- Venue
- Arteriosclerosis and Thrombosis: A Journal of Vascular Biology
- Published
- 1991-01
- Volume
- 11
- Issue
- 1
- Pages
- 2-14
- ISSN
- 1049-8834 (ISSN-L)
- OpenAlex
- W2155238815
- Cited by
- 697
- References
- 98
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 7 · 2022: 6 · 2021: 5 · 2020: 3 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 8 · 2015: 5 · 2014: 5 · 2013: 13 · 2012: 8
- FWCI
- 15.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arteriosclerosis and Thrombosis A Journal of Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (7r29hl038760-03)
- National Heart, Lung, and Blood Institute (HL38760, P01HL030086, HL3-0086)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- plasma triglycerides, coronary artery disease, cardiovascular risk factors, hypertriglyceridemia, familial hypertriglyceridemia, small dense LDL, HDL cholesterol, genetic susceptibility, primary prevention, lipid-lowering intervention
- MeSH terms
- Coronary Disease, Female, Humans, Male, Pedigree, Triglycerides, Multivariate Analysis
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