Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women.

By Børge G. Nordestgaard, M. Benn, P. Schnohr, A. Tybjaerg-hansen. Journal of the American Medical Association (JAMA), 2007

2,075 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Surgery

View Paper: https://www.semanticscholar.org/paper/1a3904622c23421a6a601b57cb5511613722b50c

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Citations in the corpus

Major Lipids, Apolipoproteins, and Risk of Vascular Disease (2009, neutral): “Finally, in contrast with previous findings based on much less data, triglyceride concentration was not independently related with CHD risk after controlling for HDL-C, non–HDL-C, and other standard risk factors, including null findings in women and under nonfasting conditions.(21,22)”
A Meta-Analysis of Low-Density Lipoprotein Cholesterol, Non-High-Density Lipoprotein Cholesterol, and Apolipoprotein B as Markers of Cardiovascular Risk (2011, background): “We used 2 of these reports12,13 instead of ERFC-cited reports because the Copenhagen City Heart Study report cited by ERFC14 did not contain the necessary risk associations, and the Women’s Health Study report15 excluded women taking hormone replacement therapy.”
Triglyceride-Rich Lipoproteins and Atherosclerotic Cardiovascular Disease: New Insights From Epidemiology, Genetics, and Biology. (2016, positive): “Such higher risks in women than in men have also been observed previously(49) and were in the Copenhagen City Heart Study partly explained by confounding from higher alcohol intake in men than in women.(42) In other words, in men with low alcohol intake, the risks of ASCVD and all-cause mortality we”
Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. (2009, neutral): “Participants in the 1991-1994 examination by age, y 21-46 (n = 2204) 52 (48-55) 27 (25-30) 16 (14-18) 12 (11-13)”
Elevated Remnant Cholesterol Causes Both Low-Grade Inflammation and Ischemic Heart Disease, Whereas Elevated Low-Density Lipoprotein Cholesterol Causes Ischemic Heart Disease Without Inflammation (2013, methodology): “The Copenhagen City Heart Study (CCHS) is a prospective study of the Danish general population initiated in 1976 to 1978 with followup examinations in 1981 to 1983, 1991 to 1994, and 2001 to 2003.(13) Participants were recruited and examined exactly as in the CGPS.”
Major Lipids, Apolipoproteins, and Risk of Vascular Disease (2010, result): “Finally, in contrast with previous findings based on much less data, triglyceride concentration was not independently related with CHD risk after controlling for HDL-C, non–HDL-C, and other standard risk factors, including null findings in women and under nonfasting conditions.(21,22)”
European Guidelines on Cardiovascular Disease Prevention in Clinical Practice (Version 2012) (2012, positive): “There is evidence that non-fasting triglycerides may predict CHD risk even better, as individuals are in the postprandial state most of the time.(477) However, due to the lack of standardization, measuring non-fasting triglycerides is not recommended.”
Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management (2011, methodology): “Reproduced with modification from Nordestgaard et al.89 and Freiberg et al.90 Copyright& (2007, 2008) American Medical Association.”
2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. (2016, background): “PUFAs of the n-3 series have no hypocholesterolaemic effect; conversely, when they are used at high dosages (>3 g/day), the effect on LDL-C levels is either neutral or a slight increase [particularly with docosahexaenoic acid (DHA)] with a concomitant decrease of TGs. 165 A positive relationship exi”
The metabolic syndrome. (2003, positive): “Two recent large cohort studies found that nonfasting triglycerides were a significant risk factor for CHD and death in men and women and were a more robust indicator of risk than fasting levels [12, 13].”
Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points—a joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Med (2016, background): “Una razón, entre otras, para elegir el perfil lipídico en ayunas es el aumento de la concentración de triglicéridos observado durante una prueba de tolerancia grasa (26)(27); sin embargo, el aumento de triglicéridos plasmáticos observados en la mayoría de los individuos después de la ingesta habitua”