Triglycerides and cardiovascular disease

Nordestgaard, Børge G.; Varbo, Anette

doi:10.1016/s0140-6736(14)61177-6

Cited by 1,151 publications

(937 citation statements)

References 72 publications

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“…Elevated levels of triglyceride are associated with increasing risk of coronary heart disease 26. As expected, triglyceride levels were significantly reduced in the omega‐3 ethyl‐ester group compared with the control group.…”

Section: Discussionsupporting

confidence: 69%

Effect of Eicosapentaenoic and Docosahexaenoic Acids Added to Statin Therapy on Coronary Artery Plaque in Patients With Coronary Artery Disease: A Randomized Clinical Trial

Alfaddagh

Elajami

Ashfaque

et al. 2017

JAHA

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BackgroundAlthough statins reduce cardiovascular events, residual risk remains. Therefore, additional modalities are needed to reduce risk. We evaluated the effect of eicosapentaenoic acid and docosahexaenoic acid in pharmacologic doses added to statin treatment on coronary artery plaque volume.Methods and ResultsA total of 285 subjects with stable coronary artery disease on statins were randomized to omega‐3 ethyl‐ester (1.86 g of eicosapentaenoic acid and 1.5 g of docosahexaenoic acid daily) or no omega‐3 (control) for 30 months. Coronary plaque volume was assessed by coronary computed tomographic angiography. Mean (SD) age was 63.0 (7.7) years; mean low‐density lipoprotein cholesterol ≤80 mg/dL. In the intention‐to‐treat analysis, our primary endpoint, noncalcified plaque volume, was not different between groups (P=0.14) but approached significance in the per protocol analysis (P=0.07). When stratified by age in the intention‐to‐treat analysis, younger omega‐3 subjects had significantly less progression of the primary endpoint, noncalcified plaque (P=0.013), and fibrous, calcified and total plaque. In plaque subtype analysis, controls had significant progression of fibrous plaque compared to no change in the omega‐3 ethyl‐ester group (median % change [interquartile range], 5.0% [−5.7, 20.0] versus −0.1% [−12.3, 14.5], respectively; P=0.018). Among those on low‐intensity statins, omega‐3 ethyl‐ester subjects had attenuation of fibrous plaque progression compared to controls (median % change [interquartile range], 0.3% [−12.8, 9.0] versus 4.8% [−5.1, 19.0], respectively; P=0.032). In contrast, those on high‐intensity statins had no difference in plaque change in either treatment arm.ConclusionsHigh‐dose eicosapentaenoic acid and docosahexaenoic acid provided additional benefit to statins in preventing progression of fibrous coronary plaque in subjects adherent to therapy with well‐controlled low‐density lipoprotein cholesterol levels. The benefit on low‐intensity statin, but not high‐intensity statin, suggests that statin intensity affects plaque volume.Clinical Trial Registration URL: http://www.ClinicalTrials.gov. Unique identifier: NCT01624727.

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Section: Discussionsupporting

confidence: 69%

Effect of Eicosapentaenoic and Docosahexaenoic Acids Added to Statin Therapy on Coronary Artery Plaque in Patients With Coronary Artery Disease: A Randomized Clinical Trial

Alfaddagh

Elajami

Ashfaque

et al. 2017

JAHA

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“…This index performed better than other surrogates (including fasting insulin, HOMA‐IR, insulin‐to‐glucose ratio, and the Bennett index) in predicting IR in normoglycemic individuals in New Zealand, with a specificity of 0.91 and a sensitivity of 0.75 10. In addition, there is evidence from a number of studies that increased triglyceride levels are an additional causal risk factor for CVD 33, 34, 35. Taken together, these findings suggest that the McAuley index may be superior to other steady‐state measures such as HOMA‐IR in predicting CHD, and also in assessing IR among blacks, but this index has not been validated in this population.…”

Section: Discussionmentioning

confidence: 90%

Sex Differences in the Association Between Insulin Resistance and Incident Coronary Heart Disease and Stroke Among Blacks Without Diabetes Mellitus: The Jackson Heart Study

Effoe

Wagenknecht

Tcheugui

et al. 2017

JAHA

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BackgroundStudies exploring the association between insulin resistance (IR) and cardiovascular disease in blacks have not been conclusive, especially for coronary heart disease (CHD). The McAuley index and homeostasis model assessment of IR (HOMA‐IR) perform differently in predicting cardiovascular disease. We investigated this association in the Jackson Heart Study, a large longitudinal cohort of blacks.Methods and Results IR was estimated for 3565 participants without diabetes mellitus and cardiovascular disease at baseline using the McAuley index and HOMA‐IR, and their associations with incident CHD and stroke (composite outcome) were compared. A lower McAuley index and higher HOMA‐IR are indicative of IR. Cox regression analysis was used to estimate adjusted hazard ratios for incident CHD and/or stroke. There were 158 events (89 CHD‐only, 58 stroke‐only, and 11 CHD/stroke) over a median follow‐up of 8.4 years. After adjustment for demographic factors, the risk of the composite outcome decreased with each SD increase in the McAuley index (hazard ratio 0.80; 95% CI: 0.67–0.96), with no attenuation after further accounting for CHD and stroke risk factors. When considered individually, McAuley index and HOMA‐IR were associated with CHD (hazard ratio 0.71, 95% CI: 0.55–0.92 and hazard ratio 1.33, 95% CI: 1.03–1.72, respectively), but not stroke risk. The logHOMA‐IR and CHD association was present in men, but not in women (P interaction=0.01).ConclusionsBoth HOMA‐IR and the McAuley index demonstrate strong associations with CHD but not stroke risk in blacks. The logHOMA‐IR and CHD association was present in men, but not in women.

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“…However, among individuals with achieved lower levels of LDL‐C, atherosclerotic cardiovascular disease (ASCVD) events continue to occur with unacceptable frequency 4. Such residual risk may reflect aspects of atherogenesis not captured by LDL‐C, including effects of very‐low‐density lipoproteins (VLDLs) and their contents (cholesterol and triglycerides) 5, 6, 7, 8, 9. Enzymatic hydrolysis of VLDL results in the formation of smaller, cholesterol‐enriched lipoprotein particles,5, 10, 11 which experimental studies suggest could contribute to the development of ASCVD 5, 7, 10, 12, 13, 14, 15, 16.…”

mentioning

confidence: 99%

Residual Risk of Atherosclerotic Cardiovascular Events in Relation to Reductions in Very‐Low‐Density Lipoproteins

Lawler

Akinkuolie

Harada

et al. 2017

JAHA

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BackgroundIt is uncertain whether pharmacological reductions in very‐low‐density lipoproteins (VLDLs), and their component triglyceride and cholesterol could reduce residual risk of atherosclerotic cardiovascular disease (ASCVD) events among individuals in whom low‐density lipoprotein cholesterol (LDL‐C) has been adequately lowered. We examined whether individuals with greater on‐statin reductions in VLDL‐related measures—beyond reductions in LDL‐C—were at further reduced risk of ASCVD.Methods and ResultsIn 9423 participants in the JUPITER (Justification for the Use of Statins in Prevention) trial (NCT00239681), at baseline and on statin we measured standard lipids, 400‐MHz proton nuclear magnetic resonance spectroscopy‐measured VLDL particle subclasses (small, medium, and large VLDL lipoprotein particle concentration), and total VLDL cholesterol mass. Compared with individuals allocated to placebo, we examined risk of incident ASCVD (N=211) among statin‐allocated participants who achieved minimal (

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Triglycerides and cardiovascular disease

Cited by 1,151 publications

References 72 publications

Effect of Eicosapentaenoic and Docosahexaenoic Acids Added to Statin Therapy on Coronary Artery Plaque in Patients With Coronary Artery Disease: A Randomized Clinical Trial

Effect of Eicosapentaenoic and Docosahexaenoic Acids Added to Statin Therapy on Coronary Artery Plaque in Patients With Coronary Artery Disease: A Randomized Clinical Trial

Sex Differences in the Association Between Insulin Resistance and Incident Coronary Heart Disease and Stroke Among Blacks Without Diabetes Mellitus: The Jackson Heart Study

Residual Risk of Atherosclerotic Cardiovascular Events in Relation to Reductions in Very‐Low‐Density Lipoproteins

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