Endocrine Reviews

2018

DOI: 10.1210/er.2018-00184

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The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk

Pratik B. Sandesara

¹

,

Salim S. Virani

²

,

³

et al.

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Cited by 303 publications

(254 citation statements)

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“…The mechanisms leading to accelerated atherosclerosis in hypertriglyceridemic states are complex and involve multiple lipoproteins. For instance, the direct causal determinants of atherosclerosis in hypertriglyceridemia are not triglycerides per se, but triglyceride-rich lipoproteins, which include VLDLs, chylomicrons, and their remnants (small VLDLs or intermediate density lipoprotein particles whose triglyceride has been hydrolyzed by lipoprotein lipase) (9). These lipoproteins are capable of entering the subintimal space and promote atherosclerosis through deposition of their cholesterol content in the atherosclerotic lesion (10).…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein B, Triglyceride-Rich Lipoproteins, and Risk of Cardiovascular Events in Persons with CKD

Lamprea‐Montealegre¹,

et al. 2019

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Background and objectives Triglyceride-rich lipoproteins may contribute to the high cardiovascular risk of patients with CKD. This study evaluated associations of apo-B and markers of triglyceride-rich lipoproteins with cardiovascular events in people with CKD.Design, setting, participants, & measurements Analyses were conducted in 9270 participants with CKD in the Study of Heart and Renal Protection (SHARP): 6245 not on dialysis (mean eGFR 26.5 ml/min per 1.73 m 2 ), and 3025 on dialysis when recruited. Cox regression methods were used to evaluate associations of lipids with incident atherosclerotic and nonatherosclerotic vascular events, adjusting for demographics and clinical characteristics. Hazard ratios (HRs) were calculated per 1 SD higher level for apo-B, HDL cholesterol, LDL cholesterol, triglyceride-rich lipoprotein cholesterol (i.e., total cholesterol minus LDL cholesterol minus HDL cholesterol), non-HDL cholesterol, log triglyceride, and log ratio of triglyceride to HDL cholesterol.Results During a median follow-up of 4.9 years (interquartile range, 4.0-5.5 years), 1406 participants experienced at least one atherosclerotic vascular event. In multivariable adjusted models, positive associations with atherosclerotic vascular events were observed for apo-B (HR per 1 SD, 1.19; 95% confidence interval, 1.12 to 1.27), triglycerides (1.06; 1.00 to 1.13), the ratio of triglyceride to HDL cholesterol (1.10; 1.03 to 1.18), and triglyceride-rich lipoprotein cholesterol (1.14; 1.05 to 1.25). By contrast, inverse associations with nonatherosclerotic vascular events were observed for each of these lipid markers: apo-B (HR per 1 SD, 0.92; 0.85 to 0.98), triglycerides (0.86; 0.81 to 0.92), the ratio of triglyceride to HDL cholesterol (0.88; 0.82 to 0.94), and triglyceride-rich lipoprotein cholesterol (0.85; 0.77 to 0.94).Conclusions Higher apo-B, triglycerides, ratio of triglyceride to HDL cholesterol, and triglyceride-rich lipoprotein cholesterol concentrations were associated with increased risk of atherosclerotic vascular events in CKD. Reducing triglyceride-rich lipoproteins using novel therapeutic agents could potentially lower the risk of atherosclerotic cardiovascular disease risk in the CKD population.

“…The mechanisms leading to accelerated atherosclerosis in hypertriglyceridemic states are complex and involve multiple lipoproteins. For instance, the direct causal determinants of atherosclerosis in hypertriglyceridemia are not triglycerides per se, but triglyceride-rich lipoproteins, which include VLDLs, chylomicrons, and their remnants (small VLDLs or intermediate density lipoprotein particles whose triglyceride has been hydrolyzed by lipoprotein lipase) (9). These lipoproteins are capable of entering the subintimal space and promote atherosclerosis through deposition of their cholesterol content in the atherosclerotic lesion (10).…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein B, Triglyceride-Rich Lipoproteins, and Risk of Cardiovascular Events in Persons with CKD

Lamprea‐Montealegre¹,

et al. 2019

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Background and objectives Triglyceride-rich lipoproteins may contribute to the high cardiovascular risk of patients with CKD. This study evaluated associations of apo-B and markers of triglyceride-rich lipoproteins with cardiovascular events in people with CKD.Design, setting, participants, & measurements Analyses were conducted in 9270 participants with CKD in the Study of Heart and Renal Protection (SHARP): 6245 not on dialysis (mean eGFR 26.5 ml/min per 1.73 m 2 ), and 3025 on dialysis when recruited. Cox regression methods were used to evaluate associations of lipids with incident atherosclerotic and nonatherosclerotic vascular events, adjusting for demographics and clinical characteristics. Hazard ratios (HRs) were calculated per 1 SD higher level for apo-B, HDL cholesterol, LDL cholesterol, triglyceride-rich lipoprotein cholesterol (i.e., total cholesterol minus LDL cholesterol minus HDL cholesterol), non-HDL cholesterol, log triglyceride, and log ratio of triglyceride to HDL cholesterol.Results During a median follow-up of 4.9 years (interquartile range, 4.0-5.5 years), 1406 participants experienced at least one atherosclerotic vascular event. In multivariable adjusted models, positive associations with atherosclerotic vascular events were observed for apo-B (HR per 1 SD, 1.19; 95% confidence interval, 1.12 to 1.27), triglycerides (1.06; 1.00 to 1.13), the ratio of triglyceride to HDL cholesterol (1.10; 1.03 to 1.18), and triglyceride-rich lipoprotein cholesterol (1.14; 1.05 to 1.25). By contrast, inverse associations with nonatherosclerotic vascular events were observed for each of these lipid markers: apo-B (HR per 1 SD, 0.92; 0.85 to 0.98), triglycerides (0.86; 0.81 to 0.92), the ratio of triglyceride to HDL cholesterol (0.88; 0.82 to 0.94), and triglyceride-rich lipoprotein cholesterol (0.85; 0.77 to 0.94).Conclusions Higher apo-B, triglycerides, ratio of triglyceride to HDL cholesterol, and triglyceride-rich lipoprotein cholesterol concentrations were associated with increased risk of atherosclerotic vascular events in CKD. Reducing triglyceride-rich lipoproteins using novel therapeutic agents could potentially lower the risk of atherosclerotic cardiovascular disease risk in the CKD population.

“…It is well known that patients with coronary heart disease (CHD) have high rates of event recurrence, 1 supporting the presence of "residual cardiovascular risk" in which, low high-density lipoprotein cholesterol (HDL-c) or high triglycerides (TG) and large triacylglycerol-rich lipoproteins (TRLs)-TG play a crucial role, suggesting the need of lifestyle changes to modulate the progression of disease. 2,3 More recently, the application of Mendelian randomization to large prospective studies supports that elevated TG (fasting and nonfasting) are causally implicated in cardiovascular disease (CVD), 4 and its treatment is now recommended. 5 Environmental conditions such as tobacco and alcohol consumption, sedentary habits, saturated fatty acids (SFA)rich diets 6 and genetic background 7 have been involved in the degree of postprandial hypertriglyceridemia (ppHTG).…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein E genetic variants interact with Mediterranean diet to modulate postprandial hypertriglyceridemia in coronary heart disease patients: CORDIOPREV study

¹

,

Alcalá‐Díaz

²

,

³

et al. 2019

Eur J Clin Investigation

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Background: We try to explore whether long-term consumption of two healthy dietary patterns (low-fat [LF] diet or Mediterranean diet [MedDiet]) interacts with the apolipoprotein E (APOE) single-nucleotide polymorphisms (SNPs: rs439401, rs440446 and rs7412) modulating postprandial hypertriglyceridemia (ppHTG) in coronary heart disease (CHD) patients. Methods and results: We selected patients from the CORDIOPREV study with genotyping and who underwent an oral fat load test (FLT) at baseline and after 3 years follow-up (n = 506). After 3 years of follow-up, we found a gene-diet interaction between the APOE rs439401 SNP and MedDiet. Specifically, T-allele carriers in the MedDiet group showed a more significant decrease in postprandial triglycerides (TG: P = 0.03) and large triacylglycerol-rich lipoproteins (TRLs) TG (large TRLs TG; P = 0.01) compared with CC subjects. Consistently, the area under the curve of TG (AUC-TG; P-interaction = 0.03) and AUC-large TRLs TG (P-interaction = 0.02)were significantly lower in T-allele carriers compared with CC subjects.

“…Persistent hypertriglyceridaemia indicates a significant residual cardiovascular risk, even in patients with well-controlled LDL cholesterol levels achieved by high-intensity statin regimens [18]. Currently, some components are available that can decrease TG, namely, fibrates, Omega-3 fatty acids, and nicotinic acid [19]. However, high-purity Omega-3 fatty acids products are not clinically available, and nicotinic acid drugs may raise blood sugar in patients [20].…”

Section: Discussionmentioning

confidence: 99%

Effects of Xuezhitong in Patients with Hypertriglyceridemia: a Multicentre, Randomized, Double-Blind, Double Simulation, Positive Drug and Placebo Parallel Control Study

¹

,

²

,

³

et al. 2020

Cardiovasc Drugs Ther

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Backgroud Xuezhitong (XZT) is an extract of Allium macrostemon Bunge that has lipid-lowering properties. Objective To evaluate the effects of XZT on lipids in subjects with hypertriglyceridemia (HTG) without severe dyslipidaemia. Methods A total of 358 subjects with HTG were enrolled and randomly assigned to receive XZT (2700 mg daily), xuezhikang (XZK) (1200 mg daily) or placebo. The primary endpoint was the reduction or percent reduction in the TG level over 12 weeks of treatment. Results At the 12-week follow-up, a reduction in the TG level from baseline was observed in both groups, but the XZT and XZK groups demonstrated a significantly greater reduction than the placebo group (30.77%, 24.02% vs 11.59%, P < 0.0167); 70.54% of subjects in the XZT group and 62.30% of subjects in the XZK group demonstrated reductions in TG levels of at least 20%, compared with 41.67% of the subjects in the placebo group (P < 0.0167). Treatment with XZT capsules also demonstrated superior performance compared with the placebo with respect to the control of lipids (17.97% vs 5.00%), total cholesterol (TC) (14.18% vs 3.89%), low-density lipoprotein cholesterol (LDL-C) (17.98% vs 2.95%), and high-density lipoprotein cholesterol (HDL-C) (21.47% vs 2.16%). Daily use of XZT for 12 weeks resulted in statistically significant (65.22% vs 38.30%, 25.00%; P < 0.0167) and clinically meaningful increases in HDL-C levels by ≥4 mg/dl compared with XZK and placebo. XZT was safe and well tolerated; the safety and tolerability profiles were similar across treatment groups. No subject experienced myopathy or markedly elevated liver transaminases or creatine kinase. Conclusions XZT significantly reduced TG levels and was well tolerated. Longer-term studies in more diverse patient populations are needed to corroborate these findings. Clinical Trial Registration www.chictr.org.cn Identifier: ChiCTR1900025854.

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