REVIEWS, ABSTRACTS, AND ORIGINAL ARTICLES
Authored Publications
NUMBER OF PUBLICATIONS:
91
Journal of the American Heart Association
Cardiovascular Outcomes with Icosapent Ethyl by Baseline Low‐Density Lipoprotein Cholesterol: A Secondary Analysis of the REDUCE‐IT Randomized Trial
14(5):e038656
2025 Feb 19
Background: The efficacy of icosapent ethyl among patients with very well-controlled baseline low-density lipoprotein cholesterol (LDL-C) is unknown.
Methods: In this post hoc analysis of the REDUCE-IT (Reduction of Cardiovascular Events With Icosapent Ethyl-Intervention Trial) randomized clinical trial, statin-treated patients with high cardiovascular risk, elevated triglycerides (135-499 mg/dL), and baseline LDL-C of 41 to 100 mg/dL were included. Patients were randomized to icosapent ethyl (2 g twice daily) or placebo and then post hoc stratified by baseline LDL-C (<55 mg/dL versus ≥55 mg/dL). The primary composite end point included cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, coronary revascularization, or unstable angina.
Results: Among 8175 patients with baseline LDL-C data, 7117 (87.1%) had LDL-C ≥55 mg/dL and 1058 (12.9%) had LDL-C <55 mg/dL. In patients with LDL-C <55 mg/dL, the rate of the primary composite end point was lower in the icosapent ethyl group (16.2% versus 22.8%) than in the placebo group (hazard ratio [HR], 0.66 [95% CI, 0.50-0.87]; absolute risk reduction, 6.6%; P=0.003). Among patients with LDL-C ≥55 mg/dL, a primary composite end point event occurred in a lower proportion of patients in the icosapent ethyl group (17.4% versus 21.9%) than in the placebo group (HR, 0.76 [95% CI, 0.69-0.85]; absolute risk reduction, 4.5%; P<0.0001). No significant interaction was observed between baseline LDL-C and treatment group (P for interaction=0.40). Findings were consistent among secondary cardiovascular end points and in sensitivity analyses.
Conclusions: Among statin-treated patients with elevated triglycerides and high cardiovascular risk, icosapent ethyl reduced the rate of cardiovascular end points irrespective of baseline LDL-C, including among eligible patients with optimal LDL-C control.
Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01492361.
Keywords: cardiovascular outcomes; icosapent ethyl; low‐density lipoprotein cholesterol.
The Lancet Diabetes & Endocrinology
Effect of sotagliflozin on major adverse cardiovascular events: a prespecified secondary analysis of the SCORED a randomised trial
S2213-8587(24)00362-0
2025 Feb 13
Background: Sodium-glucose co-transporter (SGLT)-2 inhibitors have shown consistent benefit in improving heart failure-related outcomes but not ischaemic cardiovascular events such as myocardial infarction or stroke. We assessed if the dual SGLT1/2 inhibitor sotagliflozin improves ischaemic outcomes.
Methods: We did a prespecified secondary analysis of the SCORED trial, which was a double-blind, placebo-controlled, randomised clinical trial enrolling patients (aged ≥18 years) with type 2 diabetes, chronic kidney disease (estimated glomerular filtration rate [eGFR] 25-60 mL/min per 1·73 m2), and additional cardiovascular risk factors. Patients at 750 sites in 44 countries were randomly assigned (1:1) to oral sotagliflozin or placebo via an interactive response technology system (block size of four; stratified by heart failure-related criteria and geographical region), with participants, investigators, and study staff, including those who assessed outcomes, masked to group assignment. Sotagliflozin treatment was prescribed at 200 mg once a day, with the dose increased to 400 mg once a day within the first 6 months if tolerated. Matching placebo was prescribed at the same treatment frequency as the intervention regimen. A prespecified secondary outcome was total major adverse cardiovascular events (MACE), which was defined as a composite of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke, assessed as first and subsequent events. Other outcomes included total myocardial infarction and total stroke (fatal and non-fatal events) as individual post-hoc endpoints. Outcomes were assessed by intention to treat with competing-risk proportional hazard models in the overall population, and, for total MACE, in prespecified subgroups stratified by baseline demographic and clinical features (sex, age, geographical region, heart failure-related criteria, eGFR, urine albumin-creatinine ratio, and cardiovascular disease history). The SCORED trial was registered at ClinicalTrials.gov, NCT03315143, and was ended early due to loss of funding.
Findings: 10 584 patients were enrolled and randomly assigned to sotagliflozin (n=5292 [50·0%]) or placebo (n=5292 [50·0%]) between Dec 8, 2017 and Jan 20, 2020 (median age 69 years [IQR 63-74]; 4754 [44·9%] female patients and 5830 [55·1%] male patients). 5144 (48·6%) patients had a history of cardiovascular disease, of whom 2108 (19·9% of the total population) had a history of myocardial infarction, 946 (8·9%) had a history of stroke, and 2375 (22·4%) had a history of coronary revascularisation. Patients in the sotagliflozin group had a significantly lower rate of total MACE than those in the placebo group (4·8 events per 100 person-years vs 6·3 events per 100 person-years; hazard ratio [HR] 0·77 [95% CI 0·65-0·91]; p=0·0020). Interaction analyses suggested a consistent effect of sotagliflozin on total MACE among stratified subgroups without evidence of heterogeneity. Additionally, sotagliflozin significantly reduced the rate of myocardial infarction (1·8 events per 100 person-years vs 2·7 events per 100 person-years; HR 0·68 [0·52-0·89]; p=0·0041) and stroke (1·2 events per 100 person-years vs 1·8 events per 100 person-years; HR 0·66 [0·48-0·91]; p=0·012) compared with placebo.
Interpretation: Sotagliflozin reduced MACE, with independent reductions in myocardial infarction and stroke, among patients with type 2 diabetes, chronic kidney disease, and additional cardiovascular risk. The ischaemic benefit on both myocardial infarction and stroke has not been previously observed with other SGLT inhibitors and warrants investigation of combined SGLT1 and SGLT2 inhibition as a possible underlying mechanism.
Funding: Lexicon Pharmaceuticals.
Copyright © 2025 Elsevier Ltd. All rights reserved, including those for text and data mining, AI training, and similar technologies.
Arteriosclerosis, Thrombosis, and Vascular Biology
“A Time to Tear Down and a Time to Mend” – The Role of Eicosanoids in Atherosclerosis
44(11):2258-2263
2024 Oct 23
The wisdom of Solomon manifests throughout the natural world, in which the cycle of destruction and rebuilding sustains life and health. For example, the body’s response to pathogens or acute tissue injury sets in motion the pathophysiologic process of inflammation. In precise fashion, the activated innate immune system triggers resident immune cells (eg, CCR2− [C-C motif chemokine receptor 2] macrophages) to recruit circulating leukocytes to the inflamed tissue (neutrophils are generally the first responders) and...
European Journal of Preventive Cardiology
Omega-3 fatty acids for Cardiovascular Event Lowering
31(8):1005-1014
2024 Jun 3
Low-density lipoprotein cholesterol (LDL-C) is the main target for therapeutics aimed at reducing the risk of atherosclerotic cardiovascular disease (ASCVD) and downstream cardiovascular (CV) events. However, multiple studies have demonstrated that high-risk patient populations harbour residual risk despite effective LDL-C lowering. While data support the causal relationship between triglycerides and ASCVD risk, triglyceride-lowering therapies such as omega-3 fatty acids have shown mixed results in CV outcomes trials. Notably, icosapent ethyl, a purified formulation of eicosapentaenoic acid (EPA), has garnered compelling evidence in lowering residual CV risk in patients with hypertriglyceridaemia and treated with statins. In this review, we summarize studies that have investigated omega-3-fatty acids for CV event lowering and discuss the clinical implementation of these agents based on trial data and guidelines.
Keywords: atherosclerotic cardiovascular disease; icosapent ethyl; omega-3 fatty acids.
© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.
Journal of the American Heart Association
Eicosapentaenoic acid improves endothelial nitric oxide bioavailability via changes in protein expression during inflammation
13(14):e034076
2024 Jul 16
Background: Endothelial cell (EC) dysfunction involves reduced nitric oxide (NO) bioavailability due to NO synthase uncoupling linked to increased oxidation and reduced cofactor availability. Loss of endothelial function and NO bioavailability are associated with inflammation, including leukocyte activation. Eicosapentaenoic acid (EPA) administered as icosapent ethyl reduced cardiovascular events in REDUCE-IT (Reduction of Cardiovascular Events With Icosapent Ethyl-Intervention Trial) in relation to on-treatment EPA blood levels. The mechanisms of cardiovascular protection for EPA remain incompletely elucidated but likely involve direct effects on the endothelium.
Methods and results: In this study, human ECs were treated with EPA and challenged with the cytokine IL-6 (interleukin-6). Proinflammatory responses in the ECs were confirmed by ELISA capture of sICAM-1 (soluble intercellular adhesion molecule-1) and TNF-α (tumor necrosis factor-α). Global protein expression was determined using liquid chromatography-mass spectrometry tandem mass tag. Release kinetics of NO and peroxynitrite were monitored using porphyrinic nanosensors. IL-6 challenge induced proinflammatory responses from the ECs as evidenced by increased release of sICAM-1 and TNF-α, which correlated with a loss of NO bioavailability. ECs pretreated with EPA modulated expression of 327 proteins by >1-fold (P<0.05), compared with IL-6 alone. EPA augmented expression of proteins involved in NO production, including heme oxygenase-1 and dimethylarginine dimethylaminohydrolase-1, and 34 proteins annotated as associated with neutrophil degranulation. EPA reversed the endothelial NO synthase uncoupling induced by IL-6 as evidenced by an increased [NO]/[peroxynitrite] release ratio (P<0.05).
Conclusions: These direct actions of EPA on EC functions during inflammation may contribute to its distinct cardiovascular benefits.
Keywords: eicosapentaenoic acid; endothelial function; nitric oxide; proteomics.
Cardiovascular Research
Do Patients Benefit from Omega-3 Fatty Acids?
119(18):2884-2901
2024 Feb 17
Omega-3 fatty acids (O3FAs) possess beneficial properties for cardiovascular (CV) health and elevated O3FA levels are associated with lower incident risk for CV disease (CVD.) Yet, treatment of at-risk patients with various O3FA formulations has produced disparate results in large, well-controlled and well-conducted clinical trials. Prescription formulations and fish oil supplements containing low-dose mixtures of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have routinely failed to prevent CV events in primary and secondary prevention settings when added to contemporary care, as shown most recently in the STRENGTH and OMEMI trials. However, as observed in JELIS, REDUCE-IT, and RESPECT-EPA, EPA-only formulations significantly reduce CVD events in high-risk patients. The CV mechanism of action of EPA, while certainly multifaceted, does not depend solely on reductions of circulating lipids, including triglycerides (TG) and LDL, and event reduction appears related to achieved EPA levels suggesting that the particular chemical and biological properties of EPA, as compared to DHA and other O3FAs, may contribute to its distinct clinical efficacy. In vitro and in vivo studies have shown different effects of EPA compared with DHA alone or EPA/DHA combination treatments, on atherosclerotic plaque morphology, LDL and membrane oxidation, cholesterol distribution, membrane lipid dynamics, glucose homeostasis, endothelial function, and downstream lipid metabolite function. These findings indicate that prescription-grade, EPA-only formulations provide greater benefit than other O3FAs formulations tested. This review summarizes the clinical findings associated with various O3FA formulations, their efficacy in treating CV disease, and their underlying mechanisms of action.
Keywords: Atherosclerosis; Cardiovascular outcome trials; Cholesterol; Docosahexaenoic acid; Eicosapentaenoic acid; Endothelial function; Lipid oxidation; Omega-3 fatty acids.
© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.
Cardiovascular Research
Do patients benefit from omega-3 fatty acids?
119(18):2884-2901
2024 Feb 17
Omega-3 fatty acids (O3FAs) possess beneficial properties for cardiovascular (CV) health and elevated O3FA levels are associated with lower incident risk for CV disease (CVD.) Yet, treatment of at-risk patients with various O3FA formulations has produced disparate results in large, well-controlled and well-conducted clinical trials. Prescription formulations and fish oil supplements containing low-dose mixtures of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have routinely failed to prevent CV events in primary and secondary prevention settings when added to contemporary care, as shown most recently in the STRENGTH and OMEMI trials. However, as observed in JELIS, REDUCE-IT, and RESPECT-EPA, EPA-only formulations significantly reduce CVD events in high-risk patients. The CV mechanism of action of EPA, while certainly multifaceted, does not depend solely on reductions of circulating lipids, including triglycerides (TG) and LDL, and event reduction appears related to achieved EPA levels suggesting that the particular chemical and biological properties of EPA, as compared to DHA and other O3FAs, may contribute to its distinct clinical efficacy. In vitro and in vivo studies have shown different effects of EPA compared with DHA alone or EPA/DHA combination treatments, on atherosclerotic plaque morphology, LDL and membrane oxidation, cholesterol distribution, membrane lipid dynamics, glucose homeostasis, endothelial function, and downstream lipid metabolite function. These findings indicate that prescription-grade, EPA-only formulations provide greater benefit than other O3FAs formulations tested. This review summarizes the clinical findings associated with various O3FA formulations, their efficacy in treating CV disease, and their underlying mechanisms of action.
Journal of the American College of Cardiology
Lipoprotein(a) Blood Levels and Cardiovascular Risk Reduction with Icosapent Ethyl
83 (16):1529-1539
2024 Apr 23
Background: Elevated lipoprotein(a) (Lp[a]) concentrations are associated with increased cardiovascular event risk even in the presence of well-controlled low-density lipoprotein cholesterol levels, but few treatments are documented to reduce this residual risk.
Objectives: The aim of this post hoc analysis of REDUCE-IT (Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial) was to explore the cardiovascular benefit of icosapent ethyl (IPE) across a range of Lp(a) levels.
Methods: A total of 8,179 participants receiving statin therapy with established cardiovascular disease or age ≥50 years with diabetes and ≥1 additional risk factor, fasting triglyceride 1.69 to 5.63 mmol/L, and low-density lipoprotein cholesterol 1.06 to 2.59 mmol/L were randomized to receive 2 g twice daily of IPE or matching placebo. Relationships between continuous baseline Lp(a) mass concentration and risk for first and total (first and subsequent) major adverse cardiovascular events (MACE) were analyzed, along with the effects of IPE on first MACE among those with Lp(a) concentrations ≥50 or <50 mg/dL.
Results: Among 7,026 participants (86% of those randomized) with baseline Lp(a) assessments, the median concentration was 11.6 mg/dL (Q1-Q3: 5.0-37.4 mg/dL). Lp(a) had significant relationships with first and total MACE (P < 0.0001), while event reductions with IPE did not vary across the range of Lp(a) (interaction P > 0.10). IPE significantly reduced first MACE in subgroups with concentrations ≥50 and <50 mg/dL.
Conclusions: Baseline Lp(a) concentration was prognostic for MACE among participants with elevated triglyceride levels receiving statin therapy. Importantly, IPE consistently reduced MACE across a range of Lp(a) levels, including among those with clinically relevant elevations.
Keywords: Lp(a); icosapent ethyl; triglycerides.
Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.
Cholesterol Crystals in Atherosclerosis and Other Related Diseases
Omega-3 Fatty Acids Influence Membrane Cholesterol Distribution and Crystal Formation in Models of Atherosclerosis
pp. 297-318
2023 Nov 23
Cholesterol crystals commonly localize in atherosclerotic lesions where they promote inflammation and disease progression. These crystals are distributed throughout the necrotic lipid core as well as areas associated with active macrophage recruitment, suggesting an early role in lesion development. Cholesterol crystal formation typically begins in the cell membrane—the site where cholesterol concentrates while serving essential structural and functional roles. When membrane cholesterol levels rise above a critical point, cholesterol will self-associate into its own nanodomains, which disrupt membrane function and nucleate the formation of extracellular crystals. Are also induced by membrane lipid oxidation also favors cholesterol domain and crystal formation, especially under conditions of hyperglycemia. In the cytosol, cholesterol crystals activate inflammasomes and associated pathways following lysosomal damage, resulting in cytokine activation and inflammatory responses. These crystals can undergo rapid expansion, extending into the extracellular space of the atherosclerotic lesion, resulting in cell death and ultimately fibrous cap disruption. Omega-3 fatty acids (n3-FAs) mitigate these effects as they readily incorporate into cell membranes, and influence cholesterol distribution, lipid raft formation, and sterol crystallization. Eicosapentaenoic acid (EPA), in particular, inhibits cholesterol domain formation due to its potent antioxidant and membrane stabilizing effects. Clinical trials have shown that EPA can reduce composite CV events in statin-treated, high-risk patients while reducing plaque volume and increasing fibrous cap thickness. Other long-chain fatty acids such as docosahexaenoic acid (DHA) or mixed EPA/DHA formulations did not produce these benefits. Understanding the mechanisms by which EPA disrupts cholesterol crystal formation will provide novel insights into the cardioprotective effects of these agents and their role in treating CV disease.
European Heart Journal
Eicosapentaenoic acid, arachidonic acid, and triglyceride levels mediate most of the benefit of icosapent ethyl in REDUCE-IT
44:ehad6551309
2023 Nov 09
Background
In REDUCE-IT, icosapent ethyl (IPE) reduced major adverse cardiovascular (CV) events (MACE) relative to placebo (PBO) in 8179 statin-treated patients with residual hypertriglyceridemia and high CV risk. Questions have been raised about the mechanisms of benefit of IPE and the potential effects of the pharmaceutical grade mineral oil PBO on the results.
Purpose
The contributions of eicosapentaenoic acid (EPA), arachidonic acid (AA), triglycerides (TG), and other biomarkers (listed in Table 1) to MACE reduction by IPE relative to PBO were quantified via mediation analyses to illustrate the mechanisms of IPE.
Methods
Patients were randomised 1:1 to IPE 4 g/day or PBO and followed for a median 4.9 years. For a biomarker to be a mediator, there had to be both a treatment group difference on the biomarker and an association between the biomarker and risk of MACE. For the first condition, treatment group differences in change from baseline in each biomarker were analysed by mixed effects repeated measures models. For the second condition, time-varying values of each biomarker were related to the risk of MACE by calculating the time-weighted moving average (TWMA) for each variable, using all values for a given patient. Each was analysed in a Cox regression model with time to MACE as the outcome and TWMA values as time-varying covariates. The individual and joint mediation of those biomarkers determined to be mediators were assessed in Cox models that included treatment assignment. Biomarkers individually found to be ³10% mediators in absolute terms were included in the multivariable models. If biomarkers that would otherwise be included in multivariable models were strongly correlated (baseline values R2>0.5), the marker with the greatest univariate mediation was included. All analyses were intention-to-treat.
Results
IPE reduced MACE by 25% (HR (95% CI) = 0.75 (0.68, 0.83), p<0.0001). Treatment group differences on all potential mediators had p<0.05, and all but oxLDL were significantly related to MACE (p<0.05). Analyses of individual biomarkers showed EPA to be the strongest single mediator (Table 1). EPA, AA, and TG jointly mediated 78.9% of the IPE treatment effect, with EPA driving most of the mediation (57% as a single mediator). The marginal mediation by the remaining 3 biomarkers was 4.5% of the treatment effect, for total joint mediation of 83.4% (Figure 1).
Conclusion
In this mediation analysis of REDUCE-IT, most of the IPE benefit on MACE reduction was attributable to the two major mechanisms of the drug: (1) increasing EPA while reducing AA and, to a lesser extent, (2) reducing TG. The remainder of measured biomarker changes accounted for a minority of the benefit.
© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved.
Biomedicine & Pharmacotherapy
Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution
162:114629
2023 Apr 5
Aims: Inhalation of air pollution small particle matter (PM) is a leading cause of cardiovascular (CV) disease. Exposure to PMs causes endothelial cell (EC) dysfunction as evidenced by nitric oxide (NO) synthase uncoupling, vasoconstriction and inflammation. Eicosapentaenoic acid (EPA) has been shown to mitigate PM-induced adverse cardiac changes in patients receiving omega-3 fatty acid supplementation. We set out to determine the pro-inflammatory effects of multiple PMs (urban and fine) on pulmonary EC NO bioavailability and protein expression, and whether EPA restores EC function under these conditions.
Methods and results: We pretreated pulmonary ECs with EPA and then exposed them to urban or fine air pollution PMs. LC/MS-based proteomic analysis to assess relative expression levels. Expression of adhesion molecules was measured by immunochemistry. The ratio of NO to peroxynitrite (ONOO-) release, an indication of eNOS coupling, was measured using porphyrinic nanosensors following calcium stimulation. Urban/fine PMs also modulated 9/12 and 13/36 proteins, respectively, linked to platelet and neutrophil degranulation pathways and caused > 50% (p < 0.001) decrease in the stimulated NO/ONOO- release ratio. EPA treatment altered expression of proteins involved in these inflammatory pathways, including a decrease in peroxiredoxin-5 and an increase in superoxide dismutase-1. EPA also increased expression of heme oxygenase-1 (HMOX1), a cytoprotective protein, by 2.1-fold (p = 0.024). EPA reduced elevations in sICAM-1 levels by 22% (p < 0.01) and improved the NO/ONOO- release ratio by > 35% (p < 0.05).
Conclusion: These cellular changes may contribute to anti-inflammatory, cytoprotective and lipid changes associated with EPA treatment during air pollution exposure.
Keywords: Air pollution; Eicosapentaenoic acid; Proteomics; Pulmonary endothelial function.
Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
Biomedicine and Pharmacotherapy
Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution
162:114629
2023 Apr 5
Aims: Inhalation of air pollution small particle matter (PM) is a leading cause of cardiovascular (CV) disease. Exposure to PMs causes endothelial cell (EC) dysfunction as evidenced by nitric oxide (NO) synthase uncoupling, vasoconstriction and inflammation. Eicosapentaenoic acid (EPA) has been shown to mitigate PM-induced adverse cardiac changes in patients receiving omega-3 fatty acid supplementation. We set out to determine the pro-inflammatory effects of multiple PMs (urban and fine) on pulmonary EC NO bioavailability and protein expression, and whether EPA restores EC function under these conditions.
Methods and results: We pretreated pulmonary ECs with EPA and then exposed them to urban or fine air pollution PMs. LC/MS-based proteomic analysis to assess relative expression levels. Expression of adhesion molecules was measured by immunochemistry. The ratio of NO to peroxynitrite (ONOO-) release, an indication of eNOS coupling, was measured using porphyrinic nanosensors following calcium stimulation. Urban/fine PMs also modulated 9/12 and 13/36 proteins, respectively, linked to platelet and neutrophil degranulation pathways and caused > 50% (p < 0.001) decrease in the stimulated NO/ONOO- release ratio. EPA treatment altered expression of proteins involved in these inflammatory pathways, including a decrease in peroxiredoxin-5 and an increase in superoxide dismutase-1. EPA also increased expression of heme oxygenase-1 (HMOX1), a cytoprotective protein, by 2.1-fold (p = 0.024). EPA reduced elevations in sICAM-1 levels by 22% (p < 0.01) and improved the NO/ONOO- release ratio by > 35% (p < 0.05).
Conclusion: These cellular changes may contribute to anti-inflammatory, cytoprotective and lipid changes associated with EPA treatment during air pollution exposure.
Keywords: Air pollution; Eicosapentaenoic acid; Proteomics; Pulmonary endothelial function.
Current Atherosclerosis Reports
Role of omega-3 fatty acids in cardiovascular disease: the debate continues.
25(1):1-17
2023
ABSTRACT
Journal of the American Heart Association
Comparative effects of mineral oil, corn oil, eicosapentaenoic acid, and docosahexaenoic acid...
12(7):e029109
2023
ABSTRACT
Best Practice and Research Clinical Endocrinology and Metabolism
Omega-3-fatty acids: Do they prevent cardiovascular disease?
37(3):101681
2023
ABSTRACT
Metabolism: Clinical and Experimental
Rationale for different formulations of omega-3 fatty acids leading to differences in residual cardiovascular risk reduction.
130:155161
2022
ABSTRACT
Circulation
Effects of randomized treatment with icosapent ethyl and a mineral oil comparator on interleukin-1beta...
146(5):372-379
2022
ABSTRACT
Journal of the American College of Cardiology
Consistency of benefit of icosapent ethyl by background statin type in REDUCE-IT
79(2):220-222
2022
ABSTRACT
Pharmacology and Therapeutics
Cholesterol crystals and atherosclerotic plaque instability: therapeutic potential of eicosapentaenoic acid
240:108237
2022
ABSTRACT
Expert Opinion on Drug Safety
Icosapent ethyl: safely reducing cardiovascular risk in adults with elevated triglycerides.
21(1):31-42
2022
ABSTRACT
Journal of Clinical Lipidology
Benefits of icosapent ethyl for enhancing residual cardiovascular risk reduction.
16(4):389-402
2022
ABSTRACT
Best Practice and Research Clinical Endocrinology and Metabolism
Omega-3-fatty acids: Do they prevent cardiovascular disease?
101681
2022
ABSTRACT
European Heart Journal - Cardiovascular Pharmacotherapy
Potential effects of icosapent ethyl on cardiovascular outcomes in cigarette smokers: REDUCE-IT smoking.
2022
ABSTRACT
Prostaglandins, Leukotrienes and Essential Fatty Acids
A biological rationale for the disparate effects of omega-3 fatty acids on cardiovascular disease outcomes
182:102450
2022
ABSTRACT
Circulation
Letter by Sherratt Regarding Article…
146(20):e282-e283
2022
ABSTRACT
Current Atherosclerosis Reports
Role of omega-3 fatty acids in cardiovascular disease: the debate continues
2022
ABSTRACT
Prostaglandins, Leukotrienes and Essential Fatty Acids
Omega-3 and omega-6 fatty acids have distinct effects on endothelial fatty acid content and nitric oxide bioavailability
173:102337
2021
ABSTRACT
Circulation
Benefits of icosapent ethyl across the range of kidney function in patients with established cardiovascular disease or diabetes: REDUCE-IT RENAL
144(22):1750-1759
2021
ABSTRACT
EClinicalMedicine
Is there a role for omega-3 fatty acids in cardiovascular disease risk reduction?
39:101096
2021
ABSTRACT
American Journal of Medicine
Mechanistic insights from REDUCE-IT STRENGTHen the case against triglyceride lowering as a strategy for cardiovascular disease risk reduction
134(9):1085-1090
2021
ABSTRACT
Progress in Cardiovascular Diseases
The role of eicosapentaenoic acid in reducing important cardiovascular events, including coronary revascularization
69:3-10
2021
ABSTRACT
Journal of Lipid Research
EPA and DHA containing phospholipids have contrasting effects on membrane structure
62:100106
2021
ABSTRACT
Journal of the American College of Cardiology
Icosapent ethyl reduces ischemic events in patients with high triglycerides and low high-density lipoprotein cholesterol levels: REDUCE-IT high TC/low HDL-C analyses
77(18):155
2021
ABSTRACT
The Journal of Heart and Lung Transplantation
Kinetics of generic tacrolimus in heart transplantation: A cautionary note
40(7):569-572
2021
ABSTRACT
Biochimica et Biophysica Acta Biomembranes
Eicosapentaenoic acid (EPA) has optimal chain length and degree of unsaturation to inhibit oxidation of small dense LDL and membrane cholesterol domains as compared to related fatty acids in vitro
1862(7):183254
2020
ABSTRACT
British Medical Journal Open
Double-blind RCT of fish oil supplementation in pregnancy and lactation to improve the metabolic health in children of mothers with overweight or obesity during pregnancy: study protocol
10(12):e041015
2020
ABSTRACT
Arteriosclerosis, Thrombosis, and Vascular Biology
Emerging mechanisms of cardiovascular protection for the omega-3 fatty acid eicosapentaenoic acid
40(5):1135-1147
2020
ABSTRACT
Current Opinion in Lipidology
Are dietary fish oil supplements appropriate for dyslipidemia management? A review of the evidence
31(2):94-100
2020
ABSTRACT
Biomedicine and Pharmacotherapy
Metformin treatment decreases nitroxidative stress, restores nitric oxide bioavailability and endothelial function beyond glucose control
98:149-156
2018
ABSTRACT
Journal of the American College of Cardiology
Unmet need for adjunctive dyslipidemia therapy in hypertriglyceridemia management
72(3):330-343
2018
ABSTRACT
European Journal of Lipid Science and Technology
The nonlinear effect of alkyl chain length in the membrane interactions of phenolipids: Evidence by X-ray diffraction analysis
119(8):1600397
2017
ABSTRACT
Cardiorenal Medicine
Eicosapentaenoic acid as a potential therapeutic approach to reduce cardiovascular risk in patients with end-stage renal disease on hemodialysis: A review
8(1):18-30
2017
ABSTRACT
Lipids in Health and Disease
Prescription omega-3 fatty acid products containing highly purified eicosapentaenoic acid (EPA)
16(1):23
2017
ABSTRACT
Postgraduate Medicine
Can pleiotropic effects of eicosapentaenoic acid (EPA) impact residual cardiovascular risk?
6-Jan
2017
ABSTRACT
Biochimica et Biophysica Acta
Eicosapentaenoic acid reduces membrane fluidity, inhibits cholesterol domain formation, and normalizes bilayer width in atherosclerotic-like model membranes
1858(12):3131-3140
2016
ABSTRACT
Journal of Cardiovascular Pharmacology
Eicosapentaenoic acid inhibits oxidation of ApoB-containing lipoprotein particles of different size in vitro when administered alone or in combination with atorvastatin active metabolite compared with other triglyceride-lowering agents
68(1):33-40
2016
ABSTRACT
Trends in Pharmacological Sciences
Generics substitution, bioequivalence standards, and international oversight: complex issues facing the FDA
37(3):184-191
2016
ABSTRACT
American Journal of Cardiology
The Editor’s Round Table: Current Perspectives on Triglycerides and Atherosclerosis
117(10):1697-1702
2016
ABSTRACT
Advances in Experimental Medicine and Biology
Characterization of cholesterol crystalline domains in model and biological membranes using X-ray diffraction
842:231-245
2015
ABSTRACT
Atherosclerosis
Biologic plausibility, cellular effects, and molecular mechanisms of eicosapentaenoic acid (EPA) in atherosclerosis
242(1):357-366
2015
ABSTRACT
Journal of Physiology and Pharmacology
Atorvastatin enhanced nitric oxide release and reduced blood pressure, nitroxidative stress and rantes levels in hypertensive rats with diabetes
66(1):65-72
2015
ABSTRACT
Biochimica et Biophysica Acta
Eicosapentaenoic acid inhibits glucose-induced membrane cholesterol crystalline domain formation through a potent antioxidant mechanism
1848(2):502-509
2015
ABSTRACT
American Journal of Hypertension
Amlodipine increased endothelial nitric oxide and decreased nitroxidative stress disproportionately to blood pressure changes
27(3):482-488
2014
ABSTRACT
BioMed Central Pharmacology and Toxicology
The favorable kinetics and balance of nebivolol-stimulated nitric oxide and peroxynitrite release in human endothelial cells
14:48
2013
ABSTRACT
Journal of Cardiovascular Pharmacology
Atorvastatin active metabolite inhibits oxidative modification of small dense low-density lipoprotein
62(2):160-166
2013
ABSTRACT
Investigative Ophthalmology and Visual Science
1,2-Naphthoquinone stimulates lipid peroxidation and cholesterol domain formation in model membranes
54(12):7189-7197
2013
ABSTRACT
British Journal of Pharmacology
Effects of angiotensin receptor blockers on endothelial nitric oxide release: the role of eNOS variants
74(1):141-146
2012
ABSTRACT
Journal of Cardiovascular Pharmacology
Dipeptidyl peptidase-4 inhibition with saxagliptin enhanced nitric oxide release and reduced blood pressure and sICAM-1 levels in hypertensive rats
60(5):467-473
2012
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Feb 17, 2024
DOI: 10.1093/cvr/cvad188
Aggarwal R, Bhatt DL, Steg PG, Miller M, Brinton EA, Dunbar RL, Ketchum SB, Tardif JC, Martens FMAC, Ballantyne CM, Szarek M, Mason RP
Figures 1-5 by Elucida Communications
Aggarwal R, Bhatt DL, Steg PG, Miller M, Brinton EA, Dunbar RL, Ketchum SB, Tardif JC, Martens FMAC, Ballantyne CM, Szarek M, Mason RP
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