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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

ABSTRACT

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

ABSTRACT

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

ABSTRACT

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

REDUCE-IT, biomarkers, and confirmation bias: are we missing the forest for the trees?

31(15):e113-e114

2024 Nov 11

ABSTRACT

European Journal of Preventive Cardiology

Omega-3 fatty acids for Cardiovascular Event Lowering

31(8):1005-1014

2024 Jun 3

ABSTRACT

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

ABSTRACT

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

ABSTRACT

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

ABSTRACT

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

ABSTRACT

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

ABSTRACT

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

ABSTRACT

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

ABSTRACT

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

ABSTRACT

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

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Journal of the American Heart Association

Comparative effects of mineral oil, corn oil, eicosapentaenoic acid, and docosahexaenoic acid...

12(7):e029109

2023

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Best Practice and Research Clinical Endocrinology and Metabolism

Omega-3-fatty acids: Do they prevent cardiovascular disease?

37(3):101681

2023

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Metabolism: Clinical and Experimental

Rationale for different formulations of omega-3 fatty acids leading to differences in residual cardiovascular risk reduction.

130:155161

2022

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Circulation

Effects of randomized treatment with icosapent ethyl and a mineral oil comparator on interleukin-1beta...

146(5):372-379

2022

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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

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Pharmacology and Therapeutics

Cholesterol crystals and atherosclerotic plaque instability: therapeutic potential of eicosapentaenoic acid

240:108237

2022

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Expert Opinion on Drug Safety

Icosapent ethyl: safely reducing cardiovascular risk in adults with elevated triglycerides.

21(1):31-42

2022

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Journal of Clinical Lipidology

Benefits of icosapent ethyl for enhancing residual cardiovascular risk reduction.

16(4):389-402

2022

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Best Practice and Research Clinical Endocrinology and Metabolism

Omega-3-fatty acids: Do they prevent cardiovascular disease?

101681

2022

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European Heart Journal - Cardiovascular Pharmacotherapy

Potential effects of icosapent ethyl on cardiovascular outcomes in cigarette smokers: REDUCE-IT smoking.

2022

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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

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Circulation

Letter by Sherratt Regarding Article…

146(20):e282-e283

2022

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Current Atherosclerosis Reports

Role of omega-3 fatty acids in cardiovascular disease: the debate continues

2022

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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

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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

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EClinicalMedicine

Is there a role for omega-3 fatty acids in cardiovascular disease risk reduction?

39:101096

2021

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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

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Progress in Cardiovascular Diseases

The role of eicosapentaenoic acid in reducing important cardiovascular events, including coronary revascularization

69:3-10

2021

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Journal of Lipid Research

EPA and DHA containing phospholipids have contrasting effects on membrane structure

62:100106

2021

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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

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The Journal of Heart and Lung Transplantation

Kinetics of generic tacrolimus in heart transplantation: A cautionary note

40(7):569-572

2021

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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

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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

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Arteriosclerosis, Thrombosis, and Vascular Biology

Emerging mechanisms of cardiovascular protection for the omega-3 fatty acid eicosapentaenoic acid

40(5):1135-1147

2020

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Current Opinion in Lipidology

Are dietary fish oil supplements appropriate for dyslipidemia management? A review of the evidence

31(2):94-100

2020

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Biomedicine and Pharmacotherapy

Metformin treatment decreases nitroxidative stress, restores nitric oxide bioavailability and endothelial function beyond glucose control

98:149-156

2018

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Journal of the American College of Cardiology

Unmet need for adjunctive dyslipidemia therapy in hypertriglyceridemia management

72(3):330-343

2018

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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

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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

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Lipids in Health and Disease

Prescription omega-3 fatty acid products containing highly purified eicosapentaenoic acid (EPA)

16(1):23

2017

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Postgraduate Medicine

Can pleiotropic effects of eicosapentaenoic acid (EPA) impact residual cardiovascular risk?

6-Jan

2017

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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

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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

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Trends in Pharmacological Sciences

Generics substitution, bioequivalence standards, and international oversight: complex issues facing the FDA

37(3):184-191

2016

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American Journal of Cardiology

The Editor’s Round Table: Current Perspectives on Triglycerides and Atherosclerosis

117(10):1697-1702

2016

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Advances in Experimental Medicine and Biology

Characterization of cholesterol crystalline domains in model and biological membranes using X-ray diffraction

842:231-245

2015

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Atherosclerosis

Biologic plausibility, cellular effects, and molecular mechanisms of eicosapentaenoic acid (EPA) in atherosclerosis

242(1):357-366

2015

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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

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Biochimica et Biophysica Acta

Eicosapentaenoic acid inhibits glucose-induced membrane cholesterol crystalline domain formation through a potent antioxidant mechanism

1848(2):502-509

2015

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American Journal of Hypertension

Amlodipine increased endothelial nitric oxide and decreased nitroxidative stress disproportionately to blood pressure changes

27(3):482-488

2014

ABSTRACT

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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

View

Journal of Cardiovascular Pharmacology

Atorvastatin active metabolite inhibits oxidative modification of small dense low-density lipoprotein

62(2):160-166

2013

ABSTRACT

View

Investigative Ophthalmology and Visual Science

1,2-Naphthoquinone stimulates lipid peroxidation and cholesterol domain formation in model membranes

54(12):7189-7197

2013

ABSTRACT

View

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

View

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

ABSTRACT

View

Journal of Atherosclerosis and Thrombosis

Effect of enhanced glycemic control with saxagliptin on endothelial nitric oxide release and CD40 levels in obese rats

18(9):774-783

2011

ABSTRACT

View

Journal of Atherosclerosis and Thrombosis

Inflammation and the development of atherosclerosis

18(5):351-358

2011

ABSTRACT

View

Therapy

Combined use of calcium channel blockers and inhibitors of the renin-angiotensin system for treating hypertension

8(3):247-260

2011

ABSTRACT

View

Vascular Health and Risk Management

Optimal therapeutic strategy for treating patients with hypertension and atherosclerosis: focus on olmesartan medoxomil

7:405-416

2011

ABSTRACT

View

Molecular Genetics and Metabolism

Alterations in membrane caveolae and BKCa channel activity in skin fibroblasts in Smith-Lemli-Opitz syndrome

104(3):346-355

2011

ABSTRACT

View

Current Cardiology Reports

Advances in pharmacologic modulation of nitric oxide in hypertension

12(6):472-480

2010

ABSTRACT

View

Thrombosis Research

Novel astaxanthin prodrug (CDX-085) attenuates thrombosis in a mouse model

126(4):299-305

2010

ABSTRACT

View

Journal of Cardiovascular Pharmacology

Evolving mechanisms of action of beta blockers: focus on nebivolol

54(2):123-128

2009

ABSTRACT

View

Biochimica et Biophysica Acta

Glucose promotes membrane cholesterol crystalline domain formation by lipid peroxidation

1788(6):1398-1403

2009

ABSTRACT

View

American Journal of Hypertension

Loss of arterial and renal nitric oxide bioavailability in hypertensive rats with diabetes: effect of beta-blockers

22(11):1160-1166

2009

ABSTRACT

View

Journal of Cardiovascular Pharmacology

Effect of beta-blockers on endothelial function during biological aging: a nanotechnological approach

51(2):208-215

2008

ABSTRACT

View

Pharmaceutical Research

Synergistic effect of amlodipine and atorvastatin in reversing LDL-induced endothelial dysfunction

25(8):1798-1806

2008

ABSTRACT

View

Drugs

Scientific rationale for combination of a calcium channel antagonist and an HMG-CoA reductase inhibitor: a new approach to risk factor management

68(7):885-900

2008

ABSTRACT

View

American Journal of Hypertension

Effects of calcium channel and renin-angiotensin system blockade on intravascular and neurohormonal mechanisms of hypertensive vascular disease

21(10):1076-1085

2008

ABSTRACT

View

Journal of the American College of Cardiology

Circulating lipid hydroperoxides predict cardiovascular events in patients with stable coronary artery disease: the PREVENT study

51(12):1196-1202

2008

ABSTRACT

View

The American Journal of Cardiology

Biologic activity of carotenoids related to distinct membrane physicochemical interactions

101(10A):20D-29D

2008

ABSTRACT

View

The Journal of Biological Chemistry

Regulation of the gating of BKCa channel by lipid bilayer thickness

282(10):7276-7286

2007

ABSTRACT

View

Subcellular Biochemistry

A biological rationale for the cardiotoxic effects of rofecoxib: comparative analysis with other COX-2 selective agents and NSAIDs

42:175-190

2007

ABSTRACT

View

Experimental Eye Research

Status of caveolin-1 in various membrane domains of the bovine lens

85(4):473-481

2007

ABSTRACT

View

Biochimica et Biophysica Acta

Differential effects of carotenoids on lipid peroxidation due to membrane interactions: X-ray diffraction analysis

1768(1):167-174

2007

ABSTRACT

View

Journal of Lipid Research

A membrane defect in the pathogenesis of the Smith-Lemli-Opitz syndrome

47(1):134-143

2006

ABSTRACT

View

Journal of Cardiovascular Pharmacology

Effect of nebivolol on endothelial nitric oxide and peroxynitrite release in hypertensive animals: Role of antioxidant activity

48(1):862-869

2006

ABSTRACT

View

The Journal of Biological Chemistry

Active metabolite of atorvastatin inhibits membrane cholesterol domain formation by an antioxidant mechanism

281(14):9337-9345

2006

ABSTRACT

View

Journal of Clinical Hypertension

Targeting nitric oxide with drug therapy

8(12 Suppl 4):40-52

2006

ABSTRACT

View

Journal of Cardiovascular Pharmacology

Rofecoxib increases susceptibility of human LDL and membrane lipids to oxidative damage: a mechanism of cardiotoxicity

47 Suppl 1:S7-14

2006

ABSTRACT

View

Journal of Clinical Hypertension

Nitric oxide mechanisms in the pathogenesis of global risk

8(8 Suppl 2):31-38

2006

ABSTRACT

View

The American Journal of Cardiology

Molecular basis of differences among statins and a comparison with antioxidant vitamins

98(11A):34P-41P

2006

ABSTRACT

View

The American Journal of Cardiology

Intermolecular differences of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors contribute to distinct pharmacologic and pleiotropic actions

96(5A):11F-23F

2005 Sep 5

ABSTRACT

The Journal of Biological Chemistry

Lipid peroxidation induces cholesterol domain formation in model membranes

280(47):39380-39387

2005

ABSTRACT

View

Circulation

Nebivolol reduces nitroxidative stress and restores nitric oxide bioavailability in endothelium of black Americans

112(24):3795-3801

2005

ABSTRACT

View

Current Drug Targets. Cardiovascular and Haematological Disorders

A rationale for combined therapy with a calcium channel blocker and a statin: evaluation of basic and clinical evidence

5(6):489-501

2005

ABSTRACT

View

The American Journal of Medicine

A rationale for combination therapy in risk factor management: a mechanistic perspective

118 Suppl 12A:54-61

2005

ABSTRACT

View
  • Feb 17, 2024

    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
    CR Do patients benefit from omega-3 fatty acids.png

    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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Publications Database List

Cardiovascular Outcomes with Icosapent Ethyl by Baseline Low‐Density Lipoprotein Cholesterol: A Secondary Analysis of the REDUCE‐IT Randomized Trial

Journal of the American Heart Association

Effect of sotagliflozin on major adverse cardiovascular events: a prespecified secondary analysis of the SCORED a randomised trial

The Lancet Diabetes & Endocrinology

“A Time to Tear Down and a Time to Mend” – The Role of Eicosanoids in Atherosclerosis

Arteriosclerosis, Thrombosis, and Vascular Biology

REDUCE-IT, biomarkers, and confirmation bias: are we missing the forest for the trees?

European Journal of Preventive Cardiology

Omega-3 fatty acids for Cardiovascular Event Lowering

European Journal of Preventive Cardiology

Eicosapentaenoic acid improves endothelial nitric oxide bioavailability via changes in protein expression during inflammation

Journal of the American Heart Association

Do Patients Benefit from Omega-3 Fatty Acids?

Cardiovascular Research

Do patients benefit from omega-3 fatty acids?

Cardiovascular Research

Lipoprotein(a) Blood Levels and Cardiovascular Risk Reduction with Icosapent Ethyl

Journal of the American College of Cardiology

Omega-3 Fatty Acids Influence Membrane Cholesterol Distribution and Crystal Formation in Models of Atherosclerosis

Cholesterol Crystals in Atherosclerosis and Other Related Diseases

Eicosapentaenoic acid, arachidonic acid, and triglyceride levels mediate most of the benefit of icosapent ethyl in REDUCE-IT

European Heart Journal

Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution

Biomedicine & Pharmacotherapy

Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution

Biomedicine and Pharmacotherapy

Role of omega-3 fatty acids in cardiovascular disease: the debate continues.

Current Atherosclerosis Reports

Comparative effects of mineral oil, corn oil, eicosapentaenoic acid, and docosahexaenoic acid...

Journal of the American Heart Association

Omega-3-fatty acids: Do they prevent cardiovascular disease?

Best Practice and Research Clinical Endocrinology and Metabolism

Rationale for different formulations of omega-3 fatty acids leading to differences in residual cardiovascular risk reduction.

Metabolism: Clinical and Experimental

Effects of randomized treatment with icosapent ethyl and a mineral oil comparator on interleukin-1beta...

Circulation

Consistency of benefit of icosapent ethyl by background statin type in REDUCE-IT

Journal of the American College of Cardiology

Cholesterol crystals and atherosclerotic plaque instability: therapeutic potential of eicosapentaenoic acid

Pharmacology and Therapeutics

Icosapent ethyl: safely reducing cardiovascular risk in adults with elevated triglycerides.

Expert Opinion on Drug Safety

Benefits of icosapent ethyl for enhancing residual cardiovascular risk reduction.

Journal of Clinical Lipidology

Omega-3-fatty acids: Do they prevent cardiovascular disease?

Best Practice and Research Clinical Endocrinology and Metabolism

Potential effects of icosapent ethyl on cardiovascular outcomes in cigarette smokers: REDUCE-IT smoking.

European Heart Journal - Cardiovascular Pharmacotherapy

A biological rationale for the disparate effects of omega-3 fatty acids on cardiovascular disease outcomes

Prostaglandins, Leukotrienes and Essential Fatty Acids

Letter by Sherratt Regarding Article…

Circulation

Role of omega-3 fatty acids in cardiovascular disease: the debate continues

Current Atherosclerosis Reports

Omega-3 and omega-6 fatty acids have distinct effects on endothelial fatty acid content and nitric oxide bioavailability

Prostaglandins, Leukotrienes and Essential Fatty Acids

Benefits of icosapent ethyl across the range of kidney function in patients with established cardiovascular disease or diabetes: REDUCE-IT RENAL

Circulation

Is there a role for omega-3 fatty acids in cardiovascular disease risk reduction?

EClinicalMedicine

Mechanistic insights from REDUCE-IT STRENGTHen the case against triglyceride lowering as a strategy for cardiovascular disease risk reduction

American Journal of Medicine

The role of eicosapentaenoic acid in reducing important cardiovascular events, including coronary revascularization

Progress in Cardiovascular Diseases

EPA and DHA containing phospholipids have contrasting effects on membrane structure

Journal of Lipid Research

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

Journal of the American College of Cardiology

Kinetics of generic tacrolimus in heart transplantation: A cautionary note

The Journal of Heart and Lung Transplantation

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

Biochimica et Biophysica Acta Biomembranes

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

British Medical Journal Open

Emerging mechanisms of cardiovascular protection for the omega-3 fatty acid eicosapentaenoic acid

Arteriosclerosis, Thrombosis, and Vascular Biology

Are dietary fish oil supplements appropriate for dyslipidemia management? A review of the evidence

Current Opinion in Lipidology

Metformin treatment decreases nitroxidative stress, restores nitric oxide bioavailability and endothelial function beyond glucose control

Biomedicine and Pharmacotherapy

Unmet need for adjunctive dyslipidemia therapy in hypertriglyceridemia management

Journal of the American College of Cardiology

The nonlinear effect of alkyl chain length in the membrane interactions of phenolipids: Evidence by X-ray diffraction analysis

European Journal of Lipid Science and Technology

Eicosapentaenoic acid as a potential therapeutic approach to reduce cardiovascular risk in patients with end-stage renal disease on hemodialysis: A review

Cardiorenal Medicine

Prescription omega-3 fatty acid products containing highly purified eicosapentaenoic acid (EPA)

Lipids in Health and Disease

Can pleiotropic effects of eicosapentaenoic acid (EPA) impact residual cardiovascular risk?

Postgraduate Medicine

Eicosapentaenoic acid reduces membrane fluidity, inhibits cholesterol domain formation, and normalizes bilayer width in atherosclerotic-like model membranes

Biochimica et Biophysica Acta

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

Journal of Cardiovascular Pharmacology

Generics substitution, bioequivalence standards, and international oversight: complex issues facing the FDA

Trends in Pharmacological Sciences

The Editor’s Round Table: Current Perspectives on Triglycerides and Atherosclerosis

American Journal of Cardiology

Characterization of cholesterol crystalline domains in model and biological membranes using X-ray diffraction

Advances in Experimental Medicine and Biology

Biologic plausibility, cellular effects, and molecular mechanisms of eicosapentaenoic acid (EPA) in atherosclerosis

Atherosclerosis

Atorvastatin enhanced nitric oxide release and reduced blood pressure, nitroxidative stress and rantes levels in hypertensive rats with diabetes

Journal of Physiology and Pharmacology

Eicosapentaenoic acid inhibits glucose-induced membrane cholesterol crystalline domain formation through a potent antioxidant mechanism

Biochimica et Biophysica Acta

Amlodipine increased endothelial nitric oxide and decreased nitroxidative stress disproportionately to blood pressure changes

American Journal of Hypertension

The favorable kinetics and balance of nebivolol-stimulated nitric oxide and peroxynitrite release in human endothelial cells

BioMed Central Pharmacology and Toxicology

Atorvastatin active metabolite inhibits oxidative modification of small dense low-density lipoprotein

Journal of Cardiovascular Pharmacology

1,2-Naphthoquinone stimulates lipid peroxidation and cholesterol domain formation in model membranes

Investigative Ophthalmology and Visual Science

Effects of angiotensin receptor blockers on endothelial nitric oxide release: the role of eNOS variants

British Journal of Pharmacology

Dipeptidyl peptidase-4 inhibition with saxagliptin enhanced nitric oxide release and reduced blood pressure and sICAM-1 levels in hypertensive rats

Journal of Cardiovascular Pharmacology

Effect of enhanced glycemic control with saxagliptin on endothelial nitric oxide release and CD40 levels in obese rats

Journal of Atherosclerosis and Thrombosis

Inflammation and the development of atherosclerosis

Journal of Atherosclerosis and Thrombosis

Combined use of calcium channel blockers and inhibitors of the renin-angiotensin system for treating hypertension

Therapy

Optimal therapeutic strategy for treating patients with hypertension and atherosclerosis: focus on olmesartan medoxomil

Vascular Health and Risk Management

Alterations in membrane caveolae and BKCa channel activity in skin fibroblasts in Smith-Lemli-Opitz syndrome

Molecular Genetics and Metabolism

Advances in pharmacologic modulation of nitric oxide in hypertension

Current Cardiology Reports

Novel astaxanthin prodrug (CDX-085) attenuates thrombosis in a mouse model

Thrombosis Research

Evolving mechanisms of action of beta blockers: focus on nebivolol

Journal of Cardiovascular Pharmacology

Glucose promotes membrane cholesterol crystalline domain formation by lipid peroxidation

Biochimica et Biophysica Acta

Loss of arterial and renal nitric oxide bioavailability in hypertensive rats with diabetes: effect of beta-blockers

American Journal of Hypertension

Effect of beta-blockers on endothelial function during biological aging: a nanotechnological approach

Journal of Cardiovascular Pharmacology

Synergistic effect of amlodipine and atorvastatin in reversing LDL-induced endothelial dysfunction

Pharmaceutical Research

Scientific rationale for combination of a calcium channel antagonist and an HMG-CoA reductase inhibitor: a new approach to risk factor management

Drugs

Effects of calcium channel and renin-angiotensin system blockade on intravascular and neurohormonal mechanisms of hypertensive vascular disease

American Journal of Hypertension

Circulating lipid hydroperoxides predict cardiovascular events in patients with stable coronary artery disease: the PREVENT study

Journal of the American College of Cardiology

Biologic activity of carotenoids related to distinct membrane physicochemical interactions

The American Journal of Cardiology

Regulation of the gating of BKCa channel by lipid bilayer thickness

The Journal of Biological Chemistry

A biological rationale for the cardiotoxic effects of rofecoxib: comparative analysis with other COX-2 selective agents and NSAIDs

Subcellular Biochemistry

Status of caveolin-1 in various membrane domains of the bovine lens

Experimental Eye Research

Differential effects of carotenoids on lipid peroxidation due to membrane interactions: X-ray diffraction analysis

Biochimica et Biophysica Acta

A membrane defect in the pathogenesis of the Smith-Lemli-Opitz syndrome

Journal of Lipid Research

Effect of nebivolol on endothelial nitric oxide and peroxynitrite release in hypertensive animals: Role of antioxidant activity

Journal of Cardiovascular Pharmacology

Active metabolite of atorvastatin inhibits membrane cholesterol domain formation by an antioxidant mechanism

The Journal of Biological Chemistry

Targeting nitric oxide with drug therapy

Journal of Clinical Hypertension

Rofecoxib increases susceptibility of human LDL and membrane lipids to oxidative damage: a mechanism of cardiotoxicity

Journal of Cardiovascular Pharmacology

Nitric oxide mechanisms in the pathogenesis of global risk

Journal of Clinical Hypertension

Molecular basis of differences among statins and a comparison with antioxidant vitamins

The American Journal of Cardiology

Intermolecular differences of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors contribute to distinct pharmacologic and pleiotropic actions

The American Journal of Cardiology

Lipid peroxidation induces cholesterol domain formation in model membranes

The Journal of Biological Chemistry

Nebivolol reduces nitroxidative stress and restores nitric oxide bioavailability in endothelium of black Americans

Circulation

A rationale for combined therapy with a calcium channel blocker and a statin: evaluation of basic and clinical evidence

Current Drug Targets. Cardiovascular and Haematological Disorders

A rationale for combination therapy in risk factor management: a mechanistic perspective

The American Journal of Medicine

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