Impact of Oxidative Stress on Arterial Elasticity in Patients with Atherosclerosis

Kals, Jaak; Kampus, Priit; Kals, Mart; Zilmer, Kersti; Kullisaar, Tiiu; Teesalu, Rein; Pulges, Andres; Zilmer, Mihkel

doi:10.1016/j.amjhyper.2006.02.003

Cited by 50 publications

(42 citation statements)

References 30 publications

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“…25 Previously, we have demonstrated the relationship between urinary 8-iso-prostaglandin F 2a concentration and the indices of arterial elasticity in patients with PAD. 10 In the present study, we extended our previous findings by demonstrating an independent association between oxLDL and aPWV, the 'gold standard' measure of arterial stiffness in the patients with PAD and in healthy subjects. It may be possible that high-grade oxidative stress stimulates hypertrophy of vascular smooth cells, which would lead to an increase in arterial stiffness.…”

Section: Discussionsupporting

confidence: 71%

“…Profound oxidative stress contributes to endothelial dysfunction 9 and arterial stiffening. 10,11 Oxidized lowdensity lipoprotein (oxLDL) is a marker of oxidative stress, which is associated with the presence of atherosclerotic lesions in different parts of the vasculature system. 11 Angiographic score (ASc) assessed by digital subtraction angiography provides information about distribution and severity of atherosclerotic lesions in the arteries of the lower extremities.…”

Section: Introductionmentioning

confidence: 99%

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Structural and biochemical characteristics of arterial stiffness in patients with atherosclerosis and in healthy subjects

et al. 2012

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Arterial stiffness is an independent predictor of vascular morbidity and mortality in patients with atherosclerosis. Angiographic score (ASc) reflects severity of atherosclerosis in patients with peripheral arterial disease (PAD). Osteopontin (OPN) and oxidized low-density lipoprotein (oxLDL) are involved in the pathogenesis of atherosclerosis. The aim of the present study was to evaluate the association between arterial stiffness, ASc, serum OPN and oxLDL in patients with symptomatic PAD, and in clinically healthy subjects. We studied 79 men with symptomatic PAD (mean age 64 ± 7 years) and 84 healthy men (mean age 63 ± 8 years). Calculation of the ASc was based on severity and location of atherosclerotic lesions in the arteries of the lower extremities. Aortic pulse wave velocity (aPWV) was evaluated by applanation tonometry using the Sphygmocor device. Serum OPN and oxLDL levels were determined by enzyme-linked immunosorbent assay. The aPWV (10 ± 2.4 VS. 8.4 ± 1.7 (m s À1 ); Po0.001), ) VS. 54.8 (47.7-67.9) (ng ml À1 ); Po0.001) and oxLDL (67 (52.5-93.5) VS. 47.5 (37-65.5); Po0.001) were different for the patients and for the controls. In multiple regression models, aPWV was independently determined by ASc, log-OPN, log-oxLDL and estimated glomerular filtration rate in the patients (R 2 ¼ 0.44; Po0.001) and by log-OPN, log-oxLDL, age and heart rate in the controls (R 2 ¼ 0.38; Po0.001). The independent relationship of a PWV with serum levels of OPN and oxLDL in the patients with PAD and in the controls indicates that OPN and oxLDL might influence arterial stiffening in patients with atherosclerosis and in clinically healthy subjects.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Structural and biochemical characteristics of arterial stiffness in patients with atherosclerosis and in healthy subjects

et al. 2012

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“…OxS leads to an excess of oxLDL and the higher levels of the circulating oxLDL, even more than LDL-Chol, are strongly associated with the increased incidence of metabolic syndrome in people who are young and otherwise healthy [25]. OxLDL is an important determinant of structural changes of the arteries even in asymptomatic persons [13,26]. Recent data suggest that an increased production of atherogenic and inflammatory oxLDL within the vessel wall suppresses several immunity-related cells, including regulatory T cells [27] which normally exert antiatherogenic and anti allergic effects.…”

Section: Discussionmentioning

confidence: 99%

“…It is of human origin [9] and a safety-proven probiotic exhibiting both antimicrobial and antioxidative benefits under different in vitro and in vivo conditions [10][11][12] and having a history of safe use in foodstuffs, especially in kefir, in Finland and the Baltic countries. Encouraged by the results of our previous trials with LfME-3 [1,2,10,11,[13][14][15][16] we aimed to carry out a study to evaluate the effects of kefir enriched with probiotic L. fermentum ME-3 on postprandial oxidative stress, postprandial lipemic response and blood lipoprotein status when added to an ordinary diet.…”

Section: Introductionmentioning

confidence: 99%

An antioxidant probiotic reduces postprandial lipemia and oxidative stress

Kullisaar¹,

Shepetova

Zilmer³

et al. 2010

Open Life Sciences

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Reducing postprandial oxidative stress (OxS), decreasing postprandial blood triglyceride level (TG) and improving lipoprotein status is likely to have a preventive impact on the development of cardiovascular disease (CVD). Previously we have shown that the antioxidant probiotic Lactobacillus fermentum ME-3 (DSM14241) is characterized by antiatherogenic effects. This randomized double-blind placebo-controlled study evaluated the influence of kefir enriched with an antioxidative probiotic L. fermentum ME-3 (LfKef) on postprandial OxS, blood TG response and lipoprotein status. 100 clinically healthy subjects were recruited into the study. Blood parameters of postprandial OxS, TG and lipoprotein status were determined by oxidized LDL, baseline diene conjugation in LDL (BDC-LDL), oxidized LDL complex with beta-2 glycoprotein (Beta2-GPI-oxLDL), paraoxonase (PON) activity, LDL-Chol, HDL-Chol and TG. To evaluate general body postprandial OxS-load we measured 8-isoprostanes (8-EPI) in the urine. Consumption of LfKef significantly reduced the postprandial level of oxidized LDL, BDC-LDL, Beta2-GPI-oxLDL, urinary 8-isoprostanes and postprandial TG and caused a significant increase in HDL-Chol and PON activity. This is the first evidence that kefir enriched with an antioxidant probiotic may have a positive effect on both postprandial OxS and TG response as well as on lipoprotein status.

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“…[26][27][28] For example, it has been reported that circulating levels of 8-isoprostane were an independent risk factor associated with coronary artery disease in a Chinese population (odds ratio 2.47, P < 0.001), 26) and were associated with peripheral artery disease. 27,28) In this study, we have shown that valsartan therapy decreased urine 8-isoprostane levels up to 12 months in type 2 diabetic subjects with hypertension, despite the fact that the blood pressure levels were unchanged. Although carotid artery mean IMT did not decrease after 12 months of treatment in this study, there is a possibility that valsartan treatment of a longer period might inhibit the progression of atherosclerosis via suppression of oxidative stress in type 2 diabetic subjects.…”

Section: Discussionmentioning

confidence: 99%

Effects of 12-Month Valsartan Therapy on Glycation and Oxidative Stress Markers in Type 2 Diabetic Subjects With Hypertension

et al. 2008

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SUMMARYAlthough it has been reported that angiotensin II receptor blockers inhibited the formation and accumulation of advanced glycation endproducts (AGEs) in vitro and in vivo, whether they can do so clinically is not clear. We investigated the effects of 12-month valsartan therapy on various markers of inflammation, glycation, and oxidation in type 2 diabetic subjects with hypertension.We started 40 mg/day valsartan treatment in 15 type 2 diabetic patients with hypertension. In 6 patients, the dose of valsartan was increased to 80 mg/day after 6 months and maintained until 12 months. Metabolic parameters including BMI and serum high molecular weight (HMW)-adiponectin, high-sensitivity C-reactive protein (hs-CRP) as an inflammation marker, AGEs, paraoxonase activity, platelet-activating factor (PAF)-acetylhydrolase activity, and urine 8-isoprostane levels were measured at baseline and after 6 and 12 months of treatment. Urine microalbumin level and carotid artery intimamedia thickness (IMT) were also measured.Even after valsartan therapy, the blood pressure levels of the patients were not decreased significantly. Serum AGEs and urine 8-isoprostane levels decreased at both 6 and 12 months (P < 0.05 for both), although other metabolic and oxidative markers were unchanged. Though urine microalbumin levels tended to be decreased after 6 and 12 months of valsartan treatment, the changes were not significant. Mean IMT at 12 months was not changed from the baseline value. In conclusion, the findings suggest that treatment with valsartan, even at a low dose, may ameliorate some glycation and oxidative stress markers independently of an effect on blood pressure in hypertensive type 2 diabetic subjects. (Int Heart J 2008; 49: 681-689)

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Impact of Oxidative Stress on Arterial Elasticity in Patients with Atherosclerosis

Abstract: The possible link between arterial elasticity and F2-IsoPs in patients with PAD suggests that oxidative modifications may be involved in alterations of arterial elastic properties in atherosclerosis.

Cited by 50 publications

References 30 publications

Structural and biochemical characteristics of arterial stiffness in patients with atherosclerosis and in healthy subjects

Structural and biochemical characteristics of arterial stiffness in patients with atherosclerosis and in healthy subjects

An antioxidant probiotic reduces postprandial lipemia and oxidative stress

Effects of 12-Month Valsartan Therapy on Glycation and Oxidative Stress Markers in Type 2 Diabetic Subjects With Hypertension

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